Microbiome, Parkinson’s Disease and Molecular Mimicry

Cells. 2019;8(3):222 DOI 10.3390/cells8030222

 

Journal Homepage

Journal Title: Cells

ISSN: 2073-4409 (Online)

Publisher: MDPI AG

LCC Subject Category: Science: Biology (General)

Country of publisher: Switzerland

Language of fulltext: English

Full-text formats available: PDF, HTML

 

AUTHORS


Fabiana Miraglia (Department of Pharmacy, University of Pisa, via Bonanno 6, 56126 Pisa, Italy)

Emanuela Colla ([email protected] Laboratory, Scuola Normale Superiore, Piazza dei Cavalieri 7, 56126 Pisa, Italy)

EDITORIAL INFORMATION

Blind peer review

Editorial Board

Instructions for authors

Time From Submission to Publication: 11 weeks

 

Abstract | Full Text

Parkinson’s Disease (PD) is typically classified as a neurodegenerative disease affecting the motor system. Recent evidence, however, has uncovered the presence of Lewy bodies in locations outside the CNS, in direct contact with the external environment, including the olfactory bulbs and the enteric nervous system. This, combined with the ability of alpha-synuclein (αS) to propagate in a prion-like manner, has supported the hypothesis that the resident microbial community, commonly referred to as microbiota, might play a causative role in the development of PD. In this article, we will be reviewing current knowledge on the importance of the microbiota in PD pathology, concentrating our investigation on mechanisms of microbiota-host interactions that might become harmful and favor the onset of PD. Such processes, which include the secretion of bacterial amyloid proteins or other metabolites, may influence the aggregation propensity of αS directly or indirectly, for example by favoring a pro-inflammatory environment in the gut. Thus, while the development of PD has not yet being associated with a unique microbial species, more data will be necessary to examine potential harmful interactions between the microbiota and the host, and to understand their relevance in PD pathogenesis.