Epidemiological Evidence for an Immune Component of Parkinson's Disease

There is a growing interest in the role the immune system and inflammatory response play on the pathophysiology of Parkinson's disease (PD). Epidemiological evidence lends support for the hypothesis that PD is an immune-mediated condition. An association between inflammatory bowel disease, including Crohn's and Ulcerative colitis, and the risk of PD has been described and replicated in several population-based cohorts. Other autoimmune conditions, such as Sjogren syndrome, ankylosing spondylitis, and rheumatoid arthritis also seem to be associated with an increased risk of PD. Immunosuppressant medications seem to be associated with a decreased risk of PD. Finally, variants in genes involved in immune system regulation are also shared between PD and autoimmune conditions. In this review, we will provide an overview of epidemiological evidence from population-based cohort studies, meta-analyses, and genome-wide association studies that analyze the association between the immune system and PD, discuss current gaps in the literature and future research directions in this field.

Automated summary

There is a growing interest in understanding the role of the immune system and inflammatory response in the development of Parkinson's disease. Epidemiological evidence suggests that Parkinson's disease may be immune-mediated, with associations observed between inflammatory bowel disease and an increased risk of Parkinson's. Medications that suppress the immune system may decrease the risk of Parkinson's, and there are shared genetic variants between Parkinson's and autoimmune conditions. Further research is needed to fully understand the relationship between the immune system and Parkinson's disease.