Association of Glial Activation and α-Synuclein Pathology in Parkinson's Disease.
10.1007/s12264-022-00957-z
- Author:
Rui WANG
1
;
Haigang REN
2
;
Elena KAZNACHEYEVA
3
;
Xiaojun LU
4
;
Guanghui WANG
5
Author Information
1. Center of Translational Medicine, First People's Hospital of Taicang, Taicang Affiliated 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 Affiliated Hospital of Soochow University, Suzhou, 215400, China.
5. Center of Translational Medicine, First People's Hospital of Taicang, Taicang Affiliated Hospital of Soochow University, Suzhou, 215400, China. wanggh@suda.edu.cn.
- Publication Type:Review
- Keywords:
Astrocyte activation;
Microglial activation;
Neuroinflammation;
Parkinson's disease;
α-synuclein pathology
- MeSH:
Humans;
Parkinson Disease/pathology*;
alpha-Synuclein/metabolism*;
Dopaminergic Neurons/metabolism*;
Pars Compacta/metabolism*
- From:
Neuroscience Bulletin
2023;39(3):479-490
- CountryChina
- Language:English
-
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.
