Abstract
Accumulating evidence implicates immune dysfunction in the etiology of Parkinson's disease (PD). For instance, impaired cellular and humoral immune responses are emerging as established pathological hallmarks in PD. Further, in experimental models of PD, inflammatory cell activation and immune dysregulation are evident. Genetic and epidemiologic studies have drawn associations between autoimmune disease and PD. Distillation of these various lines of evidence indicates dysregulated immunogenetics as a primary risk factor for PD. This article will present novel perspectives on the association between genetic risk factors and immune processes in PD. The objective of this work is to synthesize the data surrounding the role of immunogenetics in PD to maximize the potential of targeting the immune system as a therapeutic modality.
| Original language | English (US) |
|---|---|
| Pages (from-to) | S5-S11 |
| Journal | Journal of Parkinson's disease |
| Volume | 12 |
| DOIs | |
| State | Published - Jul 7 2022 |
Funding
This work was supported by a National Institute of Neurologic Disease and Stroke K99/R00 Pathway to Independence Award (NS112458-01A1) (D.G.), the Cure Alzheimer’s Fund (D.G.) and a pilot project through the NIA funded Northwestern University Alzheimer’s Disease Research Center 1P30AG072977-01 (D.G.).
Keywords
- Parkinson's disease
- T cells
- adaptive immunity
- immune
- immunogenetics
ASJC Scopus subject areas
- Clinical Neurology
- Cellular and Molecular Neuroscience