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Gut bacterial composition in a mouse model of Parkinson’s disease

In: Beneficial Microbes
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P. Perez-Pardo Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, the Netherlands.

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H.B. Dodiya Department of Internal Medicine, Division of Digestive Disease and Nutrition, Rush University Medical Center, 1725 West Harrison Street, Chicago, IL 60612, USA.

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P.A. Engen Department of Internal Medicine, Division of Digestive Disease and Nutrition, Rush University Medical Center, 1725 West Harrison Street, Chicago, IL 60612, USA.

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A. Naqib DNA Services Facility, University of Illinois, 835 S Wolcott, Chicago, IL 60612, USA.

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C.B. Forsyth Department of Internal Medicine, Division of Digestive Disease and Nutrition, Rush University Medical Center, 1725 West Harrison Street, Chicago, IL 60612, USA.

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S.J. Green DNA Services Facility, University of Illinois, 835 S Wolcott, Chicago, IL 60612, USA.

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J. Garssen Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, the Netherlands.
Nutricia Research, Uppsalalaan 12, 3584 CT Utrecht, the Netherlands.

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A. Keshavarzian Department of Internal Medicine, Division of Digestive Disease and Nutrition, Rush University Medical Center, 1725 West Harrison Street, Chicago, IL 60612, USA.

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A.D. Kraneveld Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, the Netherlands.
Institute for Risk Assessment Sciences, Faculty of Veterinary Medicine, Utrecht University, Yalelaan 104, 3584 CM Utrecht, the Netherlands.

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The mechanism of neurodegeneration in Parkinson’s disease (PD) remains unknown but it has been hypothesised that the intestinal tract could be an initiating and contributing factor to the neurodegenerative processes. In PD patients as well as in animal models for PD, alpha-synuclein-positive enteric neurons in the colon and evidence of colonic inflammation have been demonstrated. Moreover, several studies reported pro-inflammatory bacterial dysbiosis in PD patients. Here, we report for the first time significant changes in the composition of caecum mucosal associated and luminal microbiota and the associated metabolic pathways in a rotenone-induced mouse model for PD. The mouse model for PD, induced by the pesticide rotenone, is associated with an imbalance in the gut microbiota, characterised by a significant decrease in the relative abundance of the beneficial commensal bacteria genus Bifidobacterium. Overall, intestinal bacterial dysbiosis might play an important role in both the disruption of intestinal epithelial integrity and intestinal inflammation, which could lead or contribute to the observed alpha-synuclein aggregation and PD pathology in the intestine and central nervous system in the oral rotenone mouse model of PD.

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