小胶质细胞
神经炎症
串扰
神经科学
微泡
阿尔茨海默病
细胞生物学
生物
淀粉样蛋白(真菌学)
β淀粉样蛋白
免疫学
小RNA
疾病
医学
炎症
生物化学
病理
肽
物理
光学
基因
植物
作者
Yuanxin Zhao,Buhan Liu,Jian Wang,Long Xu,Shuyou Yu,Jiaying Fu,Xiaoyu Yan,Jing Su
出处
期刊:Biomedicines
[MDPI AG]
日期:2022-07-27
卷期号:10 (8): 1800-1800
被引量:10
标识
DOI:10.3390/biomedicines10081800
摘要
One of the most striking hallmarks shared by various neurodegenerative diseases, including Alzheimer's disease (AD), is microglia-mediated neuroinflammation. The main pathological features of AD are extracellular amyloid-β (Aβ) plaques and intracellular tau-containing neurofibrillary tangles in the brain. Amyloid-β (Aβ) peptide and tau protein are the primary components of the plaques and tangles. The crosstalk between microglia and neurons helps maintain brain homeostasis, and the metabolic phenotype of microglia determines its polarizing phenotype. There are currently many research and development efforts to provide disease-modifying therapies for AD treatment. The main targets are Aβ and tau, but whether there is a causal relationship between neurodegenerative proteins, including Aβ oligomer and tau oligomer, and regulation of microglia metabolism in neuroinflammation is still controversial. Currently, the accumulation of Aβ and tau by exosomes or other means of propagation is proposed as a regulator in neurological disorders, leading to metabolic disorders of microglia that can play a key role in the regulation of immune cells. In this review, we propose that the accumulation of Aβ oligomer and tau oligomer can propagate to adjacent microglia through exosomes and change the neuroinflammatory microenvironment by microglia metabolic reprogramming. Clarifying the relationship between harmful proteins and microglia metabolism will help people to better understand the mechanism of crosstalk between neurons and microglia, and provide new ideas for the development of AD drugs.
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