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Microbiome–microglia connections via the gut–brain axis
Open accessAbstract
Microglia, the resident immune cells in the brain, are essential for modulating neurogenesis, influencing synaptic remodeling, and regulating neuroinflammation by surveying the brain microenvironment. Microglial dysfunction has been implicated in the onset and progression of several neurodevelopmental and neurodegenerative diseases; however, the multitude of factors and signals influencing microglial activity have not been fully elucidated. Microglia not only respond to local signals within the brain but also receive input from the periphery, including the gastrointestinal (GI) tract. Recent preclinical findings suggest that the gut microbiome plays a pivotal role in regulating microglial maturation and function, and altered microbial community composition has been reported in neurological disorders with known microglial involvement in humans. Collectively, these findings suggest that bidirectional crosstalk between the gut and the brain may influence disease pathogenesis. Herein, we discuss recent studies showing a role for the gut microbiome in modulating microglial development and function in homeostatic and disease conditions and highlight possible future research to develop novel microbial treatments for disorders of the brain.
Overview
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Written from the paper’s full text.
TL;DR
This review synthesizes evidence that the gut microbiota influences microglial maturation, identity, and function through gut–brain axis pathways including the vagus nerve, systemic circulation, and microbial metabolites. It argues that dysbiosis may contribute to microglial dysfunction in neurodevelopmental and neurodegenerative disorders such as autism spectrum disorder (ASD) and Parkinson’s disease (PD).
Key findings
- Microglia make up ∼5–15% of total brain cells and mature stepwise from early to pre- to adult microglia. Germ-free (GF) mice show immature microglial gene expression and morphology, with impaired responses to LPS and lymphocytic choriomeningitis virus; a diverse microbiota—not just bacterial exposure—is required, and antibiotic depletion in adulthood reverts microglia toward an immature phenotype.
- Gut–brain communication routes include the vagus nerve, intestinal barrier/peripheral immune signaling, and bacterial metabolites. Short-chain fatty acids (SCFAs; acetic, propionic, and butyric acid make up ∼95% of gut SCFAs) rescue the immature microglial phenotype in GF mice, while FFAR2-deficient SPF mice resemble GF mice. Other microbial neuroactive substances include serotonin (90% produced in the gut), tryptophan metabolites, GABA, and acetylcholine.
- Disease associations include ASD, where GI symptoms occur in 23–70% of patients and fecal samples show increased Clostridium and Lactobacillus with decreased Bacteroidetes and Bifidobacterium; maternal immune activation models show microglial maturation disruption, and Bacteroides fragilis administration rescues behavioral and GI defects. In PD, >80% of patients report GI dysfunction 10–20 yr before motor symptoms, SIBO occurs in 25–54.5%, and GF α-synuclein-overexpressing mice show reduced motor deficits, GI dysfunction, and microglial activation; SCFA feeding restores deficits. Table 1 also lists schizophrenia, major depressive disorder, Alzheimer’s disease, amyotrophic lateral sclerosis, and multiple sclerosis as neuropathologies with both microglial dysfunction and microbial dysbiosis.
Methods
- Narrative review; no primary data are reported. It synthesizes published human and animal studies on the gut microbiome, microglia, and gut–brain axis.
- Evidence discussed includes GF and specific pathogen–free mice, antibiotic depletion, fecal microbiota transplant, probiotics/prebiotics, SCFA supplementation, vagotomy and vagus nerve stimulation, human postmortem brain tissue, PET imaging, and fecal microbiota analyses.
- Main analysis is qualitative integration of mechanisms and disease associations; no systematic search strategy or meta-analysis is described.
Limitations
- Stated in the paper: ASD pilot studies have small sample sizes; the maternal immune activation model has limitations in replicating complex ASD symptomatology; exact SCFA signaling pathways and how GI signals propagate to the CNS are poorly understood; whether disease-associated microbial alterations are a cause or consequence of altered brain function is unclear; the role of SCFAs in PD models is uncertain due to concentration- and region-dependent effects; interindividual variation in PD microbiota is high.
- Evident from the text: as a narrative review, it does not systematically assess study quality or quantify effects; many conclusions rely on animal models and correlative human data, so causality in humans remains unestablished.
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In the paper
“microglial activity is now known to be influenced by factors originating outside the CNS, including the gut.”
§ Microbiome–microglia connections via the gut–brain axis > Introduction
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“This review highlights evidence demonstrating the various mechanisms by which the gut microbiota can influence microglia in both homeostatic and disease conditions.”
§ Microbiome–microglia connections via the gut–brain axis > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Microglia from adult GF mice also display differential expression of genes associated with microglial maturation, including down-regulation of genes that regulate cell activation and immune system defense pathways, such as Mapk8, IL-1α, Ly86, Jak3, and Stat1, all of which are normally highly expressed in adult microglia (Fig. 1; Erny et al., 2015; Matcovitch-Natan et al., 2016).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Diverse gut microbiota is a prerequisite for adult microglial maturation and function
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesNone of the sources cited for this claim have been checked yet.
In the paper
“Sophisticated crosstalk between the CNS and the gut microbiome (known as the gut–brain axis) is critical for several facets of CNS physiology, including microglial development and function (Mayer et al., 2015; Fung et al., 2017).”
§ Microbiome–microglia connections via the gut–brain axis > Introduction
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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
“Taken together, the gene expression profile and behavior of microglia from GF mice or under microbiota-depleted conditions is reminiscent of an immature microglial phenotype, indicating that input from gut microbiota is required for microglia to progress to later stages of cellular maturation and adequately fulfill their role in immune surveillance.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Diverse gut microbiota is a prerequisite for adult microglial maturation and function
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“In SPF mice, a diverse gut microbiota promotes microglial development and maturation.”
§ Microbiome–microglia connections via the gut–brain axis > Microglia during development and adulthood > Microglia maturation
What the sources say
- Not checked yetcites Erny et al., 2015 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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 influences microglial development and maturation.”
§ Microbiome–microglia connections via the gut–brain axis > Microglia during development and adulthood > Microglia maturation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA 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 presence of a complex and diverse microbial community, rather than exposure to gut bacteria per se, appears to be a prerequisite for proper microglial development and function.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Diverse gut microbiota is a prerequisite for adult microglial maturation and function
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“recent genetic studies provide evidence that microglia contribute to the pathogenesis of several neurodegenerative and neurodevelopmental disorders (Salter and Stevens, 2017).”
§ Microbiome–microglia connections via the gut–brain axis > Introduction
What the sources say
- Not checked yetcites Salter and Stevens, 2017 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIn the paper
“Consistent with patterns observed prenatally, microglia from adult GF mice, lacking constant postnatal input from gut microbiota, show distinct differences in density and morphology compared with those derived from SPF mice (Erny et al., 2015).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Diverse gut microbiota is a prerequisite for adult microglial maturation and function
What the sources say
- Not checked yetcites Erny et al., 2015 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes
- It may state two separate claims as one. 39
- Probably not a substantial claim. 11
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
“A role for the gut microbiome in facilitating microglial maturation and shaping microglial physiology has emerged in recent years.”
§ Microbiome–microglia connections via the gut–brain axis > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
- Rests on an assumption: Environmental factors and mechanisms shaping the developmental, homeostatic, and pathogenic program of microglia remain poorly understood.
In the paper
“Microglial development appears arrested in GF mice, as supported by high expression of genes characteristic of early and premicroglia in microglia from adult GF mice.”
§ Microbiome–microglia connections via the gut–brain axis > Microglia during development and adulthood > Microglia maturation
What the sources say
- Not checked yetcites Erny et al., 2015 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Another microbial metabolite that influences microglia activity is tryptophan, a serotonin precursor.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Bacterial-derived neuroactive substances
What the sources say
- Not checked yetcites Feng et al., 2017 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“In female offspring, by contrast, disruption was most notable in adults, and differentially expressed genes were primarily involved in immune and transcriptional signaling (Thion et al., 2018).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Maternal microbiota shapes prenatal microglial maturation and function
What the sources say
- Not checked yetcites Thion et al., 2018 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Once in the circulation, these substances activate a pro-inflammatory immune response mediated by peripheral T cells and macrophages and compromise the integrity of the BBB (Rochfort et al., 2014).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Regulation of the intestinal barrier and peripheral immune response
What the sources say
- Not checked yetcites Rochfort et al., 2014 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“SCFAs have been shown to activate sympathetic nervous system activity and alleviate intestinal inflammation, and altered SCFA production has been demonstrated in a variety of neuropathologies such as PD and ASD (Smith et al., 2013; MacFabe, 2015; Unger et al., 2016).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Bacterial-derived neuroactive substances
What the sources say
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“For example, microglia from E18.5 embryos from GF mothers show an increased density in various brain regions, with increased numbers of microglia exhibiting a ramified morphology, indicative of a resting state.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Maternal microbiota shapes prenatal microglial maturation and function
What the sources say
- Not checked yetcites Thion et al., 2018 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Approximately 70–80% of immune cells in the human body are found in the gut, allowing for direct gut–immune cell interactions (Vighi et al., 2008).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Regulation of the intestinal barrier and peripheral immune response
What the sources say
- Not checked yetcites Vighi et al., 2008 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Vagus nerve stimulation combined with LPS challenge has also been reported to decrease microglial production of the pro-inflammatory cytokines IL-6, IL-1β, and TNFα in the brain, an effect no longer observed following vagotomy (Meneses et al., 2016).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > The vagus nerve
What the sources say
- Not checked yetcites Meneses et al., 2016 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Metabolism of tryptophan by activated microglia produces the neurotoxin quinolinic acid, an N-methyl-D-aspartate agonist implicated in several neurological conditions including Huntington’s disease and depression (Feng et al., 2017).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Bacterial-derived neuroactive substances
What the sources say
- Not checked yetcites Feng et al., 2017 source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“These findings suggest that microglia are highly sensitive to perturbations in the gut microbial community during adulthood and require continual input from a complex gut microbiota to maintain homeostasis in the adult.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Diverse gut microbiota is a prerequisite for adult microglial maturation and function
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“SCFAs can exert physiological effects in the CNS via two primary mechanisms: activation of G protein–coupled receptors (GPCRs) expressed in the liver, spleen, and large intestine and inhibition of histone deacetylases (Kimura et al., 2011; Tan et al., 2014b).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Bacterial-derived neuroactive substances
What the sources say
- Not checked yetcites Kimura et al., 2011 source
- Not checked yetcites Tan et al., 2014b
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Among the most abundantly produced SCFAs are acetic acid, propionic acid, and butyric acid, which collectively make up ∼95% of SCFAs synthesized in the gut (Cook and Sellin, 1998).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Bacterial-derived neuroactive substances
What the sources say
- Not checked yetcites Cook and Sellin, 1998
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“Information about the state of peripheral inflammation and GI health is received in the CNS via vagal afferents that innervate the GI tract and can influence microglial activation and neuroinflammation.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
In the paper
“Altered microglial morphology and density, as well as attenuated inflammatory responses, are also observed in offspring of GF dams immediately after birth, a time when microglia typically exhibit an activated phenotype (Castillo-Ruiz et al., 2018).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Maternal microbiota shapes prenatal microglial maturation and function
What the sources say
- Not checked yetcites Castillo-Ruiz et al., 2018 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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 heterogeneity of microglial behavior in response to both intrinsic and extrinsic factors provides further evidence of their complexity, with the gut microbiome representing a key contributing factor in microglial development and function.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Maternal microbiota shapes prenatal microglial maturation and function
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“In male offspring of GF dams, disruption of the transcriptomic profile and morphology of microglia was greatest during the embryonic phase of development, and differentially regulated genes were mostly associated with metabolic and translational pathways (Thion et al., 2018).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain axis influences microglia development and function > Maternal microbiota shapes prenatal microglial maturation and function
What the sources say
- Not checked yetcites Thion et al., 2018 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Short-chain fatty acids (SCFAs) are metabolic byproducts of bacterial dietary fiber fermentation that can enter the systemic circulation and cross the BBB (Conn et al., 1983).”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation > Bacterial-derived neuroactive substances
What the sources say
- Not checked yetcites Conn et al., 1983
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Gut–brain communication may influence microglia via two routes: the vagus nerve and the circulatory system.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably 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
“Fine-tuning of the intestinal barrier by gut microbiota and their interactions with gut immune cells modulates peripheral inflammation and can trigger downstream inflammatory responses in the CNS.”
§ Microbiome–microglia connections via the gut–brain axis > Gut–brain communication pathways: Vagal transmission and systemic circulation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt 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
“First is the critical role of gut-derived factors in regulating microglial function in the healthy state, which suggests that signals originating from the gut microbiota might also drive a pathogenic microglial phenotype that promotes disease.”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. 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
“This dysbiosis is potentially sufficient to markedly disrupt microglial function and subsequently facilitate disease pathogenesis.”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These MIA offspring also exhibit increased intestinal permeability and intestinal inflammation, two GI symptoms commonly found in children with ASD (Hsiao et al., 2013; Chaidez et al., 2014).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“While this pattern of α-synuclein spreading is not observed in all cases of sporadic PD, vagotomy may be associated with reduced risk of developing PD in humans, potentially implicating peripheral influences on disease development (Svensson et al., 2015; Liu et al., 2017).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Similar to its ameliorative effect in colitis, oral administration of Bacteroides fragilis to offspring of MIA mice at weaning rescues the integrity of the intestinal barrier, reduces anxiety, and improves communication and repetitive behaviors (Hsiao et al., 2013).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
- Not checked yetcites Hsiao et al., 2013 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Mice lacking the fractalkine receptor Cx3cr1 demonstrate a temporary reduction in the number of microglia during early postnatal development, as well as increased synaptic density, immature brain circuitry, and signal transmission deficits that persist into adulthood (Paolicelli et al., 2011; Zhan et al., 2014).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Pathological hallmarks of PD include death of dopaminergic neurons of the substantia nigra pars compacta and intraneuronal accumulation of the α-synuclein protein (Goedert et al., 2013).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
- Not checked yetcites Goedert et al., 2013 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“Postmortem analysis of brain tissue collected from ASD patients show perturbations in microglial immune surveillance and synaptic remodeling, with evidence for heightened microglial activation, including increased expression of MHC II, elevated levels of pro- and anti-inflammatory cytokines, and increased microglial density (Vargas et al., 2005; Morgan et al., 2010; Voineagu et al., 2011; Gupta et”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Studies of ASD and other neurodevelopmental disorders provide evidence for a potential pathogenic role for both dysbiosis and microglial dysfunction, and suggests that microglia may link early-life dysbiosis to long-lasting neurological abnormalities.”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Children with ASD present with a wide range of cognitive and behavioral symptoms, including delayed language development, impaired social and communication skills, and repetitive behavior, depending on where they lie on the spectrum of disease severity (Plauche Johnson, 2004).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
- Not checked yetcites Plauche Johnson, 2004 source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“PD is the second most common neurodegenerative disorder and is defined by the presence of motor symptoms including bradykinesia, rigidity, and resting tremor (Postuma et al., 2015).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
- Not checked yetcites Postuma et al., 2015 source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably 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
“Cross-sectional studies comparing the gut microbiota composition between healthy and ASD individuals have revealed an altered microbiota profile in patients with ASD, with several studies reporting increased levels of Clostridium and Lactobacillus along with elevated levels of SCFAs, including propionic and butyric acid (Wang et al., 2012, 2013; De Angelis et al., 2013; Kang et al., 2013).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“A complex interplay of genetic and environmental factors is thought to drive the pathogenesis of PD, eventually leading to mitochondrial and autophagic dysfunction (Shulman et al., 2011).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
- Not checked yetcites Shulman et al., 2011 source
Strength:hedged· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“While the MIA model has limitations in terms of replicating the complex symptomatology of ASD, the model faithfully recapitulates abnormalities in both microglial behavior and GI function that are frequently observed in patients.”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt 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
“This in turn could compromise neuronal function and eventually lead to synaptic degeneration and neuronal death.”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“Microglia from young MIA offspring show increased expression of inflammation-related genes typically associated with an adult microglial phenotype and down-regulation of genes expressed during earlier developmental stages (e.g., Pu.1 and Irf8), suggesting that maternal inflammation disrupts the timeline of normal microglial maturation (Matcovitch-Natan et al., 2016).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
- Not checked yetcites Matcovitch-Natan et al., 2016 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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
“Given their wide spectrum of physiological functions and myriad roles in development and homeostasis, microglia are believed to be involved in the pathogenesis of several neurodevelopmental and neurodegenerative disorders.”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“While commensal symbiotic bacteria are critical for proper microglial maturation, induction of infection in pregnant dams can have disruptive effects on the progression of microglial development in offspring (Pratt et al., 2013; Matcovitch-Natan et al., 2016; Mattei et al., 2017).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > ASD
What the sources say
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
In the paper
“These mice display reduced motor deficits, GI dysfunction, and microglial activation when compared with mice with an intact gut microbiota (Sampson et al., 2016).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
- Not checked yetcites Sampson et al., 2016 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt 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 shift in microbial communities may contribute to the elevated levels of peripheral inflammation and intestinal permeability that are frequently seen in PD patients and might drive misfolding of α-synuclein in the gut and its retrograde propagation to the CNS.”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“While interindividual variation is high, PD patients often exhibit increased levels of Enterobacteriaceae and decreased levels of Bacteroidetes and Prevotellaceae (Keshavarzian et al., 2015; Unger et al., 2016).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“Feeding these GF transgenic mice a mixture of three SCFAs up-regulated microglial activation and induced motor deficits similar to those observed in colonized animals (Sampson et al., 2016).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
- Not checked yetcites Sampson et al., 2016 source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Studies show altered abundance of certain bacterial strains in patients with PD, changes that may correlate with severity of motor deficits (Scheperjans et al., 2015; Mertsalmi et al., 2017).”
§ Microbiome–microglia connections via the gut–brain axis > Microglial dysfunction and microbial dysbiosis in disease > PD
What the sources say
Strength:hedged· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt 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
“Signals originating from the gut microbiota and transmitted to the brain have the potential to alleviate or exacerbate disease pathogenesis, changes that may operate through gut-mediated changes in microglial behavior.”
§ Microbiome–microglia connections via the gut–brain axis > Future directions and challenges
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
The paper relies on this without support.
Environmental factors and mechanisms shaping the developmental, homeostatic, and pathogenic program of microglia remain poorly understood.
“However, environmental factors and mechanisms shaping the developmental, homeostatic, and pathogenic program of microglia remain poorly understood.”
The paper relies on this without support.
The womb is likely a sterile environment.
“While the womb is likely a sterile environment”
The paper relies on this without support.
BBB-permeable bacterial metabolites, including SCFAs, modulate microglial maturation.
“BBB-permeable bacterial metabolites, including SCFAs, modulate microglial maturation through mechanisms that are yet to be determined.”
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?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Moreover, gut bacteria can also affect CNS inflammation by binding to specific receptors, such as the proinflammatory tachykinin/neurokinin receptors, in the vagus nerve fiber.104”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [104]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“As alluded to in earlier sections microbiota-microglia interactions are receiving much attention of late as key mechanisms underlying microbiota-immune-brain interactions (Abdel-Haq et al., 2019;Rea et al., 2016;Vuong et al., 2017).”
From The Microbiota-Gut-Brain Axis (2019) · cites this paper as Abdel-Haq et al., 2019
In the citing paper
“Throughout the host lifespan, the gut microbiome provides essential signals to microglia during health and disease.59,60,187,188”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [187]
In the citing paper
“There is increasing evidence that interactions between the gut microbiome and the CNS innate immune system (gut-brain axis) may modulate AD pathogenesis.”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Abdel-Haq et al., 2019
In the citing paper
“Various aspects of CNS physiology are regulated by the microbiome, including microglial maturation and function (Abdel-Haq et al., 2019).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Abdel-Haq et al., 2019
In the citing paper
“Both microbial dysbiosis and microglial dysfunction have been described in several neurological diseases, including behavioral, inflammatory and neurodegenerative disorders.243”
From Interaction between microbiota and immunity in health and disease (2020) · cites this paper as [243]
In the citing paper
“The GM appears to influence microglial development and maturation (120, 121), and animal models have demonstrated downstream effects on various aspects of neurocognitive function (19, 45, 60, 114, 115).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [121]
In the citing paper
“SCFAs may also improve neuronal homeostasis and function by influencing neurotrophic factors such as nerve growth factor, glial cell line-derived neurotrophic factor, and BDNF (119–122).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [121]
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.
Opposite directions reported for SCFA levels in ASD
MajorTable 1 says SCFA levels are decreased in ASD patients compared with healthy controls, whereas the ASD section says studies found elevated SCFA levels in patients with ASD.
“Decreased SCFA levels in ASD patients compared to healthy controls.”
“several studies reporting increased levels of Clostridium and Lactobacillus along with elevated levels of SCFAs, including propionic and butyric acid”
Conflicting prevalence bounds for symptoms preceding PD motor symptoms
MinorTable 1 says more than 80% of PD patients report GI dysfunction before motor symptoms. The PD section says nonmotor symptoms, including GI distress, precede motor symptoms in up to 80% of patients; the narrower GI group cannot exceed the stated bound for the broader nonmotor group.
“>80% of PD patients report GI dysfunction (e.g., increased intestinal permeability, constipation, and nausea) 10–20 yr prior to onset of motor symptoms.”
“Nonmotor symptoms, including chronic constipation and GI distress, precede motor symptoms in up to 80% of PD patients”
Citations
Cites
Diversity of the Human Intestinal Microbial Flora
Eckburg, P. B., Bik, E. M., Bernstein, C. N., Purdom, E., Dethlefsen, L., Sargent, M., Gill, S. R., Nelson, K. E., & Relman, D. A. (2005) · Science · doi:10.1126/science.1110591 · Cited by 7,913 · cited 1×
“By the age of 5, the gut microbiota stabilizes and begins to resemble that of an adult, with members of Bacteroidetes and Firmicutes becoming most abundant (Eckburg et al., 2005).”
BackgroundMDS clinical diagnostic criteria for Parkinson’s disease
Postuma, R. B., Berg, D., Stern, M., Poewe, W., Olanow, C. W., Oertel, W., Obeso, J., Marek, K., Litvan, I., Lang, A. E., et al. (2015) · Movement Disorders · doi:10.1002/mds.26424 · Cited by 7,653
The gut microbiota as an environmental factor that regulates fat storage
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“Along with preserving the integrity of the intestinal–epithelial barrier along the gastrointestinal (GI) tract, gut bacteria are critical for the development and maturation of the host’s innate and adaptive immune systems, nutrient absorption, host metabolism, and protection against foreign invaders (Hooper et al., 20…”
BackgroundResting microglial cells are highly dynamic surveillants of brain parenchyma in vivo
Nimmerjahn, A., Kirchhoff, F., & Helmchen, F. (2005) · Science · doi:10.1126/science.1110647 · Cited by 5,827 · cited 3×
“Under steady-state conditions, surveying microglia have a ramified morphology with a small cell body and many long extended processes that are used to continuously scan and assess the health of cells in close proximity—a process critical for maintaining homeostasis in the absence of pathology (Nimmerjahn et al., 2005;…”
BackgroundA Unique Microglia Type Associated with Restricting Development of Alzheimer’s Disease
Keren-Shaul, H., Spinrad, A., Weiner, A., Matcovitch-Natan, O., Dvir-Szternfeld, R., Ulland, T. K., David, E., Baruch, K., Lara-Astaiso, D., Toth, B., et al. (2017) · Cell · doi:10.1016/j.cell.2017.05.018 · Cited by 5,493
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 · cited 1×
“SCFAs have been shown to activate sympathetic nervous system activity and alleviate intestinal inflammation, and altered SCFA production has been demonstrated in a variety of neuropathologies such as PD and ASD (Smith et al., 2013; MacFabe, 2015; Unger et al., 2016).”
BackgroundFate Mapping Analysis Reveals That Adult Microglia Derive from Primitive Macrophages
Ginhoux, F., Greter, M., Leboeuf, M., Nandi, S., See, P., Gokhan, S., Mehler, M. F., Conway, S. J., Ng, L. G., Stanley, E. R., et al. (2010) · Science · doi:10.1126/science.1194637 · Cited by 5,175 · cited 3×
“The maturation and differentiation of erythromyeloid progenitors into microglia within the yolk sac requires several transcription factors, including RUNX1, JUN, PU.1, and IRF8, the expression of which coincides with that of microglial markers, including CX3CR1, CD11b, and F4/80 (Ginhoux et al., 2010; Matcovitch-Natan…”
BackgroundDominguez-Bello, M. G., Costello, E. K., Contreras, M., Magris, M., Hidalgo, G., Fierer, N., & Knight, R. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1002601107 · Cited by 4,774 · cited 1×
“Initial microbial colonization of the gut happens at birth and is heavily influenced by the mode of delivery (cesarean section versus vaginal birth; Dominguez-Bello et al., 2010; Rodríguez et al., 2015).”
BackgroundMacrophage biology in development, homeostasis and disease
Wynn, T. A., Chawla, A., & Pollard, J. W. (2013) · Nature · doi:10.1038/nature12034 · Cited by 4,684 · cited 1×
“During early development, microglia actively regulate neuronal cell numbers and synaptic refinement, ultimately shaping neural circuitry (Sierra et al., 2010; Paolicelli et al., 2011; Wynn et al., 2013).”
BackgroundMeta-Analysis of 74,046 Individuals Identifies 11 New Susceptibility Loci for Alzheimer’s Disease
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Items 301–400 of 480
Tan, Y., Xu, M., & Deng, L. (2024) · Archives of Microbiology · doi:10.1007/s00203-024-03866-z · Cited by 10
Oyovwi, M. O., & Ajayi, A. F. (2025) · Discover Medicine · doi:10.1007/s44337-025-00495-3 · Cited by 10
“The intricate relationship between gut health and a broad spectrum of neurological disorders has become an area of intense research in recent years [31].”
InfluentialNettles, R., Ricks, K. D., & Koide, R. T. (2020) · Microbial Ecology · doi:10.1007/s00248-020-01525-6 · Cited by 8
“Severe imbalance in the equilibrium of intestinal microbial communities may increase the risk of rheumatoid arthritis [3, 4], type 1 diabetes [5, 6], gastrointestinal disorders [7, 8], certain cancers [9, 10], and neurodegenerative disorders such as multiple sclerosis, Parkinson’s disease, and Alzheimer’s disease [11,…”
BackgroundUnderstanding the role of gut microbiota in the pathogenesis of schizophrenia
Ghorbani, M., Rajandas, H., Parimannan, S., Joseph, G. B. S., Tew, M. M., Ramly, S. S., Rasat, M. A. M., & Lee, S. Y. (2020) · Psychiatric Genetics · doi:10.1097/ypg.0000000000000270 · Cited by 8
“An altered gut microbiota caused by environmental factors and stress, which subsequently leads to microglia dysfunction in the CNS, has been proposed as the etiology of schizophrenia (Monji et al., 2009; Sharon et al., 2016; Wang et al., 2018; Abdel-Haq et al., 2019; Ma et al., 2019).”
BackgroundGut microbiota mediates the beneficial effects of exercise on autism-like behaviors
Zhong, J., Zhu, B., Zou, Z., Li, Y., Feng, Y., Ke, W., & Hou, X. (2026) · BMC Microbiology · doi:10.1186/s12866-025-04632-x · Cited by 10
“The bidirectional communication between the gut microbiota and the brain involves multiple pathways, primarily the immune system, neuroendocrine pathways, metabolism, and the vagal nerve pathway [11–13].”
The microbiota-brain connection in neurological diseases: the ubiquitous short-chain fatty acids
Bertin, L., Bonazzi, E., Facchin, S., Lorenzon, G., Maniero, D., BARBA, C. D., Tomasulo, A., FORTUNA, A., Zingone, F., Barberio, B., et al. (2025) · Minerva Gastroenterology · doi:10.23736/s2724-5985.25.03866-5 · Cited by 10
Diet, Microbiota and the Gut-Brain Axis
García-Gutiérrez, E., & Sayavedra, L. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819265-8.00089-9 · Cited by 10
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“MCs emerge as key mediators in these processes, as their activation can lead to the release of pro-inflammatory cytokines and contribute to an unfavorable microenvironment for neuronal health.”
The researcher's guide to selecting biomarkers in mental health studies
Verhoeven, J. E., Wolkowitz, O. M., Satz, I. B., Conklin, Q. A., Lamers, F., Lavebratt, C., Lin, J., Lindqvist, D., Mayer, S. E., Melas, P. A., et al. (2024) · BioEssays · doi:10.1002/bies.202300246 · Cited by 10
“[127] Increased gut permeability may induce chronic low-grade inflammation and gut microbiota alterations regulate microglial development [128,129] which could lead to neuroinflammation which in turn may give rise to depressive or other symptoms.”
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Bonnechère, B. (2022) · Genes · doi:10.3390/genes14010063 · Cited by 7
“The gut–brain axis is a bidirectional communication axis that includes, among other things, the intestinal microbiome, the intestinal barrier, intestinal inflammation, and the intestinal/systemic/brain immune systems [24].”
BackgroundAkkermansia Muciniphila Plays a Neuroprotective Role in HMC3 Cells Through The ‘Gut–Brain’ Axis
Zou, R., Shen, G., Wu, Y., Guo, M., Chen, J., Yang, S., Zhao, H., & Zheng, H. (2023) · Future Microbiology · doi:10.2217/fmb-2022-0007 · Cited by 7
Sweetener synapse: Exploring non-nutritive sweeteners' role in zebrafish glucose homeostasis
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IMD signaling in the gut and the brain modulates Amyloid-beta-induced deficits in Drosophila
Hsieh, T., & Chiang, H. (2023) · Life Sciences · doi:10.1016/j.lfs.2023.122118 · Cited by 6
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Yadav, A., Tadas, M., Kale, M. B., Wankhede, N. L., Umekar, M. J., Kotagale, N. R., & Taksande, B. G. (2025) · Physiology & Behavior · doi:10.1016/j.physbeh.2025.114989 · Cited by 11
Gut dysbiosis leads to cognitive decline through CNTF-mediated activation of microglia in mice
Krishnapriya, Rishikesh, R., Kishanchand, D. K., Haack, I., Hosseini, S., Deepti, A., Sudhadevi, T., Michaelsen‐Preusse, K., Sivan, U., Körte, M., et al. (2025) · BMC Biology · doi:10.1186/s12915-025-02454-x · Cited by 8
“Loss of beneficial microbes through dysbiosis can provoke microglial overactivation, contributing to neuroinflammation [87, 88].”
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The role of the gut microbiome in the regulation of astrocytes in Alzheimer's disease
Chandra, S., & Vassar, R. J. (2024) · Neurotherapeutics · doi:10.1016/j.neurot.2024.e00425 · Cited by 7
Linking the gut microbiome to microglial activation in opioid use disorder
Antoine, D., Venigalla, G., Truitt, B., & Roy, S. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.1050661 · Cited by 6
“Additionally, the microbiota plays a substantial role on the immune cells of the CNS, the microglia, as prenatal and postnatal inputs from the gut microbiota are critical for microglial maturation and function (Abdel-Haq et al., 2019).”
BackgroundStudying Laboratory Mice – Into the Wild
Savage, J. C., & Tremblay, M. (2019) · Trends in Neurosciences · doi:10.1016/j.tins.2019.05.004 · Cited by 7
“Changes in themicrobiome affect the gut–brain axis and have major effects on behavior and brain physiology, including anxiety as well as microglial function [5].”
Olwenyi, O. A., Johnson, S. D., Bidokhti, M. R. M., Thakur, V., Pandey, K., Thurman, M., Acharya, A., Uppada, S. B., Callen, S. E., Giavedoni, L. D., et al. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.1001544 · Cited by 6
“Based on the existence of a gut-brain axis, metabolites such as SCFAs secreted by the gut microbiome may influence CNS inflammation and shape microglial maturation (Erny et al., 2015; Meneses et al., 2016; Mertsalmi et al., 2017; Abdel-Haq et al., 2019).”
BackgroundMolecular Mechanisms of Depression: The Interplay Between Genes and Receptors
Oatu, A., Trifu, S. C., & Coman, E. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms262311325 · Cited by 8
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Probiotic Mechanism to Modulate the Gut-Brain Axis (GBA)
Samtiya, M., Dhewa, T., & Puniya, A. K. (2022) · Springer eBooks · doi:10.1007/978-981-16-1626-6_10 · Cited by 6
Does the Maternal Gut Microbiome Influence the Outcome of Perinatal Asphyxia?
Morozan, V.-P., Ionescu, M.-I., Zahiu, C. D. M., Catrina, A. M., Racoviță, A., Chirilă, A.-T., Dogaru, I.-A., Ciotei, C., Pîrcălăbioru, G. G., & Zăgrean, A. (2025) · Antioxidants · doi:10.3390/antiox14091134 · Cited by 8
“This protective milieu can buffer the developing brain against the detrimental effects of oxygen deprivation, while enhancing its neural repair capacity [10,11].”
Interaction Between Innate Lymphoid Cells and the Nervous System
Zhang, Y., Grazda, R., & Yang, Q. (2022) · Advances in experimental medicine and biology · doi:10.1007/978-981-16-8387-9_9 · Cited by 5
Lipid metabolism, microglia, and stroke
Chen, L., Zhang, M., Wei, W., Li, Q., Wang, L., Zhao, M., He, L., Xu, H., Yang, P., & Zhang, P. (2025) · Neural Regeneration Research · doi:10.4103/nrr.nrr-d-24-01523 · Cited by 7
“They clear cellular debris and take part in information transmission (Abdel-Haq et al., 2019).”
Deficiency of intestinal alkaline phosphatase affects behavior and microglia activity in mice
Dai, J., Yang, J., Han, S., Li, N., Wang, S., Xia, S., Kim, H.-H., Jun, Y., Lee, S., Kitagawa, Y., et al. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.02.006 · Cited by 5
Basgaran, A., Lymberopoulos, E., Burchill, E., Reis-Dehabadi, M., & Sharma, N. (2025) · Brain Communications · doi:10.1093/braincomms/fcaf059 · Cited by 8
“5 In a similar manner to peripheral macrophages, microglia play an important role in CNS homeostasis during development, adulthood and ageing.”
Neklesova, M. V., Sogomonyan, K. S., Golovkin, I. A., Shirokiy, N. I., Vershinina, S. O., Tsvetikova, S. A., Korzhova, J. E., Zakharova, M. N., & Gnedovskaya, E. V. (2025) · Biomedicines · doi:10.3390/biomedicines13081806 · Cited by 6
Neurodevelopment and the gut microbiome
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Biagioli, V., Matera, M., & Striano, P. (2025) · Global Pediatrics · doi:10.1016/j.gpeds.2025.100301 · Cited by 8
Stressor-Specific Microbiota Intervention
Chuang, J.-Y. (2022) · Frontiers in Nutrition · doi:10.3389/fnut.2022.870665 · Cited by 4
“, acetylcholine, gamma-aminobutyric acid [GABA], serotonin, and short-chain fatty acids [SCFAs]) into the circulation, thus compromising the integrity of the blood–brain barrier and influencingmicroglia (6).”
BackgroundInfluentialKano, M., & Fukudo, S. (2023) · Elsevier eBooks · doi:10.1016/b978-0-12-820480-1.00036-x · Cited by 6
Gut Bacteria Provide Genetic and Molecular Reporter Systems to Identify Specific Diseases
Dicks, L. M. T. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25084431 · Cited by 5
Lupu, V. V., Nedelcu, A. H., Miron, I. C., Anton, S. C., Săsăran, M. O., Frăsinariu, O. E., Jechel, E., Bozomitu, L. I., Chisnoiu, T., Anton, C., et al. (2026) · Nutrients · doi:10.3390/nu18101541 · Cited by 4
Role of microbiota in pain: From bench to bedside
Ren, H., Cao, B., Xu, Q., Zhao, R., Li, H., & Wei, B. (2025) · iMetaOmics. · doi:10.1002/imo2.58 · Cited by 7
“The gut microbiota integrates gut ‐ brain communication via vagal transmission and the circulatory system, which are essential for maintaining microglial function [104].”
Changes of Dopamine and Tyrosine Hydroxylase Levels in the Brain of Germ-free Mice.
Wang, Y., Qiao, H., & Zhang, Y. (2023) · PubMed Central · doi:10.30498/ijb.2022.236732.2798 · Cited by 6
“Moreover, previous studies have found that the microglia interact with various components of the microflora-intestine-brain axis (28, 29).”
BackgroundTranslational pediatrics: clinical perspective for Phelan–McDermid syndrome and autism research
Sakai, Y., Okuzono, S., Schaaf, C. P., & Ohga, S. (2021) · Pediatric Research · doi:10.1038/s41390-021-01806-x · Cited by 4
Novel opportunity of treatment for psycho-cardiologic disease by gut microbiome
Lai, Y., Fang, C., Jiang, Y., Yang, C., Zhou, Q., Cai, Y., Yan, W., & Fan, X. (2025) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2025.1604962 · Cited by 4
“In addition, Relevant studies have proved that microglial dysfunction is closely related to the occurrence and development of neurodegenerative diseases and mental diseases (131).”
Phatak, M., Nair, B., Soni, U., & Pujari, R. (2025) · Current Drug Metabolism · doi:10.2174/0113892002361676250325082424 · Cited by 3
Neurodevelopmental and Neuropsychiatric Disorders
Traetta, M. E., Filho, A. M. C., Akinluyi, E. T., & Tremblay, M. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-55529-9_26 · Cited by 4
Microbiome, Exposome, and Cognitive Development: The Known Unknowns
Aburto, M. R., Nagpal, J. K., Majumdar, A., O’Riordan, K. J., Clarke, G. A., & Cryan, J. F. (2025) · Annual Review of Developmental Psychology · doi:10.1146/annurev-devpsych-111323-120638 · Cited by 4
Christodoulou, M. V., Alexiou, G. Α., Lampros, M. G., Astrakas, L. G., Katsanos, K. H., & Argyropoulou, M. I. (2025) · Neuroradiology · doi:10.1007/s00234-025-03756-1 · Cited by 4
“These cytokines may underlie the limbic, ACC and prefrontal alterations reported in CD [34, 35, 39, 42 ] - brain regions richly innervated by gut vagal afferents [ 60 ] and highly sensitive to TNF-α signal - ing [61 ].”
Microbiome in Neuroblastoma: A Virgin Island in the World of Onco-Microbiome
Giri, A. K., Subramanian, P., Periyasamy, L., Aravindan, S., & Aravindan, N. (2025) · Cells · doi:10.3390/cells14151218 · Cited by 3
“The gut microbiota is crucial for the maturation and activation of microglia, the resident immune cells of the CNS, with microbial signals necessary for development [187].”
Gut microbiota and brain development: A review
Varier, K. M., Karandikar, A., Liu, W., Chen, J., Ben‐David, Y., Shen, X., Chinnasamy, A., & Gajendran, B. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-821265-3.00018-9 · Cited by 3
Wyatt‐Johnson, S. K., Desai, J. M., Wireman, A., Eipers, P. G., Morrow, C. D., Vornhagen, J., & Brutkiewicz, R. R. (2025) · Alzheimer s & Dementia · doi:10.1002/alz.70493 · Cited by 3
“5,6 7 However, the immune system’scontributionstendtobeonlymeasuredthroughinflammation and not as a key player in the gut–brain axis.”
Lu, X. (2022) · AIP conference proceedings · doi:10.1063/5.0095072 · Cited by 4
Mi, K., Cao, M., Zhang, L., Zhang, Q., Zhou, W., Deng, C., Zhang, Y., Zhao, Q., Wei, Y., Liu, X., et al. (2026) · Cell Reports Medicine · doi:10.1016/j.xcrm.2026.102655 · Cited by 6
“64,65 To investigate the possible mediation pathways within the multi-omics data, we constructed a two-stage model (Microbiota → Metabolite → sMRI → Behavior).”
Gut–Brain Inflammation and Disrupted Homeostasis Due to Activation of Mast Cells and Microglia
Katiraei, P., Frye, R. E., & Theoharides, T. C. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27041768 · Cited by 3
“Peripheral gut inflammation and damage can activate the microglia [162,163].”
The Role of the Gut Microbiome in Bipolar Disorder and its Common Medical Comorbidities
Jones, G. H., Pinjari, O. F., Vecera, C. M., Smith, K., Barrera, A., & Machado‐Vieira, R. (2023) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2023.101078 · Cited by 5
Yang, H., Wang, A., Yang, J., Luo, R., & Yang, Y. (2025) · Frontiers in Microbiology · doi:10.3389/fmicb.2025.1650212 · Cited by 6
Food for thought: probiotic modulation of microglial activity in Parkinson's disease
Kimber, I. K., & Tremblay, M. (2025) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2025.1690507 · Cited by 4
Hofford, R. S., Sens, J. P., Shipman, A. L., Kimble, V. M., Coric, C., Meckel, K. R., & Kiraly, D. D. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.07.005 · Cited by 4
Dossena, C., Bergamaschi, L., Rossignoli, F., Licata, A. G., Gasparini, P., Venturini, L. V., Marra, M., Oriani, M., Biassoni, V., Schiavello, E., et al. (2025) · Neuro-Oncology Advances · doi:10.1093/noajnl/vdaf042 · Cited by 4
“Therefore, the BBB integrity is disrupted by this inflammation, causing the infiltration of inflammatory mediators, immune cells, and bacterial toxins in the CNS, 50,51 which could activate resident microglia’s immune response.”
Microbiota-Brain-Gut Axis and Neurodegenerative Disorders
Abughazaleh, S. J., Euers, L. A., & Quigley, E. M. M. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-819265-8.00031-0 · Cited by 3
Ma, P., Mo, R.-F., Liao, H., et al. (2021) · Research Square · doi:10.21203/rs.3.rs-970681/v1 · Cited by 3
Song, B., Qiu, Y., Wang, Z., Tao, Y., Wang, M., Duan, A., Xie, M., Yin, Z., Chen, Z., Ma, C., et al. (2025) · Biomedicines · doi:10.3390/biomedicines13030753 · Cited by 3
“…Table S11: Results of MR analysis of GM and the possible mediating factors; Supplementary Table S12: The result of the mapped genes; Supplementary Table S13: MR analysis results of all five methods for significant genes; Supplementary Table S14: Sensitivity analysis results for significant genes.”
The microbiota-microglia axis: A novel clue for diet and brain health
Song, Z., Song, R., Liu, Y., Zhu, Y., & Zhang, X. (2025) · Trends in Food Science & Technology · doi:10.1016/j.tifs.2025.104942 · Cited by 4
Lee, M., Ahn, K., & Kim, M. (2024) · PLoS ONE · doi:10.1371/journal.pone.0312670 · Cited by 6
Targeting gut dysbiosis as a means to enhance recovery from surgical brain injury
Danehower, S. (2021) · Surgical Neurology International · doi:10.25259/sni_72_2021 · Cited by 3
“First, during development, they modulate neuronal development and synaptic connections to establish CNS circuitry.[2] Following the development, microglial plays an important role in CNS homeostasis.”
BackgroundWei, W., Zhang, G., Zhang, Y., Zhang, L., Wu, S., Li, X., & Yang, D. (2023) · Frigid Zone Medicine · doi:10.2478/fzm-2023-0003 · Cited by 3
Mangoni, A. A., Hulin, J.-A., & Tommasi, S. (2026) · Pharmacological Reviews · doi:10.1016/j.pharmr.2026.100147 · Cited by 2
“432 — 435 Overall, the potential beneficial effects of methotrexate in Alzheimer disease, vascular dementia, and mixed dementia are biologically plausible because it targets protein aggregation, autophagy failure, neuroinflammation, oxidative stress, cerebro-vascular dysfunction, blood-brain…”
Osteoarthritis Related Pain: Which Procedure is the Optimal Choice?
Pedersini, P., Bishop, M. D., & Villafañe, J. H. (2021) · Electronic Journal of General Medicine · doi:10.29333/ejgm/11014 · Cited by 2
Pan, H., & Liu, Z. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-90256-4.00024-2 · Cited by 2
Vagus Nerve Stimulation in Peripheral Targets
Özden, A. V. (2023) · Neuromethods · doi:10.1007/978-1-0716-3465-3_1 · Cited by 2
A prebiotic diet modulates microglial states and motor deficits in α-synuclein overexpressing micePreprint
Abdel-Haq, R., Schlachetzki, J. C. M., Boktor, J. C., et al. (2022) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2022.06.27.497828 · Cited by 2
Self-citationBağırsak-Beyin Eksenine Biyokimyasal Bakış
Aydın, Ü. F., & Tuli, A. (2021) · Arşiv Kaynak Tarama Dergisi · doi:10.17827/aktd.910674 · Cited by 2
Pribac, M., Moțățăianu, A., Andone, S. R., Mardale, E., & Nemeth, S. (2024) · Current Issues in Molecular Biology · doi:10.3390/cimb46050271 · Cited by 3
Mora-Ortiz, M., García-Fernández, H., Pérez‐Martínez, P., & Camargo, A. (2024) · Open Research Europe · doi:10.12688/openreseurope.18568.1 · Cited by 2
Ruciński, J., Kurowska, E., Myślińska, D., Grembecka, B., Piekarczyk, N., Necel, A., Kosznik-Kwaśnicka, K., & Majkutewicz, I. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26094353 · Cited by 4
Dietary influences on the gut-brain pathways: Mechanisms and therapeutic potential
Ajay, A., Gaur, S. S., Singh, J., Shams, R., Dash, K. K., Shaikh, A. M., & Kovács, B. (2025) · Human Nutrition & Metabolism · doi:10.1016/j.hnm.2025.200349 · Cited by 2
The role of alpha-sinuclein in the neurodegenerative process
Sobolev, V. B., & Худоерков, Р. М. (2019) · CLINICAL AND EXPERIMENTAL MORPHOLOGY · doi:10.31088/cem2019.8.3.5-12 · Cited by 2
“К сожалению, систематическая группа бактерий или их некая совокупность не определены, так же, как неизвестен механизм влияния, но предположительными агентами влияния микробиома могут выступать короткие цепочки жирных кислот [42].”
Neurocognitive Impairment After COVID-19: Mechanisms, Phenotypes, and Links to Alzheimer’s Disease
Doskas, T. K., Vavougios, G. D., Kormas, C., Kokkotis, C., Tsiptsios, D., Spiliopoulos, K. C., Tsiakiri, A., Christidi, F., Aravidou, T., Dekavallas, L., et al. (2025) · Brain Sciences · doi:10.3390/brainsci15060564 · Cited by 7
Yang, X., Chen, C., Wang, J., Gao, Z., Yuan, W., & Gao, B. (2026) · Neurobiology of Disease · doi:10.1016/j.nbd.2026.107425 · Cited by 2
Newton, K. A., & Biase, L. M. D. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-55529-9_19 · Cited by 3
Causal Effects of Gut Microbiome on Tinnitus: A Mendelian Randomization Study
Zeng, Q., Xie, W., Dong, H., Liu, X., Shao, S., Chen, L., & Zhang, W. (2025) · Journal of Multidisciplinary Healthcare · doi:10.2147/jmdh.s525502 · Cited by 4
Microbiota-derived short chain fatty acids promote Aβ plaque depositionPreprint
Colombo, A. V., Sadler, R., Llovera, G., et al. (2020) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2020.06.09.141879 · Cited by 2
“The microbiome plays an important role in microglial maturation during development and in adulthood (Abdel-Haq et al., 2019).”
Backgroundda Fonseca, E. N., Piedade, A. B. T., & da Silva, M. C. (2022) · Research Society and Development · doi:10.33448/rsd-v11i16.38185 · Cited by 4
Association between the Distal Gut Microbiome and Anxiety in Highly Active IndividualsPreprint
Morales, E., Fletcher, E., Hwang, P. S., Kim, C. S., Padgett, R. N., Smeding, S., Scullin, M. K., Gordon, P. M., & Greathouse, K. L. (2020) · doi:10.21203/rs.3.rs-26541/v1 · Cited by 2
Tizabi, Y., Getachew, B., Mendieta, L., Palafox-Sánchez, V., Tsytsarev, V., Manaye, K. F., Tinkov, A. A., da Silva, V. D. A., & Aschner, M. (2025) · Neurotoxicity Research · doi:10.1007/s12640-025-00768-w · Cited by 2
Microglial Plasticity in Vascular Dementia: Mechanisms and Therapeutic Reprogramming
Shukla, M., Li, J., Sun, Y., Jin, R., & Li, G. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27093719 · Cited by 3
“In addition, increasing attention is being directed toward systemic modulators of neuroinflammation, particularly the microbiota–gut–brain axis [96].”
ADITIVOS ALIMENTARES E O IMPACTO SOBRE A MICROBIOTA INTESTINAL HUMANA E SEUS EFEITOS SOBRE A SAÚDE
da Cunha, M. C., & Paula, B. M. D. (2023) · Revista Interfaces Saúde Humanas e Tecnologia · doi:10.16891/2317-434x.v11.e3.a2023.pp3079-3091 · Cited by 1
The Enigmatic Gut-Brain-Immune Trio in Brain and Behavior Disorders
Mythri, R. B. (2025) · Advances in medical diagnosis, treatment, and care (AMDTC) book series · doi:10.4018/979-8-3693-7432-0.ch019 · Cited by 1
Reynolds, A., Glenn, E., Lavoie, B. A., Ishaq, S. L., & Li, Y. (2026) · Frontiers in Neuroscience · doi:10.3389/fnins.2026.1815972 · Cited by 1
Tang, Y., & Tang, R. (2024) · Elsevier eBooks · doi:10.1016/b978-0-443-15602-1.00005-7 · Cited by 1
The gut microbiome in neurodegenerative disorders
Abughazaleh, S. J., Euers, L. A., & Quigley, E. M. M. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-821039-0.00006-x · Cited by 1
Mediators between gut microbiota and Alzheimer's disease: A mediation Mendelian randomization study
Dong, X., Han, Y., Wang, T.-B., Han, Y., & Liu, L. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251401157 · Cited by 1
“The interaction between the microglia and microbiota in fl uences immune regulation, 27 which can impair A β clearance mechanisms and ultimately contribute to AD.”
Shaik, S. M., Schiro, G., Laubitz, D., Madan, J. C., Kelley, C. P., Daines, M., Rice, S. A., Ghishan, F. K., & Kiela, P. R. (2026) · Microorganisms · doi:10.3390/microorganisms14051036 · Cited by 1
On the Pathophysiology of Stroke‐Associated Pneumonia: A Brief Review
Zhong, A. (2025) · Neurology and Clinical Neuroscience · doi:10.1111/ncn3.70030 · Cited by 1
The Gut Vascular Barrier: Linking the Intestinal Environment with Blood Circulation
Carloni, S., & Strati, F. (2025) · The microbiomes of humans, animals, plants, and the environment · doi:10.1007/978-3-031-84065-4_4 · Cited by 2
Bosch, M. E., Dodiya, H. B., Michalkiewicz, J., Lee, C., Shaik, S. M., Weigle, I. Q., Zhang, C. M., Osborn, J., Nambiar, A., Patel, P. A., et al. (2023) · Research Square · doi:10.21203/rs.3.rs-3394003/v1 · Cited by 1
Forgham, H., Albornoz, E. A., Pietrogrande, G., Zhu, J., Chung, K. H. K., Tahir, M. S., Ali, S. A., Qiao, R., Käkinen, A., Wolvetang, E. J., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.01.15.633290 · Cited by 1
Impact of Cesarean Delivery on Childhood Neurocognitive Development
Lupu, V. V., Miron, I. C., Răileanu, A. A., Jechel, E., Cianga, A. L., Buga, A. M. L., Stârcea, I. M., Ioniuc, I. K., Mocanu, A., & Lupu, A. (2024) · BRAIN BROAD RESEARCH IN ARTIFICIAL INTELLIGENCE AND NEUROSCIENCE · doi:10.18662/brain/15.1/541 · Cited by 1
Microbiota–Gut–Brain Axis and Neurodegenerative Disorder
Soni, A., Verma, A., & Gupta, P. (2022) · Nutritional neurosciences · doi:10.1007/978-981-19-4530-4_3 · Cited by 3
Metadata
- Authors
- Abdel-Haq, R., Schlachetzki, J. C. M., Glass, C. K., & Mazmanian, S. K.
- Affiliations
- California Institute of Technology (US)
- University of California San Diego (US)
- Corresponding author
- Abdel-Haq, Reem
- Mazmanian, Sarkis K.
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2018-11-01
- Volume
- 216
- Issue
- 1
- Pages
- 41-59
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC6314531
- OpenAlex
- W2899046125
- Cited by
- 471
- References
- 214
- Citations by year
- 2026: 51 · 2025: 78 · 2024: 70 · 2023: 76 · 2022: 77 · 2021: 46 · 2020: 38 · 2019: 33
- FWCI
- 2.77
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The Journal of Experimental Medicine (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by-nc-sa)
- eScholarship (California Digital Library) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion, cc-by-nc-sa)
- Funders
- U.S. Department of Defense (PD160030)
- Donna and Benjamin M. Rosen Bioengineering Center
- National Institutes of Health (AG057706, NS096170, MH100556, NS085910)
- Heritage Medical Research Institute
- Simons Foundation (322839)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- gut microbiota, microglia, gut-brain axis, neuroinflammation, microglial maturation, neurodevelopmental disorders, neurodegenerative diseases, microbial treatment, brain microenvironment
- MeSH terms
- Gastrointestinal Microbiome, Animals, Brain, Humans, Intestines, Microglia, Neurodegenerative Diseases, Neurodevelopmental Disorders
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