Altered gut microbiome in parkinson’s disease and the influence of lipopolysaccharide in a human α-synuclein over-expressing mouse model
Open accessAbstract
The interaction between the gut microbiota and alpha-synuclein (Syn) aggregation in Parkinson’s disease (PD) is receiving increasing attention. The objective of this study was to investigate gut microbiota, and effects of an inflammatory lipopolysaccharide (LPS) trigger in a human Syn over-expressing mouse model of PD (Thy1-αSyn). Stool samples from patients with confirmed PD and Thy1-Syn mice were analysed using 16S ribosomal RNA sequencing. Compared to healthy controls, the relative abundance of mucin-degrading Verrucomicrobiae and LPS-producing Gammaproteobacteria were greater in PD patients. In mice, the abundance of Gammaproteobacteria was negligible in both Thy1-αSyn and wild-type (WT) animals, while Verrucomicrobiae were reduced in Thy1-αSyn mice. The effect of LPS on intestinal barrier function was investigated in vitro using intestinal epithelial (IEC-6) cells, and in vivo via administration of LPS in drinking water to Thy1-Syn mice. Acute exposure to LPS in vitro resulted in a reduction and altered distribution of the tight junction markers ZO-1 and e-Cadherin around the cell membrane in IEC-6 cells, as shown by immunohistochemistry. LPS administration in Thy1-Syn mice resulted in the emergence of early motor manifestations at 10 weeks, compared to untreated mice who were still asymptomatic at this age. This study reaffirms that an altered microbiome exists in patients with PD, and supports the notion of a proinflammatory gut microbiome environment as a trigger for PD pathogenesis.
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LPS intervention results in a significant decrease in the tight junction proteins ZO-1 and e-cadherin in intestinal epithelial cells of Thy1-a-synuclein mice.
“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”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [36]
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)
Experimental — accuracy not yet measuredA decreased abundance of mucin-degrading Verrucomicrobiae was found in a human alpha-synuclein overexpressing mouse model.
“A decreased abundance of mucin-degrading Verrucomicrobiae was found in a human a-synuclein overexpressing mouse model.36”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [36]
There is a relationship between gut microbiota and the pathogenesis of Parkinson's disease.
“indicating that there is a relationship between gut microbiota and the pathogenesis of Parkinson's disease”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [36]
a-synuclein spreads from the intestine to the CNS in the pathogenesis of Parkinson's disease.
“thus supporting the hypothesis that a-synuclein spreads from the intestine to the CNS in the pathogenesis of Parkinson's disease.36”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [36]
An increase in Gammaproteobacteria, an LPS-producing Gram-negative bacterium, was found in the faeces of patients with Parkinson's disease.
“An increase in Gammaproteobacteria, an LPS-producing Gram-negative bacterium, was found in the faeces of patients with Parkinson's disease.36”
From The role of gut dysbiosis in Parkinson’s disease: mechanistic insights and therapeutic options (2021) · cites this paper as [36]
Age-related changes in the microbiota may contribute to cognitive decline and other neurodegenerative disorders.
“There is growing evidence that age-related changes in the microbiota may contribute to cognitive decline and other neurodegenerative disorders (102, 103).”
From Signalling cognition: The gut microbiota and hypothalamic-pituitary-adrenal axis (2023) · cites this paper as [103]
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- Authors
- Gorecki, A. M., Preskey, L., Bakeberg, M. C., Kenna, J. E., Gildenhuys, C., MacDougall, G., Dunlop, S. A., Mastaglia, F. L., Akkari, P. A., Koengten, F., & Anderton, R. S.
- Affiliations
- The University of Western Australia (AU)
- The University of Notre Dame Australia (AU)
- Perron Institute for Neurological and Translational Science (AU)
- Murdoch University (AU)
- Corresponding author
- Anderton, Ryan S.
- ORCID
- Venue
- Frontiers in Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2019-08-07
- Volume
- 13
- Pages
- 839-839
- ISSN
- 1662-453X (ISSN-L)
- PMC
- PMC6693556
- OpenAlex
- W2965437143
- Cited by
- 184
- References
- 76
- Citations by year
- 2026: 7 · 2025: 22 · 2024: 35 · 2023: 28 · 2022: 30 · 2021: 43 · 2020: 19
- FWCI
- 15.56
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Neuroscience (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Murdoch University Research Portal (submittedVersion)
- UWA Profiles and Research Repository (UWA) (submittedVersion, cc-by)
- ResearchOnline@ND (The University of Notre Dame) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Armstrong Foundation
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Parkinson's disease, gut microbiota, alpha-synuclein, lipopolysaccharide, Gammaproteobacteria, intestinal barrier function, tight junctions, ZO-1, E-cadherin, motor symptoms, neuroinflammation, microbiome-gut-brain axis
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.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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