Author: Archana Pant1, Krishna Singh Bisht1, Swati Aggarwal1, Tushar Kanti Maiti2
Affiliation: <sup>1</sup> Regional Centre for Biotechnology, Faridabad, Haryana, India.
<sup>2</sup> Regional Centre for Biotechnology, Faridabad, Haryana, India. Electronic address: tkmaiti@rcb.res.in.
Conference/Journal: Prog Mol Biol Transl Sci
Date published: 2022 Oct 25
Other:
Volume ID: 192 , Issue ID: 1 , Pages: 281-307 , Special Notes: doi: 10.1016/bs.pmbts.2022.08.004. , Word Count: 208
The bidirectional communication between the gut and the brain has come up very fascinating in recent years. Many studies have reported that the onset of gastrointestinal issues appears long before the actual manifestation of Parkinson's disease (PD) symptoms. Disturbances in the gut-brain axis have been found to be linked with PD. PD-linked neuropathological changes in the enteric nervous system and significant alteration of gut microbiota suggest a vital role of gut microbiota in PD pathogenesis. Studies have also suggested that aggregation of α-synuclein, one of the major proteins associated with PD neuropathology, might start from the gut and move to the central nervous system (CNS) through the vagus nerve and olfactory bulb. Inflammation in the gut has been suggested to be associated with PD initiation and progression. The flushing out of healthy gut microbiota and replacing with pathogens induces gut inflammation and promotes neuroinflammation in the CNS. Therefore, it is intriguing to understand the mechanism of gut-brain communications associated with the development of PD. This review sheds light on the PD pathology, the gut dysbiosis that is associated with PD and its medications, altered gene expression, pathways and microbial metabolites during PD.
Keywords: Central nervous system; Gut microbiota; Gut-brain axis; Metabolites; Neuroinflammation; Parkinson's disease.
PMID: 36280322 DOI: 10.1016/bs.pmbts.2022.08.004