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The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options
Open accessAbstract
Parkinson's disease is a common neurodegenerative disorder in which gastrointestinal symptoms may appear prior to motor symptoms. The gut microbiota of patients with Parkinson's disease shows unique changes, which may be used as early biomarkers of disease. Alterations in the gut microbiota composition may be related to the cause or effect of motor or non-motor symptoms, but the specific pathogenic mechanisms are unclear. The gut microbiota and its metabolites have been suggested to be involved in the pathogenesis of Parkinson's disease by regulating neuroinflammation, barrier function and neurotransmitter activity. There is bidirectional communication between the enteric nervous system and the CNS, and the microbiota-gut-brain axis may provide a pathway for the transmission of α-synuclein. We highlight recent discoveries about alterations to the gut microbiota in Parkinson's disease and focus on current mechanistic insights into the microbiota-gut-brain axis in disease pathophysiology. Moreover, we discuss the interactions between the production and transmission of α-synuclein and gut inflammation and neuroinflammation. In addition, we draw attention to diet modification, the use of probiotics and prebiotics and faecal microbiota transplantation as potential therapeutic approaches that may lead to a new treatment paradigm for Parkinson's disease.
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Every source the paper cites for this claim was checked and supports it.
In the paper
“which can maintain and protect the normal dopamine function of the substantia nigra and striatum by changing mitochondrial respiration and reactive oxygen species production.41”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [41] Andrews, 2009, Ghrelin promotes and protects nigrostriatal dopamine function via a UCP2-dependent mitochondrial mechanism, J Neurosci source
The Discussion reports that ghrelin promotes nigrostriatal dopamine output and protects dopamine neurons in a mouse model of Parkinson’s disease through UCP2-dependent mitochondrial respiration. The section “Ghrelin controls ROS in a UCP2-dependent manner in the SN” also reports that ghrelin lowers ROS in substantia nigra dopamine neurons of wild-type mice. These passages support the claim’s paraphrase, within the study’s mouse-model context. (LLM, conf=0.92)
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In the paper
“A decreased abundance of mucin-degrading Verrucomicrobiae was found in a human a-synuclein overexpressing mouse model.36”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [36] Gorecki, 2019, Altered gut microbiome in Parkinson's disease and the influence of lipopolysaccharide in a human alpha-synuclein over-expressing mouse model, Front Neurosci source
The Results section reports significantly lower Verrucomicrobiae abundance in Thy1-αSyn mice than in wild-type controls. The Discussion describes members of Verrucomicrobiae as mucin degraders. Page numbers are not available in our copy. (LLM, conf=0.94)
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In the paper
“The gut microbiota sends signals to the CNS and enteric nervous system through different pathways through metabolites, hormones, the immune system and afferent nerves.14,15”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [14] Heiss, 2019, The role of the gut microbiota in development, function and disorders of the central nervous system and the enteric nervous system, J Neuroendocrinol source
- Could not verifycites [15] Lahiri, 2019, The gut microbiota influences skeletal muscle mass and function in mice, Sci Transl Med sourceExperimental — accuracy not yet measured
The Introduction says the gut microbiota influences immunity and behavior, and the Discussion describes microbial metabolites mediating host interactions. Neither passage says that the microbiota signals to the central and enteric nervous systems through metabolites, hormones, immune pathways, and afferent nerves. Searches for those nervous-system targets and pathways found no passage establishing the claim. (LLM, conf=0.72)
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In the paper
“Reduced levels of intestinal mucus and the production of microbe-derived SCFAs may therefore be a mechanism by which the host experiences increased intestinal permeability, resulting in an increased risk of local inflammation across the intestinal canal.37,39”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [37] Li, 2019, Alteration of the faecal microbiota in North-Eastern Han Chinese population with sporadic Parkinson's disease, Neurosci Lett source
- Partly supportedcites [39] Kundu, 2017, Our gut microbiome: The evolving inner self, Cell sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
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The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Intriguingly, the increase in Lactobacillaceae and decrease in Prevotellaceae are related to the decrease in the gastrointestinal hormone ghrelin, which can maintain and protect the normal dopamine function of the substantia nigra and striatum by changing mitochondrial respiration and reactive”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Could not verifycites [41] Andrews, 2009, Ghrelin promotes and protects nigrostriatal dopamine function via a UCP2-dependent mitochondrial mechanism, J Neurosci sourceExperimental — accuracy not yet measured
The sections on striatal dopamine levels and mitochondrial responses discuss ghrelin’s effects on neurons, not gut bacteria. Searches for Lactobacillaceae, Prevotellaceae, and a gut-microbiota relationship found no passage linking changes in those families to decreased ghrelin. (LLM, conf=0.76)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“There was a strong correlation between the alterations in oral-specific microbial taxa and functional indexes in patients with Parkinson's disease.48”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Partly supportedcites [48] Mihaila, 2019, The oral microbiome of early stage Parkinson's disease and its relationship with functional measures of motor and non-motor function, PLoS One sourceExperimental — accuracy not yet measured
The Discussion reports strong correlations between specific oral microbiota and subsets of functional measures in patients with Parkinson’s disease. But the Results describe the analysis as exploratory and say that only one of the ten strongest correlations linked a significantly altered taxon to a significantly altered functional measure. The claim overgeneralizes that narrower finding. (LLM, conf=0.85)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“indicating that there is a close connection between gut microbiota and neurological disorders; therefore, microbial intervention could provide a novel strategy for the prevention and treatment of Alzheimer's disease.47”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [47] Ou, 2020, Protective effects of Akkermansia muciniphila on cognitive deficits and amyloid pathology in a mouse model of Alzheimer's disease, Nutr Diabetes source
The Discussion states that a close relationship exists between gut microbiota and neurological disorders. It also suggests that supplementation with Akkermansia, a gut microbe, could be a new strategy for preventing and treating Alzheimer’s disease. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“suggesting that the gut microbiota may be seriously influenced by disease progression.57”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Supportedcites [57] Minato, 2017, Progression of Parkinson's disease is associated with gut dysbiosis: Two-year follow-up study, PLoS One source
The Discussion (page unavailable) suggests that gut microbiota may be critically influenced by time after Parkinson’s disease onset, based on differing declines in bacterial counts. The paper also reports that total fecal bacterial counts decreased over two years in the patients studied. This supports the citing sentence’s hedged claim, though it does not establish that disease progression causes the changes. (LLM, conf=0.90)
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In the paper
“Minato et al. 57 investigated the relationship between intestinal disorders and disease progression through a 2-year follow-up of patients with Parkinson's disease and found that the decreased abundance of Bifidobacterium and Bacteroides fragilis was related to the deterioration of the Unified Parkinson's Disease Rating Scale (UPDRS)-I score”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Supportedcites [57] Minato, 2017, Progression of Parkinson's disease is associated with gut dysbiosis: Two-year follow-up study, PLoS One source
The Results section (‘Correlations between the bacterial counts at year 0 and the progression of clinical symptoms in 2 years’) reports that lower baseline counts of Bifidobacterium and the B. fragilis group correlated with worsening UPDRS I scores over two years (Fig. 1C–D). The association concerns counts at year 0, not a measured decline in those bacteria during follow-up. (LLM, conf=0.93)
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In the paper
“Astrocytes have been found to express co-stimulatory molecules that are necessary to activate CD4 + T cells.91,92”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Partly supportedcites [91] Li, 2019, Reactive astrocytes in neurodegenerative diseases, Aging Dis sourceExperimental — accuracy not yet measured
The Up regulation section (page not provided) says astrocytes display MHC molecules and can present antigens to T lymphocytes. It does not say they express co-stimulatory molecules or that those molecules are necessary to activate CD4+ T cells. (LLM, conf=0.83)
- Supportedcites [92] Rostami, 2020, Astrocytes have the capacity to act as antigen-presenting cells in the Parkinson’s disease brain, J Neuroinflamm source
The Discussion states that human astrocytes exposed to fibrillary α-synuclein express CD80, CD86, and CD40, which it describes as crucial for CD4+ T-cell activation. The results section also reports that these co-stimulatory molecules were detected following that exposure. (LLM, conf=0.93)
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In the paper
“Concentrations of norepinephrine, dopamine and 5-HT in the striatum of germ-free mice were significantly increased compared to those of specific pathogen-free mice with normal gut microbiota.81”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Partly supportedcites [81] Diaz Heijtz, 2011, Normal gut microbiota modulates brain development and behaviour, Proc Natl Acad Sci U S A sourceExperimental — accuracy not yet measured
The Results section reports significantly higher turnover rates of noradrenaline, dopamine and 5-HT in the striatum of germ-free mice than in SPF mice. It says their concentrations were measured, but does not report that the concentrations themselves were significantly higher; the claim substitutes concentration for turnover. (LLM, conf=0.87)
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In the paper
“indicating that the normal development of the intestinal mucosal EGC network depends on gut microbiota.74”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Supportedcites [74] Kabouridis, 2015, Microbiota controls the homeostasis of glial cells in the gut lamina propria, Neuron source
The Results section, “Microbiota Is Required for the Postnatal Development of mEGCs,” explicitly concludes that normal development of the mucosal EGC network depends on gut microbiota. It reports fewer mucosal EGCs in germ-free mice and restoration of the glial network after microbiota were introduced. (LLM, conf=0.95)
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“This suggests that infiltrating peripheral adaptive immune cells are involved in activating resident immune cells in the brain, thus enhancing neuroinflammation.88”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [88] Iba, 2020, Neuroinflammation is associated with infiltration of T cells in Lewy body disease and alpha-synuclein transgenic models, J Neuroinflamm source
The Background passage explicitly says that infiltrating T cells near microglia and astrocytes imply participation in activating brain-resident immune cells and enhancing inflammation. The Discussion likewise reports their proximity to glial cells alongside glial activation. (LLM, conf=0.94)
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A strong CD4 + T cell response to a-synuclein epitopes can be detected before the onset and diagnosis of Parkinson's disease.95”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [95] Lindestam Arlehamn, 2020, α-Synuclein-specific T cell reactivity is associated with preclinical and early Parkinson’s disease, Nat Commun source
The Results report that a longitudinal case study found strong CD4+ T cell responses to an α-synuclein epitope detectable 10 years before the onset of motor symptoms and clinical diagnosis. The claim says these responses can be detected, without asserting that they occur in all patients. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Peripheral monocytes have been shown to enhance phagocytosis in autologous serum of patients with Parkinson's disease, supporting the involvement of innate immunity.84”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [84] Wijeyekoon, 2018, Monocyte function in Parkinson's disease and the impact of autologous serum on phagocytosis, . Front Neurol source
The Discussion reports increased bead phagocytosis by monocytes in early-to-moderate Parkinson’s disease compared with controls, largely driven by factors in patient serum. It also states that the difference emerged in autologous serum but not standard medium, adding to evidence of altered innate immune function in Parkinson’s disease. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The NLRP3 inflammasome has been found to play a critical role in microbiota-mediated intestinal/peripheral inflammation and neuroinflammation in CNS diseases.102”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Partly supportedcites [102] Pellegrini, 2020, Microbiota-gut-brain axis in health and disease: Is NLRP3 inflammasome at the crossroads of microbiota-gut-brain communications?, Prog Neurobiol sourceExperimental — accuracy not yet measured
The Introduction describes NLRP3 as a potential key player in peripheral and central inflammatory responses in CNS diseases, and section 4 links its interaction with gut microbiota to intestinal disease. But section 6.2 says the evidence suggests relevance to central neuroinflammation while noting that a direct causal relationship has not been evaluated. The claim overstates this qualified evidence as an established role in microbiota-mediated inflammation. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In another mouse model, the peripheral injection of lipopolysaccharide (LPS) increased the expression of proinflammatory cytokines in the brain and microglia activation in the substantia nigra via the NLRP3-IL-1b signalling pathway, resulting in neurodegeneration.101”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Partly supportedcites [101] Zhao, 2020, A novel role of NLRP3-generated IL-1beta in the acute-chronic transition of peripheral lipopolysaccharide-elicited neuroinflammation: Implications for sepsis-associated neurodegeneration, J Neuroinflamm sourceExperimental — accuracy not yet measured
The Abstract reports that peripheral LPS increased brain mature IL-1β, and that high-dose LPS led to persistent nigral microglial activation and neuronal degeneration dependent on NLRP3 or IL-1R1. But the section ‘Deficiency in NLRP3-IL-1β-IL-1R1…’ says the initial rise in other proinflammatory cytokines and acute microglial activation occurred without that pathway. The claim omits this acute-versus-chronic distinction and the high-dose condition; page numbers were not available in our copy. (LLM, conf=0.89)
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In the paper
“Previous evidence has indicated that systemic inflammation can increase the reactive oxygen species, activation of microglia and degeneration of dopaminergic neurons in the brain through peripheral inflammatory factors.103,104”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Partly supportedcites [103] Qin, 2007, Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration, Glia sourceExperimental — accuracy not yet measured
The Abstract reports that systemic LPS or TNFα activated brain microglia and that LPS caused progressive loss of dopaminergic neurons; the Discussion identifies TNFα as a proposed link between peripheral inflammation and brain inflammation. The Introduction says activated microglia can produce superoxide, a reactive oxygen species, but the paper does not show that systemic inflammation increased reactive oxygen species in the brain. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites [104] Qin, 2013, NADPH oxidase and aging drive microglial activation, oxidative stress, and dopaminergic neurodegeneration following systemic LPS administration, Glia source
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In the paper
“These findings suggest that gut microbiota may trigger immune activation of the colonic mucosa through the TLR4 signalling pathway, leading to neuroinflammation and subsequent neurodegeneration in Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [120] Terán-Ventura, 2014, Specific changes of gut commensal microbiota and TLRs during indomethacin-induced acute intestinal inflammation in rats, J Crohns Colitis sourceExperimental — accuracy not yet measured
The Discussion reports altered gut microbiota and increased ileal and ceco-colonic TLR-4 expression during indomethacin-induced inflammation in rats, and suggests that altered host–bacterial interactions may perpetuate intestinal inflammation. It does not connect this pathway to neuroinflammation, neurodegeneration, or Parkinson’s disease; it also does not establish that microbiota triggered the observed inflammation. (LLM, conf=0.88)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“indicating that peripheral infection can lead to neuroinflammation in the brain via disruption of the blood-CSF barrier and systemic immune response.107”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [107] Gorle, 2018, The choroid plexus epithelium as a novel player in the stomach-brain axis during Helicobacter infection, Brain Behav Immun source
The Discussion (p. 11) reports that H. suis infection induced systemic inflammation in mice, followed by loss of blood-CSF barrier integrity and brain inflammation. This supports the claim that a peripheral infection can lead to neuroinflammation through those processes. (LLM, conf=0.93)
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In the paper
“In particular, TLR2 is expressed in enteric neurons, glial cells and smooth muscle cells of the intestinal wall.118”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [118] Brun, 2013, Toll-like receptor 2 regulates intestinal inflammation by controlling integrity of the enteric nervous system, Gastroenterology source
The section “Distinct Cell Populations of the Small Intestine Express Functional TLR2” reports TLR2 expression in neurons, glia, and smooth muscle cells from the smooth muscle layers of mouse ileum. The Discussion likewise identifies functional TLR2 expression in these three cell types. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
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Every source the paper cites for this claim was checked and supports it.
In the paper
“suggesting that alterations in the microbiota may be closely related to the systemic inflammatory response.40”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [40] Lin, 2019, Altered gut microbiota and inflammatory cytokine responses in patients with Parkinson's disease, J Neuroinflamm source
The Discussion states that altered gut microbiota are linked to aberrant systemic immune responses and reports correlations between bacterial abundances and elevated plasma inflammatory cytokines in patients with Parkinson’s disease. This supports the citing sentence’s hedged claim of a relationship. (LLM, conf=0.91)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Microarray analysis of sigmoid mucosa samples illustrated that the expression of TLR4 mRNA was significantly higher compared with that in controls.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [120] Terán-Ventura, 2014, Specific changes of gut commensal microbiota and TLRs during indomethacin-induced acute intestinal inflammation in rats, J Crohns Colitis sourceExperimental — accuracy not yet measured
Section 3.7 (page unavailable) reports increased TLR-4 expression in inflamed rat ileal and ceco-colonic tissue compared with controls. But the Methods (section 2.10, page unavailable) describe semi-quantitative RT-PCR, not microarray analysis, and the samples were not sigmoid mucosa. The text does not establish that the specific TLR-4 comparison claimed was statistically significant. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Genomewide association studies have alluded to a significant genetic overlap between Parkinson's disease and autoimmune diseases.97”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [97] Witoelar, 2017, Genome-wide pleiotropy between Parkinson disease and autoimmune diseases, JAMA Neurol source
The Results section, “Shared Susceptibility Loci for PD and Autoimmune Disorders” (page unavailable), reports 17 pleiotropic loci shared between Parkinson disease and seven autoimmune diseases at a conjunction false discovery rate below 0.05. The Discussion also describes an overlap between their genetic risk factors. (LLM, conf=0.94)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition, inflammatory bowel diseases and Parkinson's disease share some common genetic factors.98”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [98] Brudek, 2019, Inflammatory bowel diseases and Parkinson's disease, J Parkinsons Dis source
The “PD AND IBD: GENETIC BACKGROUND” section reports shared genetic loci between Parkinson’s disease and Crohn’s disease and ulcerative colitis. It identifies LRRK2 as a susceptibility factor shared by Parkinson’s and Crohn’s disease, directly supporting the claim. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“intestinal biopsies from patients with Parkinson's disease, it was reported that the immune response of TLR4, cytokines and chemokines, as well as the number of CD3 + T cells, increased in the lamina propria of colonic tissue.120”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [120] Terán-Ventura, 2014, Specific changes of gut commensal microbiota and TLRs during indomethacin-induced acute intestinal inflammation in rats, J Crohns Colitis sourceExperimental — accuracy not yet measured
Section 3.7 reports increased TLR-4 expression in the ceco-colonic tissue of rats with indomethacin-induced inflammation. It does not establish this finding in biopsies from patients with Parkinson’s disease, and our copy does not report increased cytokines, chemokines, or CD3+ T cells in the colonic lamina propria. (LLM, conf=0.88)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Studies have shown that patients with inflammatory bowel diseases have a higher risk of Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [98] Brudek, 2019, Inflammatory bowel diseases and Parkinson's disease, J Parkinsons Dis source
The ‘EPIDEMIOLOGICAL EVIDENCE FOR A LINK BETWEEN IBD AND PD’ section reports increased Parkinson’s disease risk in several cohort studies and a meta-analysis finding a 46% increased risk in patients with IBD. It also notes one case–control study with an inverse finding, but the claim that studies have shown higher risk is supported. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Cytokines and chemokines related to gut microbiota or pathogen-derived products may be involved in the pathogenesis of intestinal inflammation via TLRs.122”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Could not verifycites [122] Joers, 2020, Microglia, inflammation and gut microbiota responses in a progressive monkey model of Parkinson's disease: A case series, Neurobiol Dis sourceExperimental — accuracy not yet measured
The Gastrointestinal Assessments methods describe measuring gut microbiota and circulating LPS, while the Introduction discusses the pro-inflammatory cytokine TNF in Parkinson’s disease. Neither passage links microbiota- or pathogen-derived products to intestinal inflammation through TLRs; searches for TLR and toll-like receptors found no passage addressing that mechanism. (LLM, conf=0.76)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“Microbial functional amyloids can also induce the accumulation of neuronal proteins such as A-b, a-synuclein and tau, mediating the transmission of the disease through the gut-brain axis.130”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [130] Friedland, 2020, What are the molecular mechanisms by which functional bacterial amyloids influence amyloid beta deposition and neuroinflammation in neurodegenerative disorders?, Int J Mol Sci source
Section 2 proposes that bacterial amyloids may cross-seed Aβ, alpha-synuclein and tau aggregation, with prion-like propagation potentially traveling from the gut to the brain through the gut–brain axis. This supports the citing sentence as a statement of possibility, not an established mechanism. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In Parkinson's disease, the vagus nerve seems to play a fundamental role in the gut-brain transmission of pathological asynuclein.141”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [141] Knudsen, 2018, In-vivo staging of pathology in REM sleep behaviour disorder: A multimodality imaging case-control study, Lancet Neurol source
The Introduction describes a hypothesis in which pathological α-synuclein spreads from gastrointestinal nerve terminals through autonomic nerves to the dorsal motor nucleus of the vagus, and cites evidence that truncal vagotomy is protective against Parkinson’s disease. The citing sentence’s “seems” reflects the paper’s presentation of this gut–brain pathway as a hypothesis, not a proven mechanism. (LLM, conf=0.85)
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Moreover, LPS intervention resulted in a significant decrease in the tight junction proteins zona occludens 1 (ZO-1) and e-cadherin in intestinal epithelial cells of Thy1-a-synuclein mice”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [36] Gorecki, 2019, Altered gut microbiome in Parkinson's disease and the influence of lipopolysaccharide in a human alpha-synuclein over-expressing mouse model, Front Neurosci sourceExperimental — accuracy not yet measured
The Results section, “LPS Alters Quantity and Distribution of ZO-1 and e-Cadherin in IEC-6 Cells in vitro” (page not provided), reports a noticeable reduction of both proteins after LPS treatment. That experiment used cultured IEC-6 cells, not intestinal epithelial cells from Thy1-αSyn mice, and the passage does not report a statistically significant decrease in those proteins. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, the increase in Bacteroides spp., Enterobacteriaceae and Clostridium in rats with acute colitis mediates the occurrence of intestinal inflammation by upregulating TLR2 and TLR4.120”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [120] Terán-Ventura, 2014, Specific changes of gut commensal microbiota and TLRs during indomethacin-induced acute intestinal inflammation in rats, J Crohns Colitis sourceExperimental — accuracy not yet measured
The Results (section 3.7) report increased TLR-2 and TLR-4 expression during inflammation, and the Discussion reports increases in the named bacterial groups. But the Discussion describes TLR upregulation as possibly associated with dysbiosis and says these changes coincide during indomethacin-induced acute enteritis; it does not establish that the bacteria cause inflammation by upregulating TLRs. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The gut microbiota also activated intestinal cells that produce IL-10 in MyD88/TLR2/ PI3K-dependent pathways to maintain mucosal homeostasis.123”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [123] Mishima, 2019, Microbiota maintain colonic homeostasis by activating TLR2/MyD88/PI3K signaling in IL-10-producing regulatory B cells, J Clin Invest source
The Introduction states that resident enteric bacteria activate intestinal IL-10-producing B cells through TLR2, MyD88, and PI3K pathways, and that these cells maintain mucosal homeostasis. The claim paraphrases this finding, though it calls the B cells more generally ‘intestinal cells.’ (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“indicating that there is a relationship between gut microbiota and the pathogenesis of Parkinson's disease”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [36] Gorecki, 2019, Altered gut microbiome in Parkinson's disease and the influence of lipopolysaccharide in a human alpha-synuclein over-expressing mouse model, Front Neurosci source
The Discussion states that gut dysbiosis and gastrointestinal dysfunction may contribute to α-synuclein pathophysiology and eventual neurodegeneration in Parkinson’s disease. The study also reports an altered gut microbiome in patients with Parkinson’s disease, supporting the claimed relationship without establishing causation. (LLM, conf=0.93)
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“The increase in TLR4, TLR5 and the proinflammatory factor IL-6 and the decrease in the anti-inflammatory factor IL-10 in the mucosa of patients with irritable bowel syndrome were related to alterations in the gut microbiota.122”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Could not verifycites [122] Joers, 2020, Microglia, inflammation and gut microbiota responses in a progressive monkey model of Parkinson's disease: A case series, Neurobiol Dis sourceExperimental — accuracy not yet measured
The Discussion addresses gut-microbiota changes in a monkey model of Parkinson’s disease, while the Materials and Methods describe gastrointestinal measurements in those monkeys. Searches for irritable bowel syndrome, TLR4, TLR5, IL-6 and IL-10 found no passage linking the claimed mucosal changes to gut microbiota in patients with irritable bowel syndrome. (LLM, conf=0.78)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Could not verify
Every source the paper cites for this claim was checked and supports it.
In the paper
“thus supporting the hypothesis that a-synuclein spreads from the intestine to the CNS in the pathogenesis of Parkinson's disease.36”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [36] Gorecki, 2019, Altered gut microbiome in Parkinson's disease and the influence of lipopolysaccharide in a human alpha-synuclein over-expressing mouse model, Front Neurosci source
The Discussion says the authors’ findings support a previously reported pathological spread of α-synuclein from the gut to the CNS in Parkinson’s disease pathogenesis. This matches the citing sentence’s framing of the spread as a hypothesis supported by the study. (LLM, conf=0.94)
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“An increase in Gammaproteobacteria, an LPS-producing Gram-negative bacterium, was found in the faeces of patients with Parkinson's disease.36”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [36] Gorecki, 2019, Altered gut microbiome in Parkinson's disease and the influence of lipopolysaccharide in a human alpha-synuclein over-expressing mouse model, Front Neurosci source
The Methods section reports collecting stool samples from patients with Parkinson’s disease. The Results section finds higher mean Gammaproteobacteria abundance in both mild and severe PD groups than in controls, while the Discussion describes Gammaproteobacteria as a major contributor to LPS production. No page numbers are provided in our copy. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Vagotomy can prevent the transmission of pathological a-synuclein to the CNS in animal models.137,138”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [137] Kim, 2019, Transneuronal propagation of pathologic alpha-synuclein from the gut to the brain models Parkinson's disease, Neuron source
In the passage labeled “legend continued on next page” (page not supplied), the authors report that truncal vagotomy prevented pathological α-synuclein from spreading to the CNS after gut injection in mice. This directly supports the claim in an animal model. (LLM, conf=0.94)
- Supportedcites [138] Uemura, 2018, Inoculation of alpha-synuclein preformed fibrils into the mouse gastrointestinal tract induces Lewy body-like aggregates in the brainstem via the vagus nerve, Mol Neurodegener source
The Abstract reports that vagotomy before gastric inoculation of α-synuclein fibrils completely abolished aggregate formation in the mouse dorsal motor nucleus of the vagus, a brainstem nucleus. The Results section reports pathology only on the unvagotomized side, supporting the claim in this animal model. (LLM, conf=0.91)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This research suggests that TLR2 signalling can regulate intestinal inflammation by modulating enteric nervous system structure, neurochemical coding and intestinal neuromuscular function.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [118] Brun, 2013, Toll-like receptor 2 regulates intestinal inflammation by controlling integrity of the enteric nervous system, Gastroenterology source
The Discussion states that TLR2 deficiency alters ENS structure, neurochemical coding, and function, and that restoring ENS integrity and function changes the mice’s response to intestinal inflammatory stimuli. The Background & Aims passage likewise links TLR2-dependent ENS changes to gut dysmotility and greater susceptibility to intestinal inflammation. (LLM, conf=0.94)
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Neuroinflammation, including microglial proliferation, T cell infiltration, increased expression of inflammatory factors and glial cell activation, has been proven to be an important pathology of Parkinson's disease.145,146”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [145] Gao, 2020, Multimodal analysis of gene expression from postmortem brains and blood identifies synaptic vesicle trafficking genes to be associated with Parkinson's disease, Brief Bioinform source
- Partly supportedcites [146] Wang, 2020, Disease progression-dependent expression of CD200R1 and CX3CR1 in mouse models of Parkinson's disease, Aging Dis sourceExperimental — accuracy not yet measured
The Abstract identifies microglial activation as an important contributor to Parkinson’s disease pathology, and the Results report increased microglial numbers, activation, and inflammatory cytokine expression in mouse models. The paper does not establish that the increased numbers reflect proliferation, and the passages found do not address T-cell infiltration. Its findings therefore support much of the neuroinflammation claim, but not every listed feature. (LLM, conf=0.86)
boosted- Asserted: passes — The authors put it forward as true.
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Intestinal barrier dysfunction and increased intestinal permeability caused by inflammation in patients with Parkinson's disease provide conditions for the circulation of inflammatory factors and the exposure of the enteric nervous system to the microbiota and their harmful products.77”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [77] Perez-Pardo, 2019, Role of TLR4 in the gut-brain axis in Parkinson's disease: A translational study from men to mice, Gut sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TLR4 gene-deficient mice partially resist MPTP toxicity by suppressing the activation of microglia in the substantia nigra.156”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [156] Noelker, 2013, Toll like receptor 4 mediates cell death in a mouse MPTP model of Parkinson disease, Sci Rep sourceExperimental — accuracy not yet measured
The Discussion reports that TLR4-deficient mice are partially protected against MPTP toxicity and that this correlates with decreased microglial activation in the substantia nigra. The Results document fewer activated nigral microglia, but the paper does not establish that suppressing their activation causes the protection; the claim’s “by” overstates that link. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, SCFAs from intestinal microbiota are key molecules regulating the maturation, morphology and function of microglia.147”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Partly supportedcites [147] Erny, 2015, Host microbiota constantly control maturation and function of microglia in the CNS, Nat Neurosci sourceExperimental — accuracy not yet measured
The Discussion reports that gut microbiota affect microglial maturation, shape and responses to pathogens. It mentions SCFAs only as metabolites that may enter circulation and could affect immune regulation and CNS function; it does not establish them as the key molecules regulating all three microglial features. Page numbers are unavailable in our copy. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Braniste et al. 167 demonstrated that BBB permeability was increased due to the destruction of tight junction structure and the low expression of transmembrane tight junction proteins (including occludin and claudin-5) in the brains of germ-free mice compared with pathogen-free mice.167”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [167] Braniste, 2014, The gut microbiota influences blood-brain barrier permeability in mice, Sci Transl Med sourceExperimental — accuracy not yet measured
The Discussion reports increased BBB permeability in germ-free mice and says it may partly result from disorganized tight junctions and reduced occludin and claudin-5 expression. The Results section on brain endothelial tight junctions also documents disorganization and lower protein expression. The citing sentence overstates this as established causation and calls the structural change “destruction.” (LLM, conf=0.88)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The BBB was shown to be damaged in MPTP-treated mice.89,164”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [89] Liu, 2017, Th17 cells induce dopaminergic neuronal death via LFA-1/ICAM-1 interaction in a mouse model of Parkinson's disease, Mol Neurobiol source
- Supportedcites [164] Zhang, 2017, Reassessment of subacute MPTP-treated mice as animal model of Parkinson's disease, Acta Pharmacol Sin source
The Results section reports that, after MPTP treatment, astrocyte endfeet were swollen and the blood–brain barrier in the substantia nigra pars compacta was damaged. This directly supports the claim about MPTP-treated mice. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Importantly, bile acids play a neuroprotective role in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease and Parkinson's disease.213”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
What the sources say
- Partly supportedcites [213] Kiriyama, 2019, The biosynthesis, signaling, and neurological functions of bile acids, Biomolecules sourceExperimental — accuracy not yet measured
Section 5.2 reports that TUDCA reduced amyloid accumulation and rescued memory deficits in an Alzheimer’s mouse model. Other passages report protective effects of TUDCA or UDCA in animal models of Parkinson’s and Huntington’s diseases. The claim omits that the reported neuroprotection concerns specific bile acids and primarily experimental models, rather than an established protective role for bile acids generally in people with these diseases. (LLM, conf=0.87)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Tauroursodeoxycholic acid (TUDCA), an endogenous bile acid, has a neuroprotective effect in models of Parkinson's disease.[214][215][216]”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
What the sources say
- Not checked — no full text of the sourcecites [214] Castro-Caldas, 2012, Tauroursodeoxycholic acid prevents MPTP-induced dopaminergic cell death in a mouse model of Parkinson's disease, Mol Neurobiol source
- Supportedcites [215] Mendes, 2019, Neurotoxic effects of MPTP on mouse cerebral cortex: Modulation of neuroinflammation as a neuroprotective strategy, Mol Cell Neurosci source
The Introduction identifies TUDCA as an endogenous bile acid and reports protective effects in MPTP-injected mice. The Discussion describes neuroprotection by TUDCA in the presence of MPTP and its potential benefit in Parkinson’s disease. (LLM, conf=0.93)
- Supportedcites [216] Rosa, 2017, Novel insights into the antioxidant role of tauroursodeoxycholic acid in experimental models of Parkinson's disease, Biochim Biophys Acta Mol Basis Dis source
The Discussion (section 4; page not provided) explicitly calls TUDCA an endogenous bile acid that is neuroprotective in models including the MPTP model of Parkinson’s disease. It also reports protection against MPP+-induced mitochondrial damage and neuronal death in this study. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The faecal microbiota of patients with Parkinson's disease shows a decrease in the production of SCFAs or their producing microbiota in most clinical studies.28,30,37,77,182”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [28] Keshavarzian, 2015, Colonic bacterial composition in Parkinson's disease, Mov Disord source
- Not checked — no full text of the sourcecites [30] Unger, 2016, Short chain fatty acids and gut microbiota differ between patients with Parkinson's disease and age-matched controls, Parkinsonism Relat Disord source
- Not checked — no full text of the sourcecites [37] Li, 2019, Alteration of the faecal microbiota in North-Eastern Han Chinese population with sporadic Parkinson's disease, Neurosci Lett source
- Partly supportedcites [77] Perez-Pardo, 2019, Role of TLR4 in the gut-brain axis in Parkinson's disease: A translational study from men to mice, Gut sourceExperimental — accuracy not yet measured
The microbiota-composition section reports fewer putative SCFA-producing bacteria in faecal samples from patients with Parkinson’s disease than from healthy controls. The Introduction also reports reduced SCFAs, but the paper does not establish that this pattern appears in *most* clinical studies. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [182] Cirstea, 2020, Microbiota composition and metabolism are associated with gut function in Parkinson's disease, Mov Disord source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In recent years, it has been found that there is an important bidirectional relationship between intestinal microbiota and bile acids.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
What the sources say
- Supportedcites [204] Friedman, 2018, FXR-dependent modulation of the human small intestinal microbiome by the bile acid derivative obeticholic acid, Gastroenterology source
The Introduction explicitly describes an important bidirectional relationship between bacteria and bile acids. It explains both directions: bacteria alter the composition of luminal bile acids, while bile acids affect bacterial survival and growth. (LLM, conf=0.95)
- Supportedcites [205] Ridlon, 2013, Cirrhosis, bile acids and gut microbiota: Unraveling a complex relationship, Gut Microbes source
The paper's Abstract explicitly describes a two-way relationship: bile acid pool size and composition regulate microbiome structure, while the microbiome regulates the bile acid pool. It also calls the balance important for health and disease. (LLM, conf=0.95)
- Partly supportedcites [206] Song, 2020, Microbial bile acid metabolites modulate gut RORgamma(+) regulatory T cell homeostasis, Nature sourceExperimental — accuracy not yet measured
The Abstract reports that gut bacteria convert primary bile acids into intestinal bile acids and that microbial factors influence the gut bile-acid pool. It does not establish the reverse direction—that bile acids affect the intestinal microbiota—so it supports an interaction but not the claimed bidirectional relationship. (LLM, conf=0.82)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“However, several studies have revealed that butyric acid in faecal samples significantly increased compared to the control group in an MPTP-induced mouse model.121,184”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [121] Sun, 2018, Neuroprotective effects of faecal microbiota transplantation on MPTP-induced Parkinson's disease mice: Gut microbiota, glial reaction and TLR4/TNF-α signaling pathway, Brain Behavior Immunity source
- Supportedcites [184] Zhou, 2019, Neuroprotection of fasting mimicking diet on MPTP-induced Parkinson's disease mice via gut microbiota and metabolites, Neurotherapeutics source
The “Short-Chain Fatty Acids Concentrations of Feces Influenced by Gut Microbiota Alteration” section reports a striking increase in fecal butyric acid in MPTP-treated, ad-libitum-fed mice compared with normal-saline, ad-libitum-fed controls. The Fig. 8 caption reports the statistical test for fecal butyric acid (p = 0.049). (LLM, conf=0.93)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“F. prausnitzii can also reduce intestinal inflammation by affecting paracellular permeability and enhancing intestinal epithelium barrier function.270,271”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not checked — no full text of the sourcecites [270] Carlsson, 2013, Faecalibacterium prausnitzii supernatant improves intestinal barrier function in mice DSS colitis, Scand J Gastroenterol source
- Supportedcites [271] Martin, 2015, Faecalibacterium prausnitzii prevents physiological damages in a chronic low-grade inflammation murine model, BMC Microbiol source
The Results report reduced intestinal permeability and tissue cytokines in DNBS-treated mice given F. prausnitzii or its supernatant. The Discussion reports protection of the paracellular pathway, and the Conclusion suggests barrier enhancement through tight-junction proteins. The evidence is from a murine model, not patients. (LLM, conf=0.89)
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Every source the paper cites for this claim was checked and supports it.
In the paper
“A ketogenic diet was found to improve motor and nonmotor symptoms in patients with Parkinson's disease.249”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
What the sources say
- Supportedcites [249] Phillips, 2018, Low-fat versus ketogenic diet in Parkinson's disease: A pilot randomized controlled trial, Mov Disord source
The Abstract and Discussion report that patients on the ketogenic diet improved in both motor and nonmotor symptoms during the eight-week pilot trial. The ketogenic group showed greater nonmotor improvement than the low-fat group; the claim does not assert a between-group advantage for motor symptoms. (LLM, conf=0.93)
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In the paper
“With alterations in diet, the microbial abundance and production of fermentation products such as SCFAs and phytochemicals will change significantly.233”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
What the sources say
- Supportedcites [233] Wilson, 2020, Diet and the human gut microbiome: An international review, Dig Dis Sci source
The review’s concluding passage (section and page not provided in our copy) states that most studies reviewed found clear changes in microbial abundance and production of fermentation products, including short-chain fatty acids and phytochemicals, following dietary change. (LLM, conf=0.94)
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In the paper
“The level of BDNF in the hippocampus of rats increased after the administration of galacto-and fructo-oligosaccharides. 259”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
What the sources say
- Partly supportedcites [259] Savignac, 2013, Prebiotic feeding elevates central brain derived neurotrophic factor, N-methyl-D-aspartate receptor subunits and D-serine, Neurochem Int sourceExperimental — accuracy not yet measured
Section 3.2 reports increased hippocampal BDNF protein after FOS, but not GOS. Section 3.4 reports increased BDNF mRNA in the dentate gyrus after both prebiotics, alongside decreased BDNF mRNA in the CA3 region after GOS. The claim does not distinguish protein from mRNA or these hippocampal regions, so it overstates the finding for GOS. (LLM, conf=0.90)
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In the paper
“In addition, ursodeoxycholic acid (UDCA) has a protective effect on the function of mitochondria and dopaminergic neurons in a Parkinson's disease model.219”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
What the sources say
- Supportedcites [219] Mortiboys, 2015, UDCA exerts beneficial effect on mitochondrial dysfunction in LRRK2(G2019S) carriers and in vivo, Neurology source
The Abstract reports that UDCA improved mitochondrial function in LRRK2 G2019S carriers and rescued loss of visual function in flies expressing the mutation in dopaminergic neurons. This supports the claim for the paper’s specific Parkinson’s disease model; it does not establish protection across all models. (LLM, conf=0.91)
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In the paper
“In animal experiments, Sampson et al.50 found that the high expression of a-synuclein in mice that were colonized by the gut microbiota of patients with Parkinson's disease increased motor dysfunction.50”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Supportedcites Sampson et al.50 Sampson, 2016, Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease, Cell source
The PD-Derived Gut Microbiota Promotes Motor Dysfunction section (p. 9) reports significantly worse motor performance in α-synuclein-overexpressing mice colonized with PD-patient microbiota than in genotype-matched mice given healthy-control microbiota. The Discussion (p. 10) describes α-synuclein overexpression and PD-associated microbiota as combining to influence motor symptoms. (LLM, conf=0.91)
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In the paper
“In addition, these mice showed changes in SCFAs, with lower concentrations of acetate and higher concentrations of propionate and butyrate, substantiating that the alteration of gut microbiota is a crucial risk factor for Parkinson's disease.50”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Partly supportedcites [50] Sampson, 2016, Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease, Cell sourceExperimental — accuracy not yet measured
The Dysbiosis of the PD Microbiome section (p. 9) reports lower acetate and higher relative propionate and butyrate in mice receiving microbiota from PD donors. The Discussion (p. 10) says these mouse findings suggest that dysbiosis can influence disease outcomes in genetically susceptible mice, but treats their relevance to human PD as a possible extrapolation—not an established crucial risk factor. (LLM, conf=0.88)
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In the paper
“In addition, these mice showed changes in SCFAs, with lower concentrations of acetate and higher concentrations of propionate and butyrate, substantiating that the alteration of gut microbiota is a crucial risk factor for Parkinson's disease.50”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Partly supportedcites [50] Sampson, 2016, Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease, Cell sourceExperimental — accuracy not yet measured
In “Dysbiosis of the PD Microbiome” (p. 9), mice receiving PD donor-derived microbiota had lower acetate concentrations than mice receiving healthy-control microbiota. The paper reports higher *relative abundances* of propionate and butyrate, not higher absolute concentrations, so that part of the claim overstates the finding. (LLM, conf=0.87)
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In the paper
“FMT is associated with adverse reactions and side effects, including diarrhoea, fever and abdominal pain.278,279”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Partly supportedcites [278] Cui, 2015, Step-up faecal microbiota transplantation strategy: A pilot study for steroid-dependent ulcerative colitis, J Transl Med sourceExperimental — accuracy not yet measured
The Safety of FMT section reports transient fever and increased diarrhoea frequency after FMT, but does not report abdominal pain as an adverse reaction. The Response to FMT section instead says abdominal-pain scores decreased after treatment. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites [279] Cui, 2015, Fecal microbiota transplantation through mid-gut for refractory Crohn's disease: Safety, feasibility, and efficacy trial results, J Gastroenterol Hepatol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition, in a clinical study, the total and active levels of plasma ghrelin decreased in patients with Parkinson's disease, indicating that the level of plasma ghrelin may be a target for the diagnosis and treatment of the disease.43”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [43] Song, 2017, Assessments of plasma ghrelin levels in the early stages of Parkinson's disease, Mov Disord source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“indicating that the level of plasma ghrelin may be a target for the diagnosis and treatment of the disease.43”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [43] Song, 2017, Assessments of plasma ghrelin levels in the early stages of Parkinson's disease, Mov Disord source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, due to differences in research methods, living environments and individuals and the time points and types of altered gut microbiota, the specific mechanisms have not been clearly elucidated.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“There were also differences in the composition of microbiota between faecal samples and sigmoid mucosa samples in patients with Parkinson's disease.28”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [28] Keshavarzian, 2015, Colonic bacterial composition in Parkinson's disease, Mov Disord source
plain- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition, Lai et al. 51 discovered that the gut microbiota of the MPTP-induced model was significantly altered, especially in the Lachnospiraceae, Erysipelotrichaceae, Prevotellaceae, Clostridiales, Erysipelotrichales and Proteobacteria.51”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [51] Lai, 2018, Intestinal pathology and gut microbiota alterations in a methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson's disease, Neurochem Res source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model, ghrelin has a protective effect on dopaminergic neurons by inhibiting the accumulation and phosphorylation of a-synuclein, promoting autophagy and inhibiting endoplasmic reticulum-mediated apoptosis.42”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [42] Wang, 2020, Ghrelin protects dopaminergic neurons against MPTP neurotoxicity through promoting autophagy and inhibiting endoplasmic reticulum mediated apoptosis, Brain Res source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“indicating that the gut microbiota of these patients has the potential to become a reference for exploring the gut microbiota associated with premotor symptoms in Parkinson's disease as biomarkers or therapeutic targets.58”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites [58] Mertsalmi, 2017, More than constipation - Bowel symptoms in Parkinson's disease and their connection to gut microbiota, Eur J Neurol source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“and glial-derived neurotrophic factor (GDNF) plays a fundamental role in maintaining the intestinal epithelial barrier.73”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Not checked — no full text of the sourcecites [73] Vergnolle, 2018, Neurons and Glia in the enteric nervous system and epithelial barrier function, Physiology (Bethesda) source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Non-motor symptoms such as gastrointestinal dysfunction, depression and anxiety may interact with gut microbiota to play a crucial role in the microbiota-gut-brain axis in Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
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In the paper
“In addition, Th17 cells, a subset of CD4 + T lymphocytes, have been shown to infiltrate into the substantia nigra in an MPTP-induced mouse model.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [89] Liu, 2017, Th17 cells induce dopaminergic neuronal death via LFA-1/ICAM-1 interaction in a mouse model of Parkinson's disease, Mol Neurobiol source
plain- Asserted: passes — The authors put it forward as true.
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A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Research findings have suggested that both innate immunity and adaptive immunity are dysregulated in neurodegenerative diseases, especially in Parkinson's disease.82,83”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [82] Tan, 2020, Parkinson disease and the immune system - Associations, mechanisms and therapeutics, Nat Rev Neurol source
- Not checked — no full text of the sourcecites [83] Stephenson, 2018, Inflammation in CNS neurodegenerative diseases, Immunology source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“There were also differences found in gut microbiota among different clinical motor phenotypes.35”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites [35] Lin, 2018, Gut microbiota in patients with Parkinson's disease in southern China, Parkinsonism Relat Disord source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Gastrointestinal dysfunction may be closely interrelated to small intestinal bacterial overgrowth and gastrointestinal Helicobacter pylori colonization.59”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites [59] Felice, 2016, Microbiota-gut-brain signalling in Parkinson's disease: Implications for non-motor symptoms, Parkinsonism Relat Disord source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“As a result, the regulation of intestinal transmitters such as 5-HT, melatonin, GABA, histamine and acetylcholine is a possible mechanism mediating the role of gut microbiota.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
hedgedconditional- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, changes in gut microbiota composition are associated with the occurrence and development of Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > HAMD(Hamilton Depression Scale)scores
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“In a cell model of Parkinson's disease, Th17 cells exacerbated dopaminergic neuron death and glial activation, which was dependent on interaction with LFA-1/ICAM1.89”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [89] Liu, 2017, Th17 cells induce dopaminergic neuronal death via LFA-1/ICAM-1 interaction in a mouse model of Parkinson's disease, Mol Neurobiol source
plaindirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Additionally, the CNS regulates the gastrointestinal tract and enteric nervous system through the sympathetic and parasympathetic branches of the autonomic nervous system and the hypothalamic-pituitaryadrenal axis, which can indirectly affect the gut microbiota by changing the gut environment and releasing signal molecules.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“These findings support the hypothesis that peripheral derived cells may play an essential role in neuroinflammation and neurodegeneration in Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [85] Harms, 2018, Peripheral monocyte entry is required for alpha-Synuclein induced inflammation and neurodegeneration in a model of Parkinson disease, Exp Neurol source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The bidirectional communication between the CNS and enteric nervous system, known as the gutbrain axis, provides a way for microbiota to mediate brain lesions.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microbiota can mediate enteric nervous system inflammation.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In summary, these findings suggest that peripheral inflammation, including gut microbiota-induced intestinal inflammation, can induce systemic and CNS inflammation.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
hedgeddirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The decrease in Roseburia is a characteristic of patients with Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Similarly, Schwiertz et al. 114 showed that calprotectin, a marker of intestinal inflammation and alpha-1-antitrypsin and zonulin, markers of intestinal barrier dysfunction, were significantly increased in patients with Parkinson's disease”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [114] Schwiertz, 2018, Fecal markers of intestinal inflammation and intestinal permeability are elevated in Parkinson's disease, Parkinson Relat Disord source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Intestinal longitudinal smooth muscle cells activate TLR2 and TLR5 to produce specific neurotrophic factors such as GDNF under the stimulation of bacterial pathogen-associated molecular patterns, which recognize conservative microbial products, to correct the abnormal phenotype of enteric neurons in Tlr2 -/- mice.125”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [125] Brun, 2015, Toll like receptor-2 regulates production of glial-derived neurotrophic factors in murine intestinal smooth muscle cells, Mol Cell Neurosci source
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“EGCs may act as an entrance for enterotoxin into the CNS, especially in neurodegenerative diseases.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
hedgedconditional- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Gut microbiota mediates the aggregation of a-synuclein in the enteric nervous system.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“A cohort study in Denmark showed that total vagotomy can significantly reduce the risk of secondary Parkinson's disease.143”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [143] Svensson, 2015, Vagotomy and subsequent risk of Parkinson's disease, Ann Neurol source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Excessive activation of microglia can lead to the production of inflammatory cytokines such as TNF, IL-1b, IL-6 and INF-c, which may have harmful effects on dopaminergic neurons.153”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [153] Zhang, 2017, Pathological alpha-synuclein exacerbates the progression of Parkinson's disease through microglial activation, Toxicol Lett source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, peripheral inflammation also plays a vital role in the pathogenesis of Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Additionally, predictive meta-genomics showed a significant increase in genes involved in endotoxin biosynthesis and the type III bacterial secretion system (associated with pathogens) in the faecal microbiome of patients with Parkinson's disease.28”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [28] Keshavarzian, 2015, Colonic bacterial composition in Parkinson's disease, Mov Disord source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results suggest that the gut microbiota can regulate the structure and function of the enteric nervous system through the TLR signalling pathway.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microbiota may trigger CNS neuroinflammation.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Sodium butyrate (NaB) can improve BBB damage in Parkinson's disease mice by upregulating occludin and ZO-1 after its intragastric administration in an MPTP mouse model.168”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [168] Liu, 2017, Sodium butyrate exerts protective effect against Parkinson's disease in mice via stimulation of glucagon like peptide-1, J Neurol Sci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These results suggested that SCFAs can regulate the homeostasis of neuroinflammation by regulating the function of damaged microglia.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“NaB can regulate apoptosis-related proteins (Bcl-2 and Bax) in the brains of Parkinson's disease mice to reduce neuronal apoptosis.168”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [168] Liu, 2017, Sodium butyrate exerts protective effect against Parkinson's disease in mice via stimulation of glucagon like peptide-1, J Neurol Sci source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“LPS may increase the blood-to-brain uptake of a-synuclein by destroying the BBB.171”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [171] Sui, 2014, Alpha synuclein is transported into and out of the brain by the blood-brain barrier, Peptides source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Wenzel et al. 198 found that single or mixed use of SCFAs could inhibit the secretion of IL-1b, monocyte chemoattractant protein-1 and TNF by stimulated human THP-1 microglia-like cells.198”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [198] Wenzel, 2020, Short-chain fatty acids (SCFAs) alone or in combination regulate select immune functions of microglia-like cells, Mol Cell Neurosci source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microglia have dual effects on the integrity of the BBB.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, the Mediterranean diet may be a promising intervention strategy to attenuate onset and development of Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Associations between Mediterranean diet adherence and lower Parkinson's disease risk reflect a causal protective effect.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, microbiota also participate in the regulation of neurotransmitters by affecting the production of GABA, the main inhibitory neurotransmitter in the human brain.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Neurotransmitters
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, a single FMT may not be enough to induce significant changes in patients; this requires confirmation through large-scale studies.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“A clinical study has shown that probiotic bacteria can increase the production of SCFAs and decrease pro-inflammatory cytokines in patients with Parkinson's disease, indicating that probiotics may be a potential treatment for this disease (Ghyselinck et al., in press).”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Probiotics
What the sources say
- Not matchedcites Ghyselinck et al., in press
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“FMT may be a potential therapeutic method for the regulation of gut microbiota in animal models.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Zhou et al. 184 reported that a fasting-mimicking diet can reduce the loss of dopaminergic neurons in the substantia nigra of MPTP-induced Parkinson's disease mice.184”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
What the sources say
- Not matchedcites Zhou et al. 184
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- Not matched
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Recent studies have shown that probiotics play a role in relieving the gastrointestinal symptoms of Parkinson's disease, especially constipation, abdominal pain and abdominal distension.252,253”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Probiotics
What the sources say
- Not checked — no full text of the sourcecites [252] Barichella, 2016, Probiotics and prebiotic fiber for constipation associated with Parkinson disease: An RCT, Neurology source
- Not checked — no full text of the sourcecites [253] Cassani, 2011, Use of probiotics for the treatment of constipation in Parkinson's disease patients, Minerva Gastroenterol Dietol
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microbial therapy, in the form of probiotics, may be a novel strategy for the treatment of Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Probiotics
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Therefore, a high-fibre diet protects children in the Burkina Faso group from inflammation and intestinal inflammatory disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Gut microbiota can also mediate disease by affecting the release of neurotransmitters in the intestine.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Neurotransmitters
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The results proved that the proliferation of intestinal microbiota mediated by prebiotics may increase the expression of BDNF in the brain through the participation of intestinal hormones.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
In the paper
“Serotoninergic medication may therefore reduce the risk of cognitive decline in Parkinson's disease.226”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Neurotransmitters
What the sources say
- Not checked — no full text of the sourcecites [226] Kotagal, 2018, Serotonin, beta-amyloid, and cognition in Parkinson disease, Ann Neurol source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The regulatory effects of FMT on intestinal microbiota may have an impact on the symptoms or progression of nervous system diseases through immune, endocrine, metabolic and neural pathways.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Eating fermented milk containing a variety of probiotic strains and prebiotic fibre could improve the symptoms of constipation in patients with Parkinson's disease.252”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
What the sources say
- Not checked — no full text of the sourcecites [252] Barichella, 2016, Probiotics and prebiotic fiber for constipation associated with Parkinson disease: An RCT, Neurology source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At present, however, there is little clinical evidence on prebiotics in patients with Parkinson's disease, so a large number of trials are required to thoroughly investigate the mechanism.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Although animal experiments have shown that a ketogenic diet and fasting are effective in preventing Parkinson's disease”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Generally, bile acids, affected by the metabolism of intestinal microbiota, play an essential role in antioxidant, anti-inflammatory and neuroprotective activities in the pathogenesis of Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Diet-mediated therapy can be used as a new strategy for the treatment and prevention of Parkinson's disease (Fig. 4).”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Intragastric administration of Faecalibacterium prausnitzii could significantly reduce the severity of colitis in mice with moderate or severe chronic colitis, suggesting that this species is an anti-inflammatory bacterium with the potential to treat inflammatory bowel disease.268”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not checked — no full text of the sourcecites [268] Martin, 2014, The commensal bacterium Faecalibacterium prausnitzii is protective in DNBS-induced chronic moderate and severe colitis models, Inflamm Bowel Dis source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
In the paper
“Recently, pathological changes in a-synuclein in the enteric nervous system of Parkinson's disease patients were observed, which provided a new direction for hypotheses on the pathogenesis and pathological origin of Parkinson's disease.133”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
What the sources say
- Not checked — no full text of the sourcecites [133] Pouclet, 2012, A comparison between rectal and colonic biopsies to detect Lewy pathology in Parkinson's disease, Neurobiol Dis source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At present, there is limited evidence for the application of FMT in patients with Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“Recently, using non-human primate models, investigators have observed that a-synuclein aggregated from patients with Parkinson's disease can induce nigra-striatal injury and enteric nervous system pathology after intestinal or striatal injection, indicating that a-synuclein may spread not only rostrally but also caudally, that is, from the gut to the brain and from the brain to”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Case control studies show changes in gut microbiota composition in patients with Parkinson's disease compared with healthy individuals, and there are suggestions of a link between microbiota alterations and disease progression.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Case control studies show changes in gut microbiota composition in patients with Parkinson's disease compared with healthy individuals, and there are suggestions of a link between microbiota alterations and disease progression.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- It may state two separate claims as one. 116
- Probably not a substantial claim. 41
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“Intermittent fasting can protect neurons in animal models of disease, reduce the number of dopaminergic neurons and improve motor function in Parkinson's disease.250”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
What the sources say
- Disputedcites [250] Mattson, 2017, Impact of intermittent fasting on health and disease processes, Ageing Res Rev sourceExperimental — accuracy not yet measured
Section 2.1 reports that mice on alternate-day fasting had reduced loss of dopaminergic neurons and improved functional outcomes in a Parkinson’s disease model. This supports the neuroprotection and functional-outcome portions of the claim, but contradicts its statement that fasting reduces the number of dopaminergic neurons. (LLM, conf=0.90)
Checked by a reasoning model — may be wrong.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Some studies suggested that there was no significant difference in the amount of microbiota in the nasal cavity of patients with Parkinson's disease, but the nasal microbiota exhibited a higher variability in different individuals.34”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Partly supportedcites [34] Heintz-Buschart, 2018, The nasal and gut microbiome in Parkinson's disease and idiopathic rapid eye movement sleep behaviour disorder, Mov Disord sourceExperimental — accuracy not yet measured
The Discussion reports that nasal microbiota varied more across individuals and that few bacterial families differed between Parkinson’s patients and healthy controls. The Results nevertheless identify eight differentially abundant nasal families, mostly with weak significance. The paper does not establish that the total amount of nasal microbiota was the same in the two groups. (LLM, conf=0.84)
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Recently, Ou et al. 47 suggested that A. muciniphila may improve the insulin resistance of Alzheimer's disease mice, reduce the decrease in colonic mucous cells, improve intestinal barrier dysfunction and dyslipidaemia, and delay pathological changes in the brain”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [47] Ou, 2020, Protective effects of Akkermansia muciniphila on cognitive deficits and amyloid pathology in a mouse model of Alzheimer's disease, Nutr Diabetes source
The Discussion reports improved insulin resistance, increased colonic mucus cells, and repair of damaged intestinal barriers in AD-model mice. The Abstract’s Results and Conclusion report improved blood lipids and suggest that Akkermansia treatment could delay pathological changes in the brain. (LLM, conf=0.94)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“therefore, microbial intervention could provide a novel strategy for the prevention and treatment of Alzheimer's disease.47”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [47] Ou, 2020, Protective effects of Akkermansia muciniphila on cognitive deficits and amyloid pathology in a mouse model of Alzheimer's disease, Nutr Diabetes source
The Discussion says that supplementation with Akkermansia, a gut microbe, could be a new strategy for preventing and treating Alzheimer’s disease. The Conclusion likewise presents the findings in AD-model mice as a potential new strategy; it does not establish effectiveness in humans. (LLM, conf=0.92)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In addition, by investigating the effect of early antibiotics on intestinal microbiota, a study revealed that the composition of intestinal microbiota changed significantly and the metabolism of SCFAs was altered after treatment with subtherapeutic antibiotic therapy.56”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [56] Cho, 2012, Antibiotics in early life alter the murine colonic microbiome and adiposity, Nature source
In mice, the section “STAT alters the composition of intestinal microbiota” reports significant differences in microbial composition after subtherapeutic antibiotic treatment. The section “STAT exposure alters gut microbiome SCFA metabolism” reports altered SCFA-related gene counts and increased caecal SCFA concentrations. Page numbers are not available in our copy. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“More than 80% of patients with Parkinson's disease experience a variety of severe gastrointestinal symptoms such as constipation, nausea and vomiting.9”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [9] Yang, 2019, The role of the gut microbiota in the pathogenesis of Parkinson's disease, Front Neurol source
The “GM changes in PD” section directly states that more than 80% of patients with PD suffer severe gastrointestinal symptoms, including constipation, nausea, and vomiting. The citing sentence closely paraphrases that passage. (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For example, Dethlefsen and Relman 53 examined the effect of ciprofloxacin on human distal intestinal microbiota and found a decrease in bacterial diversity and a significant change in microbiota composition within a 3-4-day treatment, after which it began to return incompletely to the initial state.53”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Partly supportedcites [53] Dethlefsen, 2011, Incomplete recovery and individualized responses of the human distal gut microbiota to repeated antibiotic perturbation, Proc Natl Acad Sci U S A sourceExperimental — accuracy not yet measured
The Abstract and Results report a rapid loss of diversity and shift in composition within 3–4 days of starting ciprofloxacin, followed by an often-incomplete return toward the initial state. But the Results specify two 5-day treatment courses, and the Abstract says communities began to return by one week after each course ended—not immediately after a 3–4-day treatment. (LLM, conf=0.86)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Akkermansia utilize mucin as a source of energy and may therefore reduce barrier function and increase exposure to more microbial substrates across the epithelial lining.44”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Partly supportedcites [44] Gerhardt, 2018, Changes of colonic bacterial composition in Parkinson's disease and other neurodegenerative diseases, Nutrients sourceExperimental — accuracy not yet measured
The Discussion says Akkermansia uses mucus for energy and degrades the mucus layer, which could increase microbial-antigen exposure to immune cells. It does not say that microbial substrates cross the epithelial lining, and it also reports that A. muciniphila improves epithelial barrier function. The proposed reduction in barrier function is therefore not established by this passage. (LLM, conf=0.85)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Intriguingly, the abundance of some gut microbiota increased in mice that were colonized by the faeces of patients with Parkinson's disease, including Proteus sp., Bilophila sp. and Roseburia sp., with a decrease in the Lachnospiracae, Rikenellae, Peptostreptococacae and Butyricicoccus sp.50”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Supportedcites [50] Sampson, 2016, Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease, Cell source
The “Dysbiosis of the PD Microbiome” section (p. 9) reports the same increases and decreases in mice receiving microbiota from Parkinson’s disease donors compared with healthy controls. The citing sentence misspells several family names, but otherwise matches the reported taxa. (LLM, conf=0.95)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Investigators have shown that the gut microbiota is significantly related to the duration, 28,35 onset time, 35 and motor and non-motor symptoms 23,25,29,34,40 of Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites [28] Keshavarzian, 2015, Colonic bacterial composition in Parkinson's disease, Mov Disord source
- Not checked — no full text of the sourcecites [35] Lin, 2018, Gut microbiota in patients with Parkinson's disease in southern China, Parkinsonism Relat Disord source
- Not checked — no full text of the sourcecites [23] Barichella, 2019, Unraveling gut microbiota in Parkinson's disease and atypical parkinsonism, Mov Disord source
- Not checked — no full text of the sourcecites [25] Qian, 2018, Alteration of the faecal microbiota in Chinese patients with Parkinson's disease, Brain Behav Immun source
- Not checked — no full text of the sourcecites [29] Scheperjans, 2015, Gut microbiota are related to Parkinson's disease and clinical phenotype, Mov Disord source
- Supportedcites [34] Heintz-Buschart, 2018, The nasal and gut microbiome in Parkinson's disease and idiopathic rapid eye movement sleep behaviour disorder, Mov Disord source
The Results section (‘The Gut Microbiome in Relation to Motor and Nonmotor Phenotypes of PD’; page not provided) reports significant relationships between gut bacterial abundances and both motor and nonmotor symptoms in patients with PD. The cited paper supports the symptom-related part of the sentence; the duration and onset claims are attached to other citations. (LLM, conf=0.92)
- Partly supportedcites [40] Lin, 2019, Altered gut microbiota and inflammatory cytokine responses in patients with Parkinson's disease, J Neuroinflamm sourceExperimental — accuracy not yet measured
The Abstract and Discussion report that Bacteroides abundance correlated significantly with motor symptom severity. The paper assesses non-motor symptoms, but the passages found do not establish a microbiota association with them; searches for disease duration and age at onset likewise found no such association. Page numbers are unavailable in our copy. (LLM, conf=0.86)
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Unlike the CNS, the enteric nervous system is made up of different neural networks in the intestinal wall, where individual small ganglia are connected by dense bundles of fibres.70”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Supportedcites [70] Endres, 2018, Influence of commensal microbiota on the enteric nervous system and its role in neurodegenerative diseases, J Innate Immun source
The Introduction states that, in contrast to the CNS, the ENS forms distinct networks within the gut wall, with relatively small ganglia interconnected by dense fiber bundles. This directly supports the citing sentence. (LLM, conf=0.95)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In an a-synuclein transgenic mouse model, infiltration of CD3 + /CD4 + helper T (Th) cells was increased in the brain (in close proximity to astrocytes and microglia) and this was accompanied by glial activation and enhanced expression of tumour necrosis factor (TNF) genes.88”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [88] Iba, 2020, Neuroinflammation is associated with infiltration of T cells in Lewy body disease and alpha-synuclein transgenic models, J Neuroinflamm source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Intriguingly, T cell deficiency can decrease the loss of dopamine neurons and microglial major histocompatibility complex II expression.90”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [90] Subbarayan, 2020, T cell infiltration and upregulation of MHCII in microglia leads to accelerated neuronal loss in an alpha-synuclein rat model of Parkinson's disease, J Neuroinflamm source
The Background states that, in the paper’s α-synuclein rat model, the absence of T cells prevented microglial MHCII upregulation and subsequent dopamine neuron loss. The Results sections report less neuronal loss in T cell-deficient rats and no increase in microglial MHCII expression in those rats. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“T cells can recognize certain a-synuclein antigenic epitopes, and this is largely mediated by CD4 + T cells and CD8 + T cells in patients with Parkinson's disease.94”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Partly supportedcites [94] Sulzer, 2017, T cells from patients with Parkinson’s disease recognize α-synuclein peptides, Nature sourceExperimental — accuracy not yet measured
The passage describing responses in nine Parkinson’s disease participants (section labeled Abstract) confirms that T cells recognized α-synuclein antigenic peptides. It says responses were largely mediated by CD4+ T cells, with potential CD8+ contributions; CD8+ cells mediated most of the response in only one participant. The claim overstates the CD8+ role by presenting both cell types as largely mediating the response. (LLM, conf=0.89)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The autonomic nervous system receives afferent signals from the gastrointestinal tract and then passes them along to the CNS through the spinal cord and vagus nerve pathway and also transmits signals from the CNS to the enteric nervous system.66,67”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Not checked — no full text of the sourcecites [66] Gibbons, 2019, Basics of autonomic nervous system function, Handb Clin Neurol source
- Partly supportedcites [67] Coletto, 2019, Contractile dysfunction and nitrergic dysregulation in small intestine of a primate model of Parkinson's disease, NPJ Parkinsons Dis sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) suggests that central dopaminergic changes may affect the dorsal motor nucleus of the vagus and vagal outflow, offering limited support for CNS-to-gut signaling. It does not describe gastrointestinal afferent signals traveling to the CNS through the spinal cord or vagus nerve, or explicitly trace signals from the CNS to the enteric nervous system. (LLM, conf=0.78)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
Every source the paper cites for this claim was checked and supports it.
In the paper
“The level of autoantibodies to asynuclein has been found to be significantly increased in CSF and associated with impaired cognition in patients with Parkinson's disease.96”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [96] Akhtar, 2018, Measurements of auto-antibodies to alpha-synuclein in the serum and cerebral spinal fluids of patients with Parkinson's disease, J Neurochem source
The Abstract reports significantly higher CSF α-synuclein auto-antibody levels in patients with Parkinson’s disease than in healthy controls. The Discussion reports that higher CSF levels correlated with poorer global cognitive performance. (LLM, conf=0.94)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The increased expression of TLRs can increase the permeability of the intestinal epithelial barrier and increase the susceptibility of host colonic inflammation, indicating that they play a crucial role in maintaining intestinal immune homeostasis.119,120”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [119] Dheer, 2016, Intestinal epithelial Toll-Like receptor 4 signaling affects epithelial function and colonic microbiota and promotes a risk for transmissible colitis, Infect Immun sourceExperimental — accuracy not yet measured
The Results section ('TLR4 overexpression disrupts epithelial barrier function'; page unavailable) reports increased intestinal permeability in mice with enhanced epithelial TLR4 expression. The Introduction and Discussion also report greater susceptibility to colitis in these mice. The claim generalizes these findings from epithelial TLR4 in mice to TLRs broadly, which this paper does not establish. (LLM, conf=0.84)
- Partly supportedcites [120] Terán-Ventura, 2014, Specific changes of gut commensal microbiota and TLRs during indomethacin-induced acute intestinal inflammation in rats, J Crohns Colitis sourceExperimental — accuracy not yet measured
Section 3.7 reports increased TLR-2 and TLR-4 expression in inflamed ileal and ceco-colonic tissue. The Discussion suggests this up-regulation might help aggravate or perpetuate inflammation, but it does not say that increased TLR expression raises epithelial barrier permeability or establish that it increases susceptibility to colonic inflammation. Page numbers were not available in our copy. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In autoimmune conditions, peripheral inflammation caused by gut inflammation may trigger a-synuclein aggregation, increasing the permeability of intestinal tract and BBB and leading to neuroinflammation.98”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [98] Brudek, 2019, Inflammatory bowel diseases and Parkinson's disease, J Parkinsons Dis source
The Conclusions (page unavailable) propose that peripheral inflammation from a chronically inflamed gut may trigger α-synuclein deposition, increase gut and blood–brain barrier permeability, and lead to neuroinflammation. The same section discusses chronic inflammation in autoimmune conditions, so the citing sentence preserves the paper’s tentative framing. (LLM, conf=0.94)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Roseburia can upregulate innate immune genes, including antimicrobial peptide genes, intestinal barrier function genes, and TLR-related genes such as TLR5 to enhance intestinal barrier function and reduce intestinal inflammation.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [115] Patterson, 2017, Human gut symbiont roseburia hominis promotes and regulates innate immunity, Front Immunol source
The ‘R. hominis affects host innate signaling Pathways’ section reports induction of antimicrobial-peptide, gut-barrier and TLR-related genes, including Tlr5. The Abstract describes strengthened gut barrier function, and ‘R. hominis attenuates colitis in Dss-Treated Mice’ reports reduced colonic inflammation in treated mice. These findings concern R. hominis in mouse models. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Intriguingly, TLR4 gene knockout significantly alleviated the effects of rotenone on intestinal barrier destruction, reduced the expression of GFAP in the myenteric plexus and colonic a-synuclein aggregation, decreased microglial activation in the substantia nigra and the loss of dopaminergic cells and alleviated the impairment of motor function.120”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Could not verifycites [120] Terán-Ventura, 2014, Specific changes of gut commensal microbiota and TLRs during indomethacin-induced acute intestinal inflammation in rats, J Crohns Colitis sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 2 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Could not verify
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Porphyromonas gingivalis-induced peripheral inflammation altered the gut microbiota, increased gut permeability and microglial activation and reduced dopaminergic neurons in the substantia nigra in a genetic mouse model of Parkinson's disease.100”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Partly supportedcites [100] Feng, 2020, Oral P. gingivalis impairs gut permeability and mediates immune responses associated with neurodegeneration in LRRK2 R1441G mice, J Neuroinflamm sourceExperimental — accuracy not yet measured
The Abstract Results report fewer substantia nigra dopaminergic neurons and more activated microglia in R1441G mice given oral P. gingivalis; the Conclusions report impaired gut permeability. The Background says P. gingivalis can alter gut microbiota, but the paper does not report measuring a microbiota change in these mice. That part of the citing sentence is therefore not supported as a finding of this study. (LLM, conf=0.87)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, Roseburia has a negative regulatory effect on the NF-jB pathway, promoting immune homeostasis by downregulating this inflammatory cascade.115”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [115] Patterson, 2017, Human gut symbiont roseburia hominis promotes and regulates innate immunity, Front Immunol sourceExperimental — accuracy not yet measured
The “R. hominis affects host innate signaling Pathways” section reports negative regulation of the NF-κB pathway by R. hominis. It says this *may* contribute to immune homeostasis, whereas the claim states that effect definitively and generalizes from R. hominis to Roseburia. (LLM, conf=0.88)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Another study in Asian population observed that Bacteroides was associated with plasma TNF levels, while Verrucomicrobiaceae abundance was correlated with plasma IFNc levels”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [40] Lin, 2019, Altered gut microbiota and inflammatory cytokine responses in patients with Parkinson's disease, J Neuroinflamm sourceExperimental — accuracy not yet measured
The Results section on altered cytokine responses reports a correlation between Bacteroides abundance and plasma TNFα in patients with Parkinson’s disease, and the Discussion identifies the study population as Asian. It also reports a correlation with plasma IFNγ, but for Verrucomicrobia—not Verrucomicrobiaceae, the different taxonomic group named in the claim. Page numbers are unavailable in our copy. (LLM, conf=0.90)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“These findings suggest that autoimmunity may play a role in the pathogenesis of Parkinson's disease, although it is unclear yet whether a-synuclein antibodies are pathogenic.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Supportedcites [96] Akhtar, 2018, Measurements of auto-antibodies to alpha-synuclein in the serum and cerebral spinal fluids of patients with Parkinson's disease, J Neurochem source
The Introduction (page not provided) suggests that endogenous α-synuclein auto-antibodies may participate in Parkinson’s disease pathogenesis. The Discussion (page not provided) says their origin is unknown and only proposes that they could influence α-synuclein aggregation, consistent with the claim’s uncertainty about whether the antibodies are pathogenic. (LLM, conf=0.90)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Researchers observed that TLR2 gene-deficient (Tlr2 -/-) mice had significantly reduced enteric neurons and glial cells and showed stronger colonic inflammation in response to external stimulation.118”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [118] Brun, 2013, Toll-like receptor 2 regulates intestinal inflammation by controlling integrity of the enteric nervous system, Gastroenterology source
The section on myenteric plexus architecture reports significantly fewer enteric neurons and glial cells in Tlr2-deficient mice. The Discussion states that these mice are more susceptible to colitis after chemical mucosal insults, consistent with the claim about stronger inflammation after external stimulation. (LLM, conf=0.92)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a mouse model, it was found that gastric infection by Helicobacter suis resulted in gastric inflammation and increased gastrointestinal permeability, accompanied by an increased level of proinflammatory cytokines in serum, which was associated with systemic inflammation.107”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Partly supportedcites [107] Gorle, 2018, The choroid plexus epithelium as a novel player in the stomach-brain axis during Helicobacter infection, Brain Behav Immun sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In animal experiments, intranasal injection of LPS could activate microglia in the olfactory bulb and substantia nigra through IL-1b/IL-1R1 signalling, increase pS129 a-synucleinpositive cells in the olfactory bulb and substantia nigra and reduce the number of tyrosine hydroxylase (TH)-immunoreactive cells, suggesting the loss of dopaminergic cells.150”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [150] Niu, 2020, IL-1beta/IL-1R1 signaling induced by intranasal lipopolysaccharide infusion regulates alpha-synuclein pathology in the olfactory bulb, substantia nigra and striatum, Brain Pathol sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In contrast, another study with a follow-up of patients after vagotomy argued that vagotomy was not associated with the risk of Parkinson's disease in Sweden.144”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [144] Liu, 2017, Vagotomy and Parkinson disease: A Swedish register-based matched-cohort study, Neurology source
The Abstract Methods describe a Swedish matched-cohort study that followed patients after vagotomy. The Abstract Results report no association between vagotomy overall and Parkinson disease risk (HR 0.96, 95% CI 0.78–1.17), while noting a possible lower risk after truncal vagotomy. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Erny et al. 147 illustrated that germ-free animals display global deficiency in microglia and the genes needed to express type I interferon receptors such as Janus kinase 3 (Jak3) and signal transducer and activator of transcription 1 (Stat1), were reduced.147”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [147] Erny, 2015, Host microbiota constantly control maturation and function of microglia in the CNS, Nat Neurosci sourceExperimental — accuracy not yet measured
In “Germ-free animals display global defects in microglia,” the paper reports reduced Jak3 and Stat1 expression in germ-free microglia and describes broad defects in their maturation and function. It does not report a global deficiency in microglial cell numbers: it found significantly more microglia in every brain region investigated. (LLM, conf=0.88)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LPS produced by gut microbiota treatment can increase the accumulation of a-synuclein in the enteric nervous system and increase intestinal permeability.128”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [128] Kelly, 2014, Progression of intestinal permeability changes and alpha-synuclein expression in a mouse model of Parkinson's disease, Mov Disord sourceExperimental — accuracy not yet measured
The Discussion reports that low-dose LPS increased enteric α-synuclein expression and gut permeability in mice, predominantly in the large intestine. But the Experimental Design specifies a single intraperitoneal LPS dose, not treatment with gut microbiota or a demonstration that microbiota-produced LPS caused these effects. (LLM, conf=0.87)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The function of microglia can be restored by the reconstruction of gut microbiota or their metabolites, indicating that microbiota may also be involved in the activity of the innate immune system in the brain via microbial metabolites and intestinal secretions.147”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [147] Erny, 2015, Host microbiota constantly control maturation and function of microglia in the CNS, Nat Neurosci sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Exposure to curli-producing bacteria increases the deposition and accumulation of a-synuclein in intestinal ganglion cells (myenteric plexus and submucosa) and the brain, respectively, as well as increasing the inflammatory response in the brain.131”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [131] Chen, 2016, Exposure to the functional bacterial amyloid protein curli enhances alpha-synuclein aggregation in aged Fischer 344 rats and Caenorhabditis elegans, Sci Rep source
The Results section on rat gut and brain reports increased alpha-synuclein deposition in gut ganglion cells (myenteric plexus and submucosa) and brain neurons after exposure to curli-producing bacteria. The Results section on immune responses reports increased microgliosis, astrogliosis, and several inflammatory markers in the brains of exposed rats. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A clinical study revealed that the level of serum LPS-binding protein in patients with Parkinson's disease was lower than that in controls, indicating that increased intestinal permeability and increased invasion of Gram-negative bacteria leads to an increase in LPS in the circulatory system.148”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [148] Hasegawa, 2015, Intestinal dysbiosis and lowered serum lipopolysaccharide-binding protein in Parkinson's disease, PLoS One sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The peripheral inflammation induced by systemic LPS administration increased the activation of microglia and proinflammatory cytokines, destroyed the BBB, and aggravated the polarization of the A1 phenotype of astrocytes and the loss of dopamine neurons in the substantia nigra and striatum of MPTP mice.149”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [149] Garcia-Dominguez, 2018, Peripheral inflammation enhances microglia response and nigral dopaminergic cell death in an in vivo MPTP model of Parkinson's disease, Front Cell Neurosci sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Remarkably, a recent study did not find pathological damage to a-synuclein in the vagus nerve in an animal model of Parkinson's disease, which does not support the hypothesis that a-synuclein pathology is transmitted through the vagus nerve and the dorsal motor nucleus of the vagus nerve.140”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [140] Arotcarena, 2020, Bidirectional gut-to-brain and brain-to-gut propagation of synucleinopathy in non-human primates, Brain source
The Results report no increase in aggregated α-synuclein or significant difference in phosphorylated α-synuclein in the vagus nerve of Lewy body-injected monkeys. The Discussion explicitly says the findings do not support transmission through the vagus nerve and dorsal motor nucleus of the vagus, while limiting that conclusion to the observed time point. (LLM, conf=0.94)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Increased intestinal permeability is associated with increased bacteria and exposure to the bacterial endotoxin in Parkinson's disease, while increased intestinal a-synuclein and 3nitrotyrosine staining (associated with oxidative stress) leads to high intestinal permeability.127”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Partly supportedcites [127] Forsyth, 2011, Increased intestinal permeability correlates with sigmoid mucosa alpha-synuclein staining and endotoxin exposure markers in early Parkinson's disease, PLoS One sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Furthermore, similar to Tlr2 -/-mice, the wild-type mice lacking gut microbiota also have enteric nervous system and GDNF deficiencies, which can be partially repaired by administration of TLR2 agonists.118”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Supportedcites [118] Brun, 2013, Toll-like receptor 2 regulates intestinal inflammation by controlling integrity of the enteric nervous system, Gastroenterology source
The results section (p. 1329) reports that antibiotic-treated wild-type mice had ENS abnormalities and reduced GDNF levels and signaling. It also reports that Pam3CSK4, a TLR2 agonist identified in the Methods, partially corrected the ENS abnormalities. (LLM, conf=0.94)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The activation of neuronal TLR2 in the brains of patients with Parkinson's disease results in increased proinflammatory cytokine (TNF) levels and recruitment of microglia to amplify neuroinflammation as well as increased expression of asynuclein.158”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Partly supportedcites [158] Dzamko, 2017, Toll-like receptor 2 is increased in neurons in Parkinson's disease brain and may contribute to alpha-synuclein pathology, Acta Neuropathol sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Butyrate can protect cells from increased paracellular permeability and destruction of the epithelial barrier by LPS, increase the expression of tight junction claudins by activating the Akt/mTOR signalling pathway and downregulate the expression of TLR4 to decrease the expression of the inflammatory cytokines.191”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Partly supportedcites [191] Koval, 2017, Butyrate modifies intestinal barrier function in IPEC-J2 cells through a selective upregulation of tight junction proteins and activation of the Akt signaling pathway, PLoS One sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A recent study on the effect of propionate on rotenone-treated dopaminergic neurons showed that the survival rate of TH + dopaminergic neurons increased significantly, indicating that propionic acid increased the expression of the TH gene, decreased the expression of the a-synuclein gene, and increased the expression of intracellular STAT3 protein to promote neuroprotection.197”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Partly supportedcites [197] Ostendorf, 2020, Propionic acid and fasudil as treatment against rotenone toxicity in an in vitro model of Parkinson's disease, Molecules sourceExperimental — accuracy not yet measured
Results §§2.2–2.4 report significantly greater TH+ cell survival with propionic acid under rotenone, increased TH gene expression, and increased STAT3 protein expression. But Results §2.3 reports that propionic acid significantly increased—not decreased—aSyn gene expression relative to the untreated control. The Discussion (§3) also says STAT3 signaling showed no robust modification, so the paper does not establish increased STAT3 as the mechanism of neuroprotection. (LLM, conf=0.90)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The integrity of the BBB in germ-free mice was enhanced by transplanting faecal microbiota from the pathogen-free mice or by using microbial SCFAs, suggesting that the microbiota can regulate the function of the BBB.167”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Supportedcites [167] Braniste, 2014, The gut microbiota influences blood-brain barrier permeability in mice, Sci Transl Med source
The Discussion reports that transplanting fecal microbiota from pathogen-free mice or administering SCFA-producing bacteria reinforced BBB integrity in germ-free adult mice. The Results section also reports decreased BBB permeability after treatment with the microbial metabolite sodium butyrate, supporting the claim about SCFAs. (LLM, conf=0.94)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Bile acids can, moreover, eliminate bacterial overgrowth and reduce bacterial translocation and endotoxemia.208”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
What the sources say
- Partly supportedcites [208] Lorenzo-Zuniga, 2003, Oral bile acids reduce bacterial overgrowth, bacterial translocation, and endotoxemia in cirrhotic rats, Hepatology sourceExperimental — accuracy not yet measured
The Abstract (p. 551) reports that oral conjugated bile acids eliminated intestinal bacterial overgrowth and decreased bacterial translocation and endotoxemia in ascitic cirrhotic rats. The citing sentence omits that experimental population and the fact that the administered bile acids were conjugated, making the claim broader than the result shown. (LLM, conf=0.84)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Studies have found that SCFAs are associated with a variety of diseases such as rectal cancer, 174 pancreatitis, 175 abnormal energy metabolism, 176 constipation, 177 blood lipid metabolism, 178 sleep disorders 179 and Alzheimer's disease.180”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [174] Ma, 2020, Sodium butyrate modulates gut microbiota and immune response in colorectal cancer liver metastatic mice, Cell Biol Toxicol source
- Supportedcites [175] Pan, 2019, Butyrate ameliorates caerulein-induced acute pancreatitis and associated intestinal injury by tissue-specific mechanisms, Br J Pharmacol source
Citation 175 is attached to pancreatitis, not the other conditions in the list. Section 3.1 reports that sodium butyrate, a short-chain fatty acid, reduced the severity of caerulein-induced acute pancreatitis in mice. This supports the attributed association, within that experimental setting. (LLM, conf=0.93)
- Supportedcites [176] Li, 2018, Butyrate reduces appetite and activates brown adipose tissue via the gut-brain neural circuit, Gut source
Citation 176 follows “abnormal energy metabolism,” so the other conditions in the sentence are not attributed to this source. The paper’s Gut microbiota section (page not supplied) says SCFA supplementation can protect against obesity and describes effects of butyrate and acetate on energy metabolism and insulin resistance. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [177] Tian, 2021, Analysis of gut microbiome and metabolite characteristics in patients with slow transit constipation, Dig Dis Sci source
- Supportedcites [178] Tayyeb, 2020, Short-chain fatty acids (except hexanoic acid) lower NF-kB transactivation, which rescues inflammation-induced decreased apolipoprotein A-I transcription in HepG2 cells, Int J Mol Sci source
Citation 178 is attached to the blood-lipid-metabolism example, not the other conditions in the sentence. The Introduction links SCFAs to ApoA-I, a protein involved in HDL function and cholesterol efflux; Results §2.1 reports that several SCFAs increased ApoA-I transcription in HepG2 cells. This supports an association with lipid metabolism, though the experiment measured a cellular marker rather than blood lipid levels. (LLM, conf=0.88)
- Partly supportedcites [179] Szentirmai, 2019, Butyrate, a metabolite of intestinal bacteria, enhances sleep, Sci Rep sourceExperimental — accuracy not yet measured
Citation 179 is attached to “sleep disorders,” not the other conditions in the list. The Introduction and Discussion (page unavailable) report that butyrate, an SCFA, increased sleep in mice and rats. They do not establish an association with sleep disorders, so the cited evidence supports a link to sleep but not the disease-specific claim. (LLM, conf=0.84)
- Supportedcites [180] Ho, 2018, Protective roles of intestinal microbiota derived short chain fatty acids in Alzheimer's disease-type beta-amyloid neuropathological mechanisms, Expert Rev Neurother source
Citation 180 is attached to Alzheimer’s disease, not to the other conditions in the list. The Results (§3.1–3.2; page not provided) report that certain SCFAs inhibit amyloid-β aggregation and fibril formation in vitro, supporting the stated association with Alzheimer’s disease. (LLM, conf=0.91)
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Pathological a-synuclein aggravates the progression of Parkinson's disease by activating microglia, while the absence or overstimulation of microglia can affect the spread of a-synuclein in the brain.153,159”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [153] Zhang, 2017, Pathological alpha-synuclein exacerbates the progression of Parkinson's disease through microglial activation, Toxicol Lett source
- Partly supportedcites [159] George, 2019, Microglia affect α-synuclein cell-to-cell transfer in a mouse model of Parkinson’s disease, Mol Neurodegener sourceExperimental — accuracy not yet measured
The Abstract Conclusions (page not provided) state that microglial absence or hyperstimulation affected α-synuclein transfer in the brain. The Background says aggregated α-synuclein activates microglia and that neuroinflammation can worsen neuropathology in animal models of Parkinson’s disease. It does not establish the stronger claim that this mechanism aggravates disease progression in patients. (LLM, conf=0.85)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Increased activation of TNF/TNFR1 signalling following chronic activation of microglia can give rise to TNF-mediated necroptotic neuronal cell death, 160 which represents a possible therapeutic target in Parkinson's disease.161”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Supportedcites [160] Iannielli, 2018, Pharmacological inhibition of necroptosis protects from dopaminergic neuronal cell death in Parkinsons disease models, Cell Reports source
The citation to this paper follows the therapeutic-target clause. The Discussion states that inhibiting necroptosis might be a therapeutic option for counteracting Parkinson’s disease-related neurodegeneration. The preceding TNF/TNFR1 mechanism has a separate citation. (LLM, conf=0.93)
- Partly supportedcites [161] Yuan, 2019, Necroptosis and RIPK1-mediated neuroinflammation in CNS diseases, Nat Rev Neurosci sourceExperimental — accuracy not yet measured
The Introduction describes TNFR1-triggered necroptosis, and the section on mitochondrial and lysosomal defects reports evidence implicating necroptosis in Parkinson’s disease, including protective effects of RIPK1 inhibition in disease models (page numbers unavailable). The copy does not establish the claimed sequence in Parkinson’s disease—chronic microglial activation increasing TNF/TNFR1 signalling and thereby causing necroptotic neuronal death. Its discussion of chronic microglial inflammation and TNF concerns Alzheimer’s disease. (LLM, conf=0.84)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Butyrate can also promote the production of IL-10 by regulating the differentiation of Th1 and Th17 cells and inducing the expression of mature protein 1 (Blimp1), ameliorating colonic inflammation and maintaining intestinal homeostasis.189”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Supportedcites [189] Chen, 2019, Microbiota metabolite butyrate differentially regulates Th1 and Th17 cells' differentiation and function in induction of colitis, Inflamm Bowel Dis source
The Results report that butyrate differentially regulates Th1 and Th17 development, increases IL-10 production under both conditions, and induces Blimp1, which contributes to that increase. The Results also report less severe colitis after transfer of butyrate-treated T cells; the Introduction links this effect to maintenance of intestinal homeostasis. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“SCFAs may be able to modulate neuroinflammation in (HDACi), can reduce the degeneration of dopaminergic neurons and improve dyskinesia in a rotenone-induced Drosophila Parkinson's disease model.194”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Partly supportedcites [194] St. Laurent, 2013, Sodium butyrate improves locomotor impairment and early mortality in a rotenone-induced Drosophila model of Parkinson's disease, Neuroscience sourceExperimental — accuracy not yet measured
The Abstract and Discussion (pages unavailable) report that sodium butyrate improved rotenone-induced locomotor impairment in Drosophila and was associated with higher brain dopamine levels. They do not report reduced dopaminergic-neuron degeneration in the rotenone model; the Abstract attributes that effect to sodium butyrate in a different, α-synuclein Drosophila model. The study also tested sodium butyrate, not SCFAs as a group, and measured locomotor impairment rather than dyskinesia. (LLM, conf=0.89)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“FMT has been regarded as an effective and safe treatment for patients with recurrent C. difficile and has been approved by the Federal Drug Administration in the USA.266”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Partly supportedcites [266] Carlucci, 2016, Fecal microbiota-based therapeutics for recurrent Clostridium difficile infection, ulcerative colitis and obesity, EBioMedicine sourceExperimental — accuracy not yet measured
The FMT section reports about 90% clinical cure of recurrent C. difficile infection, supporting the effectiveness claim. The Regulation of Stool-based Therapeutics section says the FDA allows FMT for this use under specified conditions without an Investigational New Drug application; it does not say the FDA approved it. That section also calls for monitoring long-term safety and adverse events, so the unqualified safety claim is not established. (LLM, conf=0.89)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“although the mechanisms may involve relieving symptoms, inhibiting inflammation, avoiding antioxidant stress and neuronutrition.254,255”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Probiotics
What the sources say
- Supportedcites [254] Castelli, 2020, Effects of the probiotic formulation SLAB51 in and Parkinson's disease models, Aging (Albany NY source
The Discussion and Conclusion report that SLAB51 improved behavioral impairments and counteracted neuroinflammation and oxidative stress in Parkinson’s disease models. The same section describes increased BDNF and related neuroprotective pathways, supporting the claim’s reference to neurotrophic support. These are findings from in vitro and in vivo models, not demonstrated symptom relief in patients. (LLM, conf=0.88)
- Partly supportedcites [255] Tamtaji, 2019, Clinical and metabolic response to probiotic administration in people with Parkinson's disease: A randomized, double-blind, placebo-controlled trial, Clin Nutr sourceExperimental — accuracy not yet measured
Section 4.1 reports improved Parkinson’s symptom scores and markers of inflammation and oxidative stress after probiotic supplementation, and discusses possible pathways for those effects. It also mentions effects on central neurochemistry, but does not describe a neuronutrition mechanism. No page number is available in our copy. (LLM, conf=0.86)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The composition of the intestinal microbiota could affect different organ systems, including the cardiovascular, nervous, immune and metabolic systems.251”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Probiotics
What the sources say
- Supportedcites [251] Azad, 2018, Probiotic species in the modulation of gut microbiota: An overview, Biomed Res Int source
Section 3, “Modulation of Gut Microbiota and Probiotic Species,” states that gut microbiota composition is likely to affect the cardiovascular, neural, immune, and metabolic systems. The citing sentence preserves that uncertainty and names the same systems. (LLM, conf=0.95)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, recent studies have reported that Roseburia intestinalis decreased the disease activity index score, intestinal mucosal epithelial injury and mucosal lymphocyte infiltration, while inhibiting intestinal inflammation, by increasing the number of Treg cells and the expression of anti-inflammatory cytokines in a mouse model of colitis.272,273”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not checked — no full text of the sourcecites [272] Shen, 2018, Insights into Roseburia intestinalis which alleviates experimental colitis pathology by inducing anti-inflammatory responses, J Gastroenterol Hepatol source
- Partly supportedcites [273] Zhu, 2018, Roseburia intestinalis inhibits interleukin17 excretion and promotes regulatory T cells differentiation in colitis, Mol Med Rep sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A recent study in Caenorhabditis elegans Parkinson's disease models showed that the main olive oil polyphenols, hydroxytyrosol and oleuropein aglycone, can reduce the accumulation of a-synuclein in muscle cells and prevent the neurodegeneration of dopaminergic neurons containing a-synuclein.248”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
What the sources say
- Partly supportedcites [248] Brunetti, 2020, Healthspan Maintenance and Prevention of Parkinson's-like Phenotypes with Hydroxytyrosol and Oleuropein Aglycone in C. elegans, Int J Mol Sci sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Studies have shown that prebiotics (including galacto-and fructooligosaccharides) can effectively normalize motor and nonmotor abnormalities and restore the level of dopamine transporters in the striatum induced by rotenone.258”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
What the sources say
- Partly supportedcites [258] Perez-Pardo, 2017, Promising effects of neurorestorative diets on motor, cognitive, and gastrointestinal dysfunction after symptom development in a mouse model of Parkinson's disease, Front Aging Neurosci sourceExperimental — accuracy not yet measured
The Abstract and Discussion report that Diet2 improved rotenone-induced motor and nonmotor abnormalities and restored striatal dopamine transporter (DAT) levels in mice. The Diets table shows that Diet2 contained galacto- and fructooligosaccharides, but also uridine, fatty acids, vitamins, and other nutrients. The study did not isolate the effects of prebiotics, so it cannot establish that prebiotics themselves produced those outcomes. (LLM, conf=0.90)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The gut microbiota plays a key role in promoting serotonin secretion, inducing enteric nervous system maturation by releasing 5-HT and activating the 5-HT4 receptor.222”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Neurotransmitters
What the sources say
- Supportedcites [222] De Vadder, 2018, ut microbiota regulates maturation of the adult enteric nervous system via enteric serotonin networks, Proc Natl Acad Sci U S A source
The Discussion says the gut microbiota promotes 5-HT secretion and that mucosal and neuronal 5-HT contribute to ENS maturation. The Results section “Activation of the 5-HT4R in GF Mice Induces Maturation of the Adult ENS” links microbiota-stimulated 5-HT release and 5-HT4R activation to enteric-neuron maturation. Page numbers are not available in our copy. (LLM, conf=0.93)
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A case-control study reported that the higher the compliance with a Mediterranean diet, the lower the risk of Parkinson's disease and the lower the score of the Mediterranean diet, the earlier the age of onset of Parkinson's disease, but it did not indicate whether low Mediterranean dietary compliance was the result or cause of Parkinson's disease.236”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
What the sources say
- Supportedcites [236] Alcalay, 2012, The association between Mediterranean diet adherence and Parkinson's disease, Mov Disord source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, the exact mechanisms and safety of using probiotics in Parkinson's disease have not fully been clarified, although the mechanisms may involve relieving symptoms, inhibiting inflammation, avoiding antioxidant stress and neuronutrition.254,255”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Probiotics
What the sources say
- Partly supportedcites [254] Castelli, 2020, Effects of the probiotic formulation SLAB51 in and Parkinson's disease models, Aging (Albany NY sourceExperimental — accuracy not yet measured
The Discussion and Conclusion (page not provided) describes the proposed PPARγ mechanism as speculative and calls for further study, supporting the claim that probiotic mechanisms in Parkinson’s disease are not fully clarified. The paper studies SLAB51 in cell and animal models, but the passages do not assess or discuss the safety of probiotic use in people with Parkinson’s disease. (LLM, conf=0.83)
- Partly supportedcites [255] Tamtaji, 2019, Clinical and metabolic response to probiotic administration in people with Parkinson's disease: A randomized, double-blind, placebo-controlled trial, Clin Nutr sourceExperimental — accuracy not yet measured
The Discussion (sections 4.1–4.2; page unavailable) proposes possible mechanisms and says further work on gene expression could help identify them, supporting the point that mechanisms remain unclear. The Results (section 3; page unavailable) report no side effects during the 12-week trial, but the paper does not state that the safety of probiotics in Parkinson’s disease remains unclarified. (LLM, conf=0.82)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The results of a recent randomized, single-blind and controlled trial demonstrated that the endoscopic index of Crohn's disease severity decreased 6 weeks after FMT.267”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Supportedcites [267] Sokol, 2020, Fecal microbiota transplantation to maintain remission in Crohn's disease: A pilot randomized controlled study, Microbiome source
The Abstract describes the study as a randomized, single-blind, sham-controlled pilot trial. The ‘Efficacy in maintaining remission’ section reports that the Crohn’s Disease Endoscopic Index of Severity decreased significantly six weeks after FMT (p = 0.03), but not after sham transplantation (p = 0.8). (LLM, conf=0.94)
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“A survey ascertained that doctors have a relatively high awareness and acceptance of FMT but are most concerned about patients' acceptance of the treatment, followed by a lack of guidelines and ethical constraints.280”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Supportedcites [280] Ren, 2016, Chinese physicians' perceptions of faecal microbiota transplantation, World J Gastroenterol source
The Discussion describes high awareness and acceptance of FMT among the surveyed Chinese physicians. The Attitudes toward FMT section ranks patients’ acceptance as the leading barrier (79.2%), followed by the absence of guidelines (56.9%) and systemic and ethical constraints (46.5%). (LLM, conf=0.93)
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Moreover, the increased production of cytokines in the midbrain and colon indicates that microbiota play an important role in a-synuclein production and neuroinflammation.132”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
What the sources say
- Partly supportedcites [132] Sampson, 2020, A gut bacterial amyloid promotes alpha-synuclein aggregation and motor impairment in mice, Elife sourceExperimental — accuracy not yet measured
The Results and discussion section reports increased cytokine production in the midbrain and colon of mice colonized with curli-producing E. coli, supporting the neuroinflammation part of the claim. It reports increased α-synuclein aggregation despite similar transgene production, so these findings do not establish increased α-synuclein production. (LLM, conf=0.90)
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The double-hit hypothesis proposed by Hawkes et al.135 supports their theory, pointing out that a-synuclein pathology is transmitted to the midbrain through two different routes, namely, from the nasal cavity to the temporal lobe or from the stomach, followed by nasal secretions in swallowed saliva.135”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
What the sources say
- Partly supportedcites [135] Hawkes, 2007, Parkinson's disease: A dual-hit hypothesis, Neuropathol Appl Neurobiol sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Colonization of curli-producing E. coli in a-synuclein-overexpressing mice aggravated motility injury and gastrointestinal dysfunction, while promoting the accumulation and inflammatory response of a-synuclein in the intestine and brain, resulting in increased expression of the proinflammatory cytokines IL-6 and TNF in brain-derived CD11b + microglia.132”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
What the sources say
- Supportedcites [132] Sampson, 2020, A gut bacterial amyloid promotes alpha-synuclein aggregation and motor impairment in mice, Elife source
Split into 2 atoms — 2 confirmed, 0 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“A clinical study reported that constipation and movement symptoms were significantly relieved after a single FMT treatment in a patient with Parkinson's disease with constipation, and leg tremor almost disappeared 1 week after FMT treatment.277”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Partly supportedcites [277] Huang, 2019, Fecal microbiota transplantation to treat Parkinson's disease with constipation: A case report, Medicine (Baltimore sourceExperimental — accuracy not yet measured
The Case presentation reports that leg tremor almost disappeared one week after FMT, the UPDRS score decreased significantly, and constipation was significantly alleviated. But it also says the fecal suspension was administered three times, once daily, rather than as a single administration. (LLM, conf=0.88)
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, the duration and recovery time of the alterations in gut microbiota caused by antibiotics seem uncertain.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The study findings vary due to differences in methodology, geographical regions, age and dietary habits.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, the abundance of gut microbiota in patients with Parkinson's disease is significantly altered and has obvious characteristics, which may be used as potential”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
In the paper
“Akkermansia muciniphila may also have beneficial effects on metabolic disorders in obese mice as well as metabolic syndrome lipid metabolism.45”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [45] Everard, 2013, Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity, Proc Natl Acad Sci U S A source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
In the paper
“Another study analysed the alteration of gut microbiota in 12 healthy males treated with 4-day antibiotic intervention and found that the composition of gut microbiota returned to initial baseline within 1.5 months.54”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [54] Palleja, 2018, Recovery of gut microbiota of healthy adults following antibiotic exposure, Nat Microbiol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Parkinson's disease is a common neurodegenerative disease largely characterized by the loss of dopaminergic neurons with abnormal accumulation of a-synuclein in the substantia nigra and striatum.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“A study on the composition of caecal mucosa-associated and luminal microbiota in rotenoneinduced Parkinson's disease mice showed that in the caecal mucosa, the relative abundance of the phyla Bacteroidetes and Firmicutes significantly increased in the experimental group, whereas the relative abundance of Actinobacteria and beneficial symbiotic bacteria Bifidobacterium significantly decreased.49”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [49] Perez-Pardo, 2018, Gut bacterial composition in a mouse model of Parkinson’s disease, Beneficial Microb source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Several lines of evidence in recent studies have shown that the composition of gut microbiota is affected by antibiotics, leading to the imbalance of host immune homeostasis and increased susceptibility to disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
boosteddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“which may be used as potential biomarkers or therapeutic targets.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: unclear — It is unclear why the paper says it holds.
It may state two separate claims as one.
In the paper
“Most antibiotics interfere with the composition and enzyme activity of the intestinal microbiota and inhibit enzyme activity.52”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [52] Kim, 2015, Gut microbiota-mediated drug-antibiotic interactions, Drug Metab Dispos source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In recent years, clinical evidence has demonstrated the relationship between gut microbiota, clinical symptoms (including motor and non-motor symptoms) and disease stage in Parkinson's disease.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Campos-Peña et al. 46 reported that metabolic syndrome, including insulin resistance and obesity, is an essential risk factor for cognitive impairment and dementia disorders.46”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [46] Campos-Peña, 2017, Metabolic syndrome as a risk factor for Alzheimer's disease: Is Aβ a crucial factor in both pathologies?, Antioxid Redox Signal source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Antibiotic administration in specific pathogen-free mice temporarily altered the composition of the microbiota with a significant increase in Firmicutes and Actinobacteria and a decrease in Bacteroidetes and Proteobacteria and increased exploratory behaviour.55”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
What the sources say
- Not checked — no full text of the sourcecites [55] Bercik, 2011, The intestinal microbiota affect central levels of brain-derived neurotropic factor and behaviour in mice, Gastroenterology source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The results of the studies on animal models of Parkinson's disease are similar to those in humans.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Introduction
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Although studies suggest that the microbiota is associated with the pathogenesis of Parkinson's disease, the specific mechanisms have not fully been elucidated.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The myenteric plexus regulates muscle activity, while the submucosal plexus participates in mucosal function.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microbial metabolism and the associated metabolites regulate the homeostasis of the gut and affect the development of the CNS and Parkinson's disease by regulating the intestinal barrier, drug interactions, neurotrophic factors and the immune response.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The enteric nervous system is a relay station between the gut microbiota and brain and is one of the three branches of the autonomic nervous system (sympathetic, parasympathetic and enteric).69”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Not checked — no full text of the sourcecites [69] Rao, 2016, The bowel and beyond: The enteric nervous system in neurological disorders, Nat Rev Gastroenterol Hepatol source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Because of the different dietary structures in different countries and regions, the composition of gut microbiota is also different.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Patients with Parkinson's disease and irritable bowel syndrome-like symptoms (abdominal pain) had more non-motor symptoms, along with lower levels of Prevotella (genus and family)”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites [58] Mertsalmi, 2017, More than constipation - Bowel symptoms in Parkinson's disease and their connection to gut microbiota, Eur J Neurol source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Recently, the positive rate of small intestinal bacterial overgrowth in patients with Parkinson's disease was found to be significantly increased, and it was associated with the deterioration of gastrointestinal symptoms and motor function.61”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites [61] Niu, 2016, Prevalence of small intestinal bacterial overgrowth in Chinese patients with Parkinson's disease, J Neural Transm (Vienna) source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“However, most studies have been cross-sectional, involving different selected populations and research methods, with no data on the relationship between the composition of specific gut microbiota and disease progression.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > HAMD(Hamilton Depression Scale)scores
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“it remains unclear whether the peripheral immune response is the cause or a result of CNS pathology.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [93] Liu, 2019, IL-17A exacerbates neuroinflammation and neurodegeneration by activating microglia in rodent models of Parkinson's disease, Brain Behav Immun source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Overexpression of a-synuclein promoted proinflammatory C-C chemokine receptor type 2 (CCR2)-positive peripheral monocyte entry into the CNS in a mouse model of Parkinson's disease, and deletion of CCR2 could prevent monocyte infiltration, a-synuclein mediated inflammation and subsequent dopaminergic neuronal death.85”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [85] Harms, 2018, Peripheral monocyte entry is required for alpha-Synuclein induced inflammation and neurodegeneration in a model of Parkinson disease, Exp Neurol source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The microbiota-gut-brain axis consists of several components of the nervous system, including the CNS, the autonomic nervous system, the enteric nervous system and the hypothalamic-pituitary-adrenal axis.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“A recent study reported an increased number of T cells in postmortem midbrains of Parkinson's disease, and T cells induced neuronal death via interleukin (IL)-17 and NF-jB activation in human induced pluripotent stem cell-derived midbrain neurons from patients with Parkinson's disease.86”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [86] Sommer, 2018, Th17 lymphocytes induce neuronal cell death in a human iPSC-based model of Parkinson's disease, Cell Stem Cell source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Other authors have demonstrated that cytotoxic CD8 + T cell infiltration occurred earlier than a-synuclein aggregation and neuronal death, suggesting adaptive immune system involvement.87”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [87] Galiano-Landeira, 2020, CD8 T cell nigral infiltration precedes synucleinopathy in early stages of Parkinson's disease, Brain source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In the enteric nervous system, EGCs are essential to the development, normal survival and differentiation of neurons”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Not checked — no full text of the sourcecites [73] Vergnolle, 2018, Neurons and Glia in the enteric nervous system and epithelial barrier function, Physiology (Bethesda) source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“Physiologically, gastrointestinal motility, glandular secretion, epithelial barriers and other digestive system functions are controlled by the autonomic nervous system.68”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Composition of the microbiota-gut-brain axis
What the sources say
- Not checked — no full text of the sourcecites [68] Wehrwein, 2016, Overview of the anatomy, physiology, and pharmacology of the autonomic nervous system, Compr Physiol source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Since levodopa is mainly absorbed in the jejunum, small intestinal bacterial overgrowth may reduce drug absorption through intestinal mucosal inflammation or cause alterations in the metabolism of levodopa by bacteria in the lumen.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“In addition, antibiotics (rifaximin) can alleviate the gastrointestinal symptoms and motor fluctuations Table 2 Research studies on the clinical correlations between gut microbiota and Parkinson's disease”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Clinical correlations between gut microbiota and Parkinson's disease
What the sources say
- Not checked — no full text of the sourcecites [62] Fasano, 2013, The role of small intestinal bacterial overgrowth in Parkinson's disease, Mov Disord source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Additionally, Keshavarzian et al. 28 observed that the putative proinflammatory bacteria Ralstonia in the intestinal mucosa of patients with Parkinson's disease were significantly abundant, and the putative proinflammatory bacteria Akkermansia, Oscillospira and Bacteroides were significantly increased in faecal samples.28”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [28] Keshavarzian, 2015, Colonic bacterial composition in Parkinson's disease, Mov Disord source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Intestinal epithelial cells regulate the diversity and function of the gut microbiota; in turn, gut microbiota are crucial to the growth and function of these cells.108”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [108] Soderholm, 2019, Intestinal epithelial cells: At the interface of the microbiota and mucosal immunity, Immunology source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Faecal microbiota transplantation (FMT) can improve the metabolic disorder of gut microbiota in MPTP mice by inhibiting the TLR4/TBK1/NF-jB/TNF signalling pathway, thus reducing intestinal inflammation and neuroinflammation, verifying the mechanism of communication between the gut and the brain.121”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [121] Sun, 2018, Neuroprotective effects of faecal microbiota transplantation on MPTP-induced Parkinson's disease mice: Gut microbiota, glial reaction and TLR4/TNF-α signaling pathway, Brain Behavior Immunity source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The gut microbiota plays a vital part in the occurrence and development of colitis induced by dextran sulphate sodium, and the lack of gut microbiota significantly reduces colitis.109”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [109] Hernandez-Chirlaque, 2016, Germ-free and antibiotic-treated mice are highly susceptible to epithelial injury in DSS colitis, J Crohns Colitis source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In a rotenone-induced Parkinson's disease mouse model, stress aggravated intestinal hyperpermeability and caused alterations to gut microbiota and inflammation in the colon as well as increased neuroinflammation in the brain.99”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [99] Dodiya, 2020, Chronic stress-induced gut dysfunction exacerbates Parkinson's disease phenotype and pathology in a rotenone-induced mouse model of Parkinson's disease, Neurobiol Dis source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Therefore, gut microbiota and its metabolites may be involved in the pathophysiology of Parkinson's disease through intestinal inflammation, and the proinflammatory intestinal environment may trigger the pathogenesis of Parkinson's disease.116”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [116] Matheoud, 2019, Intestinal infection triggers Parkinson's disease-like symptoms in Pink1(-/-) mice, Nature source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Another study revealed that the numbers of circulating lymphocytes and neutrophils were decreased with the increased plasma levels of proinflammatory cytokines after LPS injection in a 6-hydroxydopamine (6-OHDA) rat model compared with controls, suggesting that peripheral immune disorder was involved in neurodegeneration associated with Parkinson's disease.105”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Peripheral inflammation, infection and Parkinson's disease pathology
What the sources say
- Not checked — no full text of the sourcecites [105] Engler, 2009, Time-dependent alterations of peripheral immune parameters after nigrostriatal dopamine depletion in a rat model of Parkinson's disease, Brain Behav Immun source
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Changes in the expression and phosphorylation of intestinal GFAP were found in colon biopsies of patients with Parkinson's disease, indicating that there is reactive proliferation of EGCs in Parkinson's disease, which leads to local inflammation and may spread to the CNS.110”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [110] Clairembault, 2014, Enteric GFAP expression and phosphorylation in Parkinson's disease, J Neurochem source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“In addition, TLR4 plays an important role in regulating enteric neuron survival and intestinal motility; moreover, by activating TLR4, the gut microbiota can regulate gastrointestinal motility.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Inhibition of TLR4 can downregulate this process, indicating that this receptor plays an important role in paraquat-mediated microglial inflammation.154,155”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [154] Sun, 2018, Paraquat-induced inflammatory response of microglia through HSP60/TLR4 signaling, Hum Exp Toxicol source
- Not checked — no full text of the sourcecites [155] Li, 2019, Inhibiting expression of HSP60 and TLR4 attenuates paraquat-induced microglial inflammation, Chem Biol Interact source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“FMT can reduce the increased number of astrocytes, decrease the activation of microglia in the MPTP mouse model and participate in suppressing neuroinflammation by inhibiting the TLR4/TBK1/NF-jB/TNF-a signalling pathway.121”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [121] Sun, 2018, Neuroprotective effects of faecal microbiota transplantation on MPTP-induced Parkinson's disease mice: Gut microbiota, glial reaction and TLR4/TNF-α signaling pathway, Brain Behavior Immunity source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“A recent study found that a TLR2 activator can restore the inhibition of enteric nervous system neurogenesis caused by decreased gut microbiota and modulate the structure and function of the system.124”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [124] Yarandi, 2020, Intestinal bacteria maintain adult enteric nervous system and nitrergic neurons via Toll-like receptor 2-induced neurogenesis in mice, Gastroenterology source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Additionally, the activation of TLR2 can restore intestinal neurogenesis and increase the number of nitrergic neurons in germ-free mice.124”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [124] Yarandi, 2020, Intestinal bacteria maintain adult enteric nervous system and nitrergic neurons via Toll-like receptor 2-induced neurogenesis in mice, Gastroenterology source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Microglia in the CNS express pattern recognition receptors such as TLRs, which respond to pathogen-associated molecular pattens and recognize invasive pathogens as immune mechanisms for host defense.152”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
What the sources say
- Not checked — no full text of the sourcecites [152] Ho, 2019, Microglia in Parkinson's disease, Adv Exp Med Biol source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“EGCs play a key role in maintaining intestinal permeability and regulating intestinal inflammation.126”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Microbiota, enteric nervous system inflammation and a-synuclein
What the sources say
- Not checked — no full text of the sourcecites [126] Clairembault, 2015, Enteric glial cells: New players in Parkinson's disease?, Mov Disord source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“SCFAs play a crucial role in intestinal inflammation and intestinal barrier function.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The intervention of acetate could alleviate inflammation in a dextran sulphate sodium-induced colitis mouse model, reduce the proinflammatory factors TNF-a and IL-17 in colon tissue and increase the anti-inflammatory factor IL-10 but had no significant effect on Ffar2 -/-(GPR43-deficient) mice, suggesting that SCFAs may be located in GPR43 and affect the immune response.186”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [186] Masui, 2013, G protein-coupled receptor 43 moderates gut inflammation through cytokine regulation from mononuclear cells, Inflamm Bowel Dis source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, SCFAs seem to play a protective role in Parkinson's disease, but the specific mechanism remains to be explored.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“NaB attenuated MPTP-induced neuronal loss in the nigral striatal pathway and prevented activation of astrocytes and microglia by upregulating BDNF and GDNF.201”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [201] Srivastav, 2019, Probiotics mixture increases butyrate, and subsequently rescues the nigral dopaminergic neurons from MPTP and rotenone-induced neurotoxicity, J Nutr Biochem source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The activation of the bile acid receptor FXR (farnesoid X receptor) can protect the distal small intestine from the proliferation of bacteria and their harmful effects, while maintaining the integrity of the epithelial barrier.209”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
What the sources say
- Not checked — no full text of the sourcecites [209] Inagaki, 2006, Regulation of antibacterial defense in the small intestine by the nuclear bile acid receptor, Proc Natl Acad Sci U S A source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Sayin et al. 210 analysed the bile acids of the whole gut-liver system of germ-free and routinely-fed mice and showed that in the role of gut microbiota, the bile acid levels decreased in the gall bladder and small intestine, while they increased in the caecum, colon, faeces and serum, indicating that gut microbiota influenced the composition of bile acids in various parts of the enterohepatic”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
What the sources say
- Not checked — no full text of the sourcecites [210] Sayin Sama, 2013, Gut microbiota regulates bile acid metabolism by reducing the levels of tauro-beta-muricholic acid, a naturally occurring FXR antagonist, Cell Metabolism source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“In a 6-OHDA rat model, NaB reduced oxidative stress, decreased the level of the proinflammatory cytokine TNF, increased BDNF and H3 histone acetylation, rescued the decrease in dopamine levels and prevented neuronal loss and neuronal pyknosis in the striatum.195”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [195] Sharma, 2015, Beneficial effects of sodium butyrate in 6-OHdopamine induced neurotoxicity and behavioral abnormalities: Modulation of histone deacetylase activity, Behav Brain Res source
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The decrease in SCFAs may promote intestinal inflammation and greatly increase the risk of a-synuclein deposition in the gastrointestinal tract.27”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Short chain fatty acids
What the sources say
- Not checked — no full text of the sourcecites [27] Li, 2017, Structural changes of gut microbiota in Parkinson's disease and its correlation with clinical features, Sci China Life Sci source
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In summary, diet can regulate the alteration of gut microbiota and has an impact on the brain by anti-inflammation, reducing oxidative stress and neuroprotection.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Diet
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“The level of plasma 5-HT in patients with Parkinson's disease was decreased compared with that in controls, and the decrease in plasma serotonin markers was related to the severity of depression and pain.225”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Neurotransmitters
What the sources say
- Not checked — no full text of the sourcecites [225] Tong, 2015, Reduced plasma serotonin and 5-hydroxyindoleacetic acid levels in Parkinson's disease are associated with nonmotor symptoms, Parkinsonism Relat Disord source
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Prebiotics have beneficial effects on Parkinson's disease by promoting gastrointestinal peristalsis, improving immune function and relieving constipation.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“At present, FMT has been used in patients with many diseases, such as recurrent Clostridium difficile infection, inflammatory bowel disease, metabolic syndrome and obesity.[262][263][264][265]”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not matchedcites [262][263][264][265]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
In the paper
“A clinical study has shown that probiotic bacteria can increase the production of SCFAs and decrease pro-inflammatory cytokines in patients with Parkinson's disease, indicating that probiotics may be a potential treatment for this disease (Ghyselinck et al., in press).”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Probiotics
What the sources say
- Not matchedcites Ghyselinck et al., in press
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Not matched
In the paper
“Moreover, FMT has also been proposed as a therapeutic approach in neurological diseases such as multiple sclerosis, Parkinson's disease, autism spectrum disorder, Alzheimer's disease and epilepsy.[274][275][276]”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not matchedcites [274][275][276]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Not matched
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“BDNF plays an important role in regulating the composition and function of the CNS.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Prebiotics deliver beneficial effects in Parkinson's disease by producing microbiota metabolites such as SCFAs.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
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Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“The researchers reported that the level of GABA decreased in the basal ganglia in patients with Parkinson's disease, and there were significant differences in GABA levels among the Parkinson's disease motor subtypes, indicating that GABA is involved in the pathogenesis of this disease.231”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Neurotransmitters
What the sources say
- Not checked — no full text of the sourcecites [231] Gong, 2018, Inhibitory motor dysfunction in parkinson's disease subtypes, J Magn Reson Imaging source
hedgeddirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Additionally, F. prausnitzii can produce butyrate to promote Foxp3 and block the downstream pathway of IL-6/STAT3/IL-17 by inhibiting HDAC1, maintaining the Th17/Treg balance and playing a significant antiinflammatory role in colorectal colitis rodents.269”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not checked — no full text of the sourcecites [269] Zhou, 2018, Faecalibacterium prausnitzii produces butyrate to maintain Th17/Treg balance and to ameliorate colorectal colitis by inhibiting histone deacetylase 1, Inflamm Bowel Dis source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The main function of prebiotics is to stimulate the growth and activity of beneficial microbiota in the gastrointestinal tract, thereby bringing health benefits to the host.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Prebiotics and micronutrients
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In general, TUDCA can improve the loss of dopaminergic neurons and decreased ATP levels as well as mitochondrial dysfunction and neuroinflammation in Parkinson's disease models.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Bile acids
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Intragastric administration of Faecalibacterium prausnitzii could significantly reduce the severity of colitis in mice with moderate or severe chronic colitis, suggesting that this species is an anti-inflammatory bacterium with the potential to treat inflammatory bowel disease.268”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not checked — no full text of the sourcecites [268] Martin, 2014, The commensal bacterium Faecalibacterium prausnitzii is protective in DNBS-induced chronic moderate and severe colitis models, Inflamm Bowel Dis source
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“FMT can reconstruct gut microbiota, change intestinal microbial diversity and restore abnormal intestinal microbiota comprehensively and extensively.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microbial therapies such as probiotics and FMT can relieve gastrointestinal symptoms and even motor symptoms of Parkinson's disease; however, the safety and effectiveness of FMT requires further evaluation in clinical trials.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
plaindirectSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“FMT may play a vital role in regulating the gut microbiota, but animal models have some limitations.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Whether the results of animal experiments can be extrapolated to humans is unclear.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The gut microbiota and their metabolites can modulate the immune system and regulate local and systemic inflammation, epithelial barrier function and neurotrophic factors.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“For the treatment of nervous system diseases, multiple FMTs may be needed to achieve a sustained effect.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
hedgedconditionalSingle case- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The exact mechanism by which gut microbiota plays a role in FMT through the gut-brain axis remains poorly understood.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“According to Braak's hypothesis, environmental factors may start a pathological process via the olfactory bulb or the intestinal nerve plexus.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The microbiota-gut-brain axis, which connects the peripheral and central nervous systems, provides a pathway whereby microbiota may contribute to the pathogenesis of Parkinson's disease, although the exact mechanism remains to be elucidated.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The major challenges with FMT include the high costs of sample preparation and preservation as well as the selection of faecal donors.262”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not checked — no full text of the sourcecites [262] Bakken, 2013, Treatment approaches including faecal microbiota transplantation for recurrent Clostridium difficile infection (RCDI) among infectious disease physicians, Anaerobe source
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Inflammation and oxidative stress are caused by swallowing nasal secretions, which leads to the accumulation of a-synuclein in the CNS.134”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
What the sources say
- Not checked — no full text of the sourcecites [134] Braak, 2003, Idiopathic Parkinson's disease: Possible routes by which vulnerable neuronal types may be subject to neuroinvasion by an unknown pathogen, J Neural Transm (Vienna) source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“FMT significantly relieved the metabolic disorder of gut microbiota in Parkinson's disease mice, alleviated body injury and increased the contents of dopamine and 5-HT in the striatum to protect Parkinson's disease mice by inhibiting nerve inflammation and reducing TLR4/TNF signal transduction.121”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Faecal microbiota transplantation
What the sources say
- Not checked — no full text of the sourcecites [121] Sun, 2018, Neuroprotective effects of faecal microbiota transplantation on MPTP-induced Parkinson's disease mice: Gut microbiota, glial reaction and TLR4/TNF-α signaling pathway, Brain Behavior Immunity source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Microbial therapies such as probiotics and FMT can relieve gastrointestinal symptoms and even motor symptoms of Parkinson's disease; however, the safety and effectiveness of FMT requires further evaluation in clinical trials.”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
In the paper
“At present, many animal experiments have observed the spread of a-synuclein pathology from the intestine to the brain along the gut-brain axis, and pathological changes in the CNS can be observed by injecting a-synuclein into the intestinal wall of the gastrointestinal tract.[136][137][138][139]”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > Conclusion
What the sources say
- Not matchedcites [136][137][138][139]
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Not matched
The paper relies on this without support.
Alterations in gut microbiota observed in patients with Parkinson's disease are causally involved in the pathogenesis of Parkinson's disease rather than being merely a consequence of the disease.
“Although studies suggest that the microbiota is associated with the pathogenesis of Parkinson's disease, the specific mechanisms have not fully been elucidated.”
The paper relies on this without support.
Animal models of Parkinson's disease and gut microbiota manipulations adequately model the corresponding human disease processes.
“The results of the studies on animal models of Parkinson's disease are similar to those in humans.”
The paper relies on this without support.
Findings from animal models of Parkinson's disease can be extrapolated to human Parkinson's disease.
“Vagotomy can prevent the transmission of pathological a-synuclein to the CNS in animal models.137,138”
The paper relies on this without support.
The gut microbiota-gut-brain axis is a valid causal pathway in human Parkinson's disease.
“Microbiota may trigger CNS neuroinflammation.”
The paper relies on this without support.
Associations between Mediterranean diet adherence and lower Parkinson's disease risk reflect a causal protective effect.
“Therefore, the Mediterranean diet may be a promising intervention strategy to attenuate onset and development of Parkinson's disease.”
The paper relies on this without support.
Components of the bacterial amyloid protein CsgA can accelerate the production of a-synuclein aggregation.
“In particular, the components of the bacterial amyloid protein CsgA can accelerate the production of a-synuclein aggregation.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“A growing number of studies have reported changes in the microbiota among patients with Parkinson's disease (PD), Alzheimer's disease (AD), ALS, and Huntington's disease (HD) (26–28), and although the exact mechanisms underlying these phenomena remain unclear, there is a growing body of evidence to support the concept of a “gut microbiota–brain axis” (29).”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [28]
In the citing paper
“and M2 (anti-inflammatory)-like microglial cytoplasm being associated with production of anti-inflammatory cytokines such as IL-4, IL-10, and IL-13 (28, 90).”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [28]
In the citing paper
“Alterations to the gut bacteria indirectly affect the ratio of macrophages to microglia”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [28]
In the citing paper
“with M1 (pro-inflammatory) microglia producing ROS and pro-inflammatory cytokines such as NO, IL-1β, IL-6, TNF-α, and IFN-γ”
From Modulation of the gut–brain axis via the gut microbiota: a new era in treatment of amyotrophic lateral sclerosis (2023) · cites this paper as [28]
In the citing paper
“Systemic inflammation induced by intestinal inflammation and barrier disruption is key in gut–brain communication [57,58,59].”
From Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson’s Disease (2022) · cites this paper as [58]
In the citing paper
“gut microbial dysbiosis not only leads to intestinal inflammation but also increases intestinal permeability.”
From Neuroprotective Effects of Sodium Butyrate by Restoring Gut Microbiota and Inhibiting TLR4 Signaling in Mice with MPTP-Induced Parkinson’s Disease (2023) · cites this paper as [14]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > CNS inflammation
“In contrast, another study reported that NaB significantly increased the BBB permeability of a traumatic brain injury mouse model by increasing the expression of tight junction-related proteins (occludin and ZO-1).170”
§ The role of gut dysbiosis in Parkinson's disease: mechanistic insights and therapeutic options > References
“170. Li H, Sun J, Wang F, et al. Sodium butyrate exerts neuroprotec- tive effects by restoring the blood-brain barrier in traumatic brain injury mice. Brain Res. 2016;1642:70-78.”
Cited works that were retracted
Works this paper cites that were later retracted, from the retraction notices publishers deposit. Major when the notice came out before this paper was published.
A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
In the paper
“Iba, 2020, Neuroinflammation is associated with infiltration of T cells in Lewy body disease and alpha-synuclein transgenic models, J Neuroinflamm, 17, 214, 10.1186/s12974-020-01888-0”
Cited work 10.1186/s12974-020-01888-0 · retracted 2026-08-22 · notice 10.1186/s12974-026-04011-x · this paper published 2021-04-15
A note, not an issue: for example, a cited work that was retracted only after this paper was published, which its authors could not have known.
In the paper
“Tamtaji, 2019, Clinical and metabolic response to probiotic administration in people with Parkinson's disease: A randomized, double-blind, placebo-controlled trial, Clin Nutr, 38, 1031, 10.1016/j.clnu.2018.05.018”
Cited work 10.1016/j.clnu.2018.05.018 · retracted 2025-09-26 · notice 10.1016/j.clnu.2025.08.012 · this paper published 2021-04-15
Citations
Cites
2 retracted
Tamtaji, O. R., Taghizadeh, M., Daneshvar Kakhaki, R., Kouchaki, E., Bahmani, F., Borzabadi, S., Oryan, S., Mafi, A., & Asemi, Z. (2019) · Clinical Nutrition · doi:10.1016/j.clnu.2018.05.018 · Cited by 398
RetractedIba, M., Kim, C., Sallin, M., Kwon, S., Verma, A., Overk, C., Rissman, R. A., Sen, R., Sen, J. M., & Masliah, E. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01888-0 · Cited by 120
RetractedHuman gut microbiome viewed across age and geography
Yatsunenko, T., Rey, F. E., Manary, M. J., Trehan, I., Dominguez-Bello, M. G., Contreras, M., Magris, M., Hidalgo, G., Baldassano, R. N., Anokhin, A. P., et al. (2012) · Nature · doi:10.1038/nature11053 · Cited by 7,815
De Filippo, C., Cavalieri, D., Di Paola, M., Ramazzotti, M., Poullet, J. B., Massart, S., Collini, S., Pieraccini, G., & Lionetti, P. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1005963107 · Cited by 5,579
The Microbial Metabolites, Short-Chain Fatty Acids, Regulate Colonic T reg Cell Homeostasis
Smith, P. M., Howitt, M. R., Panikov, N., Michaud, M., Gallini, C. A., Bohlooly-Y, M., Glickman, J. N., & Garrett, W. S. (2013) · Science · doi:10.1126/science.1241165 · Cited by 5,413
Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation
Arpaia, N., Campbell, C., Fan, X., Dikiy, S., van der Veeken, J., deRoos, P., Liu, H., Cross, J. R., Pfeffer, K., Coffer, P. J., et al. (2013) · Nature · doi:10.1038/nature12726 · Cited by 4,838
Host-gut microbiota metabolic interactions
Nicholson, J. K., Holmes, E., Kinross, J., Burcelin, R., Gibson, G., Jia, W., & Pettersson, S. (2012) · Science · doi:10.1126/science.1223813 · Cited by 4,760
Self-citationCross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity
Everard, A., Belzer, C., Geurts, L., Ouwerkerk, J. P., Druart, C., Bindels, L. B., Guiot, Y., Derrien, M., Muccioli, G. G., Delzenne, N. M., et al. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1219451110 · Cited by 4,511
Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease
Sampson, T. R., Debelius, J. W., Thron, T., Janssen, S., Shastri, G. G., Ilhan, Z. E., Challis, C., Schretter, C. E., Rocha, S., Gradinaru, V., et al. (2016) · Cell · doi:10.1016/j.cell.2016.11.018 · Cited by 3,622
Indigenous bacteria from the gut microbiota regulate host serotonin biosynthesis
Yano, J. M., Yu, K., Donaldson, G. P., Shastri, G. G., Ann, P., Ma, L., Nagler, C. R., Ismagilov, R. F., Mazmanian, S. K., & Hsiao, E. Y. (2015) · Cell · doi:10.1016/j.cell.2015.02.047 · Cited by 3,614
Research works printed but not linked: 2
- Castelli, 2020, Effects of the probiotic formulation SLAB51 in and Parkinson's disease models, Aging (Albany NY, 12, 4641
- Leta, 2019, Gut microbiota and Parkinson’s disease: Background and rationale of the SymPD study, Neurodigest, 5, 10
Cited by
Sorted by citations
Immunological mechanisms of inflammatory diseases caused by gut microbiota dysbiosis: A review
Zhao, M., Chu, J., Feng, S., Guo, C., Xue, B., He, K., & Li, L. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.114985 · Cited by 510
Ribosome biogenesis in disease: new players and therapeutic targets
Jiao, L., Liu, Y., Yu, X., Pan, X., Zhang, Y., Tu, J., Song, Y., & Li, Y. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01285-4 · Cited by 336
Parkinson’s disease and gut microbiota: from clinical to mechanistic and therapeutic studies
Zhang, X., Tang, B., & Guo, J. (2023) · Translational Neurodegeneration · doi:10.1186/s40035-023-00392-8 · Cited by 212
“Gut microbes are associated with motor and nonmotor PD phenotypes [42].”
BackgroundDuPont, H. L., Suescun, J., Jiang, Z.-D., Brown, E. L., Essigmann, H. T., Alexander, A. S., DuPont, A. W., Iqbal, T., Utay, N. S., Newmark, M., et al. (2023) · Frontiers in Neurology · doi:10.3389/fneur.2023.1104759 · Cited by 162
Kandpal, M., Indari, O., Baral, B., Jakhmola, S., Tiwari, D., Bhandari, V., Pandey, R. K., Bala, K., Sonawane, A., & Jha, H. C. (2022) · Metabolites · doi:10.3390/metabo12111064 · Cited by 177
Metadata
- Authors
- Wang, Q., Luo, Y., Ray Chaudhuri, K., Reynolds, R., Tan, E.-K., & Pettersson, S.
- Affiliations
- Zhujiang Hospital (CN)
- Parkinson Foundation International Centre of Excellence at King’s College Hospital, and Kings College, Denmark Hill, London SE5 9RS, UK
- Nanyang Technological University (SG)
- Singapore General Hospital (SG)
- Corresponding author
- Wang, Qing
- Tan, Eng-King
- Pettersson, Sven
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2021-04-15
- Volume
- 144
- Issue
- 9
- Pages
- 2571-2593
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W3153668192
- Cited by
- 281
- References
- 291
- Citations by year
- 2026: 43 · 2025: 64 · 2024: 65 · 2023: 63 · 2022: 42 · 2021: 4
- FWCI
- 5.57
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model (vor)
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- Research Portal (King's College London) (submittedVersion)
- Spiral (Imperial College London) (submittedVersion)
- Greater South Information System
- Funders
- National Natural Science Foundation of China (82071414)
- National Medical Research Council Singapore
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Gastroenterology › Gastrointestinal motility and disorders
- Keywords
- Parkinson's disease, gut dysbiosis, gut microbiota, microbiota-gut-brain axis, alpha-synuclein, neuroinflammation, intestinal barrier, neurotransmitter activity, enteric nervous system, intestinal inflammation, non-motor symptoms, early biomarkers, probiotics, prebiotics, fecal microbiota transplantation, dietary change, neurodegeneration
- MeSH terms
- Gastrointestinal Microbiome, Fecal Microbiota Transplantation, Brain-Gut Axis, Humans, Parkinson Disease, Probiotics, Prebiotics, Dysbiosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
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