Role of gut microbiota in regulating gastrointestinal dysfunction and motor symptoms in a mouse model of Parkinson’s disease.

Yogesh Bhattarai, Jie Si, Meng Pu, Owen A. Ross, Pamela J. McLean, Lisa Till, William Moor, Madhusudan Grover, Karunya K. Kandimalla, Kara G. Margolis, Gianrico Farrugia, Purna C. Kashyap

Research output: Contribution to journalArticlepeer-review

Abstract

Parkinson’s disease (PD) is a common neurodegenerative disorder characterized primarily by motor and non-motor gastrointestinal (GI) deficits. GI symptoms’ including compromised intestinal barrier function often accompanies altered gut microbiota composition and motor deficits in PD. Therefore, in this study, we set to investigate the role of gut microbiota and epithelial barrier dysfunction on motor symptom generation using a rotenone-induced mouse model of PD. We found that while six weeks of 10 mg/kg of chronic rotenone administration by oral gavage resulted in loss of tyrosine hydroxylase (TH) neurons in both germ-free (GF) and conventionally raised (CR) mice, the decrease in motor strength and coordination was observed only in CR mice. Chronic rotenone treatment did not disrupt intestinal permeability in GF mice but resulted in a significant change in gut microbiota composition and an increase in intestinal permeability in CR mice. These results highlight the potential role of gut microbiota in regulating barrier dysfunction and motor deficits in PD.

Original languageEnglish (US)
Article number1866974
JournalGut microbes
Volume13
Issue number1
DOIs
StatePublished - 2021

Bibliographical note

Publisher Copyright:
© 2021 The Author(s). Published with license by Taylor & Francis Group, LLC.

Keywords

  • Microbiota-gut-brain axis, intestinal epithelial barrier, idiopathic Parkinson's disease, gnotobiotic mice, Braak hypothesis

PubMed: MeSH publication types

  • Journal Article

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