Synaptic pruning mediated by glia in Alzheimer's disease
10.16438/j.0513-4870.2020-1640
- VernacularTitle:胶质细胞介导的神经突触修剪在阿尔茨海默病中的作用
- Author:
Ling-jie LI
1
;
Xiao-lin YU
2
;
Rui-tian LIU
2
Author Information
1. State Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing 100190, China; School of Chemistry and Chemical Engineering, University of Chinese Academy of Sciences, Beijing 100049, China
2. State Key Laboratory of Biochemical Engineering, Institute of Process Engineering, Chinese Academy of Sciences, Beijing 100190, China
- Publication Type:Research Article
- Keywords:
Alzheimer's disease;
cognitive deficit;
microglia;
astrocyte;
synaptic pruning
- From:
Acta Pharmaceutica Sinica
2021;56(2):383-390
- CountryChina
- Language:Chinese
-
Abstract:
Alzheimer's disease (AD) is a neurodegenerative disease characterized by memory loss and cognitive impairment. To date, however, no disease-modifying strategies to prevent or cure AD exist. Synapses are involved in the connection of neurons and present as the key component for the memory and other neural activities. Synapse loss is a critical hallmark of AD pathology. In brain, glia cells, including microglia and astrocytes, are a group of highly specific cell types other than neurons. Microglia and astrocytes play a key role in maintaining the healthy neural circuit and regulating synaptic plasticity. Under development and physiological conditions, glial cells contribute to construct and maintain mature central neural networks via synaptic pruning. However, during AD pathogenesis, glial cells engulf synapses excessively, which leads to synapse loss, neuronal dysfunction, and cognitive impairment. Here, we review recent advances in our understanding of the underlying mechanisms for glia-mediated synaptic pruning in AD, and provide a novel strategy for the development of AD drugs.
