Rui Wang1,2 · Haigang Ren2 · Elena Kaznacheyeva3 · Xiaojun Lu4 · Guanghui Wang1,21 Center of Translational Medicine, First People’s Hospital of Taicang, Taicang Afliated Hospital of Soochow University, Suzhou 215400, China
2 Laboratory of Molecular Neuropathology, Jiangsu Key Laboratory of Neuropsychiatric Diseases and College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China
3 Institute of Cytology, Russian Academy of Sciences, Saint-Petersburg, Russia 194064
4 Department of Neurosurgery, First People’s Hospital of Taicang, Taicang Afliated Hospital of Soochow University, Suzhou 215400, China
Abstract
The accumulation of pathological α-synuclein (α-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 α-syn pathology have expanded our understanding of the region-specific distribution of α-syn in PD patients. Accumulating evidence suggests that α-syn aggregates are released from neurons and endocytosed by glial cells, which contributes to the clearance of α-syn. However, the activation of glial cells by α-syn species produces pro-inflammatory factors that decrease the uptake of α-syn aggregates by glial cells and promote the transmission of α-syn between neurons, which promotes the spread of α-syn pathology. In this article, we provide an overview of current knowledge on the role of glia and α-syn pathology in PD pathogenesis, highlighting the relationships between glial responses and the spread of α-syn pathology.
Keywords
Parkinson's disease; α-synuclein pathology; Microglial activation; Astrocyte activation; Neuroinfammation
