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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Vydáno v:	Movement disorders Ročník 32; číslo 5; s. 739 - 749
Hlavní autoři:	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
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States Wiley Subscription Services, Inc 01.05.2017
Témata:	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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Abstract	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
AbstractList	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 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. 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. 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. 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. 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. BACKGROUNDThere is mounting evidence for a connection between the gut and Parkinson's disease (PD). Dysbiosis of gut microbiota could explain several features of PD.OBJECTIVEThe 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.METHODSA 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.RESULTSIndependent 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.CONCLUSIONPD 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. 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
Author	Peddada, Shyamal D. Debelius, Justine W. Payami, Haydeh Wallen, Zachary D. Wissemann, William T. Factor, Stewart A. Zabetian, Cyrus P. Morton, James T. Lewis, Matthew R. Molho, Eric Knight, Rob Hill‐Burns, Erin M.
Author_xml	– sequence: 1 givenname: Erin M. surname: Hill‐Burns fullname: Hill‐Burns, Erin M. organization: University of Alabama at Birmingham – sequence: 2 givenname: Justine W. surname: Debelius fullname: Debelius, Justine W. organization: University of California San Diego – sequence: 3 givenname: James T. surname: Morton fullname: Morton, James T. organization: University of California San Diego – sequence: 4 givenname: William T. surname: Wissemann fullname: Wissemann, William T. organization: University of Alabama at Birmingham – sequence: 5 givenname: Matthew R. surname: Lewis fullname: Lewis, Matthew R. organization: University of Alabama at Birmingham – sequence: 6 givenname: Zachary D. surname: Wallen fullname: Wallen, Zachary D. organization: University of Alabama at Birmingham – sequence: 7 givenname: Shyamal D. surname: Peddada fullname: Peddada, Shyamal D. organization: National Institute of Environmental Health Sciences – sequence: 8 givenname: Stewart A. surname: Factor fullname: Factor, Stewart A. organization: Emory University School of Medicine – sequence: 9 givenname: Eric surname: Molho fullname: Molho, Eric organization: Albany Medical College – sequence: 10 givenname: Cyrus P. orcidid: 0000-0002-7739-4306 surname: Zabetian fullname: Zabetian, Cyrus P. organization: University of Washington – sequence: 11 givenname: Rob surname: Knight fullname: Knight, Rob organization: University of California San Diego – sequence: 12 givenname: Haydeh surname: Payami fullname: Payami, Haydeh email: haydehpayami@uabmc.edu organization: HudsonAlpha Institute for Biotechnology
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/28195358$$D View this record in MEDLINE/PubMed
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Notes	Nothing to report. 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 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
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Snippet	ABSTRACT Background There is mounting evidence for a connection between the gut and Parkinson's disease (PD). Dysbiosis of gut microbiota could explain several... 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. The... Background There is mounting evidence for a connection between the gut and Parkinson's disease (PD). Dysbiosis of gut microbiota could explain several features... BACKGROUNDThere is mounting evidence for a connection between the gut and Parkinson's disease (PD). Dysbiosis of gut microbiota could explain several features...
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SubjectTerms	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
Title	Parkinson's disease and Parkinson's disease medications have distinct signatures of the gut microbiome
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