The nasal and gut microbiome in Parkinson's disease and idiopathic rapid eye movement sleep behavior disorder

ABSTRACT Background Increasing evidence connects the gut microbiota and the onset and/or phenotype of Parkinson's disease (PD). Differences in the abundances of specific bacterial taxa have been reported in PD patients. It is, however, unknown whether these differences can be observed in indivi...

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Published in:Movement disorders Vol. 33; no. 1; pp. 88 - 98
Main Authors: Heintz‐Buschart, Anna, Pandey, Urvashi, Wicke, Tamara, Sixel‐Döring, Friederike, Janzen, Annette, Sittig‐Wiegand, Elisabeth, Trenkwalder, Claudia, Oertel, Wolfgang H., Mollenhauer, Brit, Wilmes, Paul
Format: Journal Article
Language:English
Published: United States Wiley Subscription Services, Inc 01.01.2018
John Wiley and Sons Inc
Subjects:
16S rRNA gene amplicon sequencing
Behavior disorders
Demography
Digestive system
Eye movements
genome reconstructions
Genomes
Intestinal microflora
Microbiomes
Microbiota
Movement disorders
Neurodegenerative diseases
nonmotor phenotype
Parkinson's disease
RBD
REM sleep
rRNA 16S
rRNA 18S
Sleep
Sleep disorders
Synuclein
16S rRNA gene amplicon sequencing
genome reconstructions
PD
RBD
nonmotor phenotype
ISSN:0885-3185, 1531-8257, 1531-8257
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Summary:ABSTRACT Background Increasing evidence connects the gut microbiota and the onset and/or phenotype of Parkinson's disease (PD). Differences in the abundances of specific bacterial taxa have been reported in PD patients. It is, however, unknown whether these differences can be observed in individuals at high risk, for example, with idiopathic rapid eye movement sleep behavior disorder, a prodromal condition of α‐synuclein aggregation disorders including PD. Objectives To compare microbiota in carefully preserved nasal wash and stool samples of subjects with idiopathic rapid eye movement sleep behavior disorder, manifest PD, and healthy individuals. Methods Microbiota of flash‐frozen stool and nasal wash samples from 76 PD patients, 21 idiopathic rapid eye movement sleep behavior disorder patients, and 78 healthy controls were assessed by 16S and 18S ribosomal RNA amplicon sequencing. Seventy variables, related to demographics, clinical parameters including nonmotor symptoms, and sample processing, were analyzed in relation to microbiome variability and controlled differential analyses were performed. Results Differentially abundant gut microbes, such as Akkermansia, were observed in PD, but no strong differences in nasal microbiota. Eighty percent of the differential gut microbes in PD versus healthy controls showed similar trends in idiopathic rapid eye movement sleep behavior disorder, for example, Anaerotruncus and several Bacteroides spp., and correlated with nonmotor symptoms. Metagenomic sequencing of select samples enabled the reconstruction of genomes of so far uncharacterized differentially abundant organisms. Conclusion Our study reveals differential abundances of gut microbial taxa in PD and its prodrome idiopathic rapid eye movement sleep behavior disorder in comparison to the healthy controls, and highlights the potential of metagenomics to identify and characterize microbial taxa, which are enriched or depleted in PD and/or idiopathic rapid eye movement sleep behavior disorder. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.
Bibliography:Full financial disclosures and author roles may be found in the online version of this article.
The present work was supported by BIOMARKAPD—a project under the aegis of an EU Joint Programme on Neurodegenerative Diseases (JPND) co‐funded by the Luxembourg National Research Fund (FNR). The project was further supported by an FNR CORE grant (BM/10404093) and an “Espoir en tête” grant from the Rotary Club Luxembourg. The DeNoPa cohort was supported by unrestricted grants by the University Medical Center Göttingen, Paracelsus‐Elena‐Klinik, Kassel, Germany, the Michael J. Fox Foundation for Parkinson's Research (MJFF), Parkinson Fond Deutschland, and the Deutsche Parkinson Vereinigung. W.H.O. is Hertie‐Senior‐Research Professor supported by the Charitable Hertie‐Foundation, Frankfurt/Main, Germany.
The copyright line for this article was changed on 8 September 2017 after original online publication.
Drs. Mollenhauer and Wilmes made equal contributions.
Nothing to report.
Relevant conflicts of interest/financial disclosures
Funding agencies
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Relevant conflicts of interest/financial disclosures: Nothing to report.
Funding agencies: The present work was supported by BIOMARKAPD—a project under the aegis of an EU Joint Programme on Neurodegenerative Diseases (JPND) co‐funded by the Luxembourg National Research Fund (FNR). The project was further supported by an FNR CORE grant (BM/10404093) and an “Espoir en tête” grant from the Rotary Club Luxembourg. The DeNoPa cohort was supported by unrestricted grants by the University Medical Center Göttingen, Paracelsus‐Elena‐Klinik, Kassel, Germany, the Michael J. Fox Foundation for Parkinson's Research (MJFF), Parkinson Fond Deutschland, and the Deutsche Parkinson Vereinigung. W.H.O. is Hertie‐Senior‐Research Professor supported by the Charitable Hertie‐Foundation, Frankfurt/Main, Germany.
ISSN:0885-3185
1531-8257
1531-8257
DOI:10.1002/mds.27105