Unraveling gut microbiota in Parkinson's disease and atypical parkinsonism

ABSTRACT Background Although several studies have suggested that abnormalities in gut microbiota may play a critical role in the pathogenesis of PD, data are still extremely heterogeneous. Methods 16S gene ribosomal RNA sequencing was performed on fecal samples of 350 individuals, subdivided into id...

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Veröffentlicht in:Movement disorders Jg. 34; H. 3; S. 396 - 405
Hauptverfasser: Barichella, Michela, Severgnini, Marco, Cilia, Roberto, Cassani, Erica, Bolliri, Carlotta, Caronni, Serena, Ferri, Valentina, Cancello, Raffaella, Ceccarani, Camilla, Faierman, Samanta, Pinelli, Giovanna, Bellis, Gianluca, Zecca, Luigi, Cereda, Emanuele, Consolandi, Clarissa, Pezzoli, Gianni
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States Wiley Subscription Services, Inc 01.03.2019
Schlagworte:
Aged
Basal ganglia
Brain diseases
Case-Control Studies
Central nervous system diseases
clinical features
Cognitive ability
Disease Progression
Dysbacteriosis
Feces - microbiology
Female
Gait
Gastrointestinal Microbiome - physiology
Gut microbiota
Gut-brain axis
Humans
Intestinal microflora
Lachnospiraceae
Lactobacillaceae
Male
Microbiota
Middle Aged
Movement disorders
MSA
multiple system atrophy
Multiple System Atrophy - microbiology
Neurodegenerative diseases
Parkinson Disease - microbiology
Parkinson's disease
Parkinsonian Disorders - microbiology
Pathogenesis
Posture
progressive supranuclear palsy
PSP
rRNA 16S
Supranuclear Palsy, Progressive - microbiology
PD
Parkinson-s disease
MSA
multiple system atrophy
PSP
clinical features
gut-brain axis
progressive supranuclear palsy
ISSN:0885-3185, 1531-8257, 1531-8257
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Zusammenfassung:ABSTRACT Background Although several studies have suggested that abnormalities in gut microbiota may play a critical role in the pathogenesis of PD, data are still extremely heterogeneous. Methods 16S gene ribosomal RNA sequencing was performed on fecal samples of 350 individuals, subdivided into idiopathic PD (n = 193, of whom 39 were drug naïve) stratified by disease duration, PSP (n = 22), MSA (n = 22), and healthy controls (HC; n = 113). Several confounders were taken into account, including dietary habits. Results Despite the fact that unadjusted comparison of PD and HC showed several differences in relative taxa abundances, the significant results were greatly reduced after adjusting for confounders. Although most of these differences were associated with disease duration, lower abundance in Lachnospiraceae was the only difference between de novo PD and HC (remaining lower across almost all PD duration strata). Decreased Lachnospiraceae and increased Lactobacillaceae and Christensenellaceae were associated with a worse clinical profile, including higher frequencies of cognitive impairment, gait disturbances, and postural instability. When compared with HC, MSA and PSP patients shared the changes in PD, with a few exceptions: in MSA, Lachnospiraceae were not lower, and Prevotellaceae were reduced; in PSP, Lactobacillaceae were similar, and Streptococcaceae were reduced. Conclusions Gut microbiota may be an environmental modulator of the pathogenesis of PD and contribute to the interindividual variability of clinical features. Data are influenced by PD duration and several confounders that need to be taken into account in future studies. Prospective studies in de novo PD patients are needed to elucidate the net effect of dysbiosis on the progression of the disease. © 2018 International Parkinson and Movement Disorder Society
Bibliographie:Nothing to report.
Funding agency
Michela Barichella, Marco Severgnini, Roberto Cilia contributed, equally to this study. Clarissa Consolandi and Gianni Pezzoli contributed equally to this study.
Relevant conflicts of interests/financial disclosures
Correction added on December 31, 2018, after first online publication: The contributing author information has been updated in the online text and PDF versions of this article.
This work was supported by the Fondazione Grigioni per il Morbo di Parkinson.
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ISSN:0885-3185
1531-8257
1531-8257
DOI:10.1002/mds.27581