Journal
NEUROSCIENCE BULLETIN
Volume 39, Issue 3, Pages 479-490Publisher
SPRINGER
DOI: 10.1007/s12264-022-00957-z
Keywords
Parkinson's disease; alpha-synuclein pathology; Microglial activation; Astrocyte activation; Neuroinflammation
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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.
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.
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