Intestinal Inflammation and Parkinson's Disease

Parkinson's disease (PD) is the second most common neurodegenerative disease which significantly influences the life quality of patients. The protein alpha-synuclein plays an important driving role in PD occurrence and development. Braak's hypothesis suggests that alpha-synuclein is produced in intestine, and then spreads into the central nervous system through the vagus nerve. The abnormal expression of alpha-synuclein has been found in inflammatory bowel disease (IBD). Intestinal inflammation and intestinal dysbiosis have been involved in the occurrence and development of PD. The present review aimed to summarize recent advancements in studies focusing on intestinal inflammation and PD, especially the mechanisms through which link intestinal inflammation and PD. The intestinal dysfunctions such as constipation have been introduced as non-motor manifestations of PD. The possible linkages between IBD and PD, including genetic overlaps, inflammatory responses, intestinal permeability, and intestinal dysbiosis, are mainly discussed. Although it is not confirmed whether PD starts from intestine, intestinal dysfunction may affect intestinal microenvironment to influence central nervous system, including the alpha-synuclein pathologies and systematic inflammation. It is expected to develop some new strategies in the diagnosis and treatment of PD from the aspect of intestine. It may also become an exciting direction to find better ways to regulate the composition of gut microorganism to treat PD.

Automated summary

Parkinson's disease, as the second most common neurodegenerative disease, is significantly influenced by intestinal inflammation and alpha-synuclein. Research suggests that intestinal inflammation and dysbiosis may be related to the occurrence and development of PD.