Parkinson's disease and Parkinson's disease medications have distinct signatures of the gut microbiome

ABSTRACT Background There is mounting evidence for a connection between the gut and Parkinson's disease (PD). Dysbiosis of gut microbiota could explain several features of PD. Objective The objective of this study was to determine if PD involves dysbiosis of gut microbiome, disentangle effects...

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Bibliographic Details
Published in:Movement disorders Vol. 32; no. 5; pp. 739 - 749
Main Authors: Hill‐Burns, Erin M., Debelius, Justine W., Morton, James T., Wissemann, William T., Lewis, Matthew R., Wallen, Zachary D., Peddada, Shyamal D., Factor, Stewart A., Molho, Eric, Zabetian, Cyrus P., Knight, Rob, Payami, Haydeh
Format: Journal Article
Language:English
Published: United States Wiley Subscription Services, Inc 01.05.2017
Subjects:
Abundance
Age Factors
Anticholinergics
Antiparkinson Agents - therapeutic use
Bifidobacterium - genetics
Carbidopa - therapeutic use
Case-Control Studies
Catechol
Catechol O-methyltransferase
Catechol O-Methyltransferase Inhibitors - therapeutic use
Cholinergic Antagonists - therapeutic use
confounding
Confounding Factors, Epidemiologic
Demography
Deoxyribonucleic acid
Diet
Digestive system
DNA
DNA sequencing
Drug Combinations
Dysbacteriosis
Dysbiosis - epidemiology
Dysbiosis - microbiology
Female
Fruit
functional pathways
Gastrointestinal Microbiome - genetics
Gastrointestinal tract
gut microbiome
Humans
Intestinal microflora
Lactobacillaceae - genetics
Levodopa
Levodopa - therapeutic use
Male
medications
Methyltransferase
Microbiota
Movement disorders
Neurodegenerative diseases
Parkinson Disease - drug therapy
Parkinson Disease - epidemiology
Parkinson Disease - microbiology
Parkinson's disease
Pasteurellaceae - genetics
Plants
Risk Factors
RNA, Ribosomal, 16S - genetics
rRNA 16S
Sex Factors
United States - epidemiology
Vegetables
Verrucomicrobia - genetics
Xenobiotics
United States
confounding
Parkinson's disease
gut microbiome
functional pathways
medications
ISSN:0885-3185, 1531-8257
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Summary:ABSTRACT Background There is mounting evidence for a connection between the gut and Parkinson's disease (PD). Dysbiosis of gut microbiota could explain several features of PD. Objective The objective of this study was to determine if PD involves dysbiosis of gut microbiome, disentangle effects of confounders, and identify candidate taxa and functional pathways to guide research. Methods A total of 197 PD cases and 130 controls were studied. Microbial composition was determined by 16S rRNA gene sequencing of DNA extracted from stool. Metadata were collected on 39 potential confounders including medications, diet, gastrointestinal symptoms, and demographics. Statistical analyses were conducted while controlling for potential confounders and correcting for multiple testing. We tested differences in the overall microbial composition, taxa abundance, and functional pathways. Results Independent microbial signatures were detected for PD (P = 4E‐5), participants' region of residence within the United States (P = 3E‐3), age (P = 0.03), sex (P = 1E‐3), and dietary fruits/vegetables (P = 0.01). Among patients, independent signals were detected for catechol‐O‐methyltransferase‐inhibitors (P = 4E‐4), anticholinergics (P = 5E‐3), and possibly carbidopa/levodopa (P = 0.05). We found significantly altered abundances of the Bifidobacteriaceae, Christensenellaceae, [Tissierellaceae], Lachnospiraceae, Lactobacillaceae, Pasteurellaceae, and Verrucomicrobiaceae families. Functional predictions revealed changes in numerous pathways, including the metabolism of plant‐derived compounds and xenobiotics degradation. Conclusion PD is accompanied by dysbiosis of gut microbiome. Results coalesce divergent findings of prior studies, reveal altered abundance of several taxa, nominate functional pathways, and demonstrate independent effects of PD medications on the microbiome. The findings provide new leads and testable hypotheses on the pathophysiology and treatment of PD. © 2017 International Parkinson and Movement Disorder Society
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Relevant conflicts of interests/financial disclosures
The study was supported by National Institute of Neurological Disorders and Stroke grant R01036960 to H.P. Udall grant (P50 NS062684) provided additional support for sample collection at the Seattle site (C.P.Z.).
Funding agencies
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ISSN:0885-3185
1531-8257
DOI:10.1002/mds.26942