Metagenomics of Parkinson’s disease implicates the gut microbiome in multiple disease mechanisms
Open accessPublished version of a preprint
Abstract
Parkinson’s disease (PD) may start in the gut and spread to the brain. To investigate the role of gut microbiome, we conducted a large-scale study, at high taxonomic resolution, using uniform standardized methods from start to end. We enrolled 490 PD and 234 control individuals, conducted deep shotgun sequencing of fecal DNA, followed by metagenome-wide association studies requiring significance by two methods (ANCOM-BC and MaAsLin2) to declare disease association, network analysis to identify polymicrobial clusters, and functional profiling. Here we show that over 30% of species, genes and pathways tested have altered abundances in PD, depicting a widespread dysbiosis. PD-associated species form polymicrobial clusters that grow or shrink together, and some compete. PD microbiome is disease permissive, evidenced by overabundance of pathogens and immunogenic components, dysregulated neuroactive signaling, preponderance of molecules that induce alpha-synuclein pathology, and over-production of toxicants; with the reduction in anti-inflammatory and neuroprotective factors limiting the capacity to recover. We validate, in human PD, findings that were observed in experimental models; reconcile and resolve human PD microbiome literature; and provide a broad foundation with a wealth of concrete testable hypotheses to discern the role of the gut microbiome in PD.
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A recent metagenomic analysis of the PD gut microbiome revealed a reduction in glutamate/glutamine synthesis genes and pathways, along with an increase in the glutamate degradation pathway.
“a recent metagenomic analysis of PD gut microbiome revealed a reduction in glutamate/glutamine synthesis genes and pathways, along with an increase in glutamate degradation pathway.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [331]
Gene families involved in TMA production were elevated in the PD gut microbiome, leading to increased choline metabolism and subsequent TMA production.
“the gene families involved in TMA production were found to be elevated in the PD gut microbiome, leading to increased choline metabolism and subsequent TMA production.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [331]
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Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases
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- Authors
- Wallen, Z. D., Demirkan, A., Twa, G., Cohen, G., Dean, M. N., Standaert, D. G., Sampson, T. R., & Payami, H.
- Affiliations
- University of Alabama at Birmingham (US)
- Emory University (US)
- Corresponding author
- Payami, Haydeh
- ORCID
- Venue
- Nature Communications
- Published
- 2022-11-15
- Volume
- 13
- Issue
- 1
- Pages
- 6958-6958
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC9663292
- OpenAlex
- W4309109636
- Cited by
- 346
- References
- 78
- Citations by year
- 2026: 97 · 2025: 99 · 2024: 90 · 2023: 57 · 2022: 3
- FWCI
- 20.33
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Parkinson's Foundation (PF-SF-JFA-830658)
- United States Department of Defense | United States Army | Army Medical Command | Medical Research and Materiel Command (W81XWH1810508)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Gut microbiota and health
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Dentistry › Periodontics › Oral microbiology and periodontitis research
- Keywords
- Parkinson's disease, gut microbiota, dysbiosis, metagenome-wide association study, alpha-synuclein pathology, neuroinflammation, neuroprotective factors, fecal microbiota
- MeSH terms
- Gastrointestinal Microbiome, Humans, Parkinson Disease, Metagenome, Metagenomics, 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.
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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