Association of Glial Activation and α-Synuclein Pathology in Parkinson's Disease

The accumulation of pathological alpha-synuclein (alpha-syn) in the central nervous system and the progressive loss of dopaminergic neurons in the substantia nigra pars compacta are the neuropathological features of Parkinson's disease (PD). Recently, the findings of prion-like transmission of alpha-syn pathology have expanded our understanding of the region-specific distribution of alpha-syn in PD patients. Accumulating evidence suggests that alpha-syn aggregates are released from neurons and endocytosed by glial cells, which contributes to the clearance of alpha-syn. However, the activation of glial cells by alpha-syn species produces pro-inflammatory factors that decrease the uptake of alpha-syn aggregates by glial cells and promote the transmission of alpha-syn between neurons, which promotes the spread of alpha-syn pathology. In this article, we provide an overview of current knowledge on the role of glia and alpha-syn pathology in PD pathogenesis, highlighting the relationships between glial responses and the spread of alpha-syn pathology.

Automated summary

This article provides an overview of the role of glia and alpha-syn pathology in the pathogenesis of Parkinson's disease (PD), highlighting the relationships between glial responses and the spread of alpha-syn pathology.