自噬
神经炎症
炎症
神经科学
免疫系统
神经退行性变
疾病
生物
细胞生物学
细胞内
小胶质细胞
免疫学
医学
细胞凋亡
病理
生物化学
作者
Xuehua Cheng,Yong Wei,Zijun Qian,Li Han
标识
DOI:10.1007/s10571-022-01269-6
摘要
Autophagy is a highly evolutionary conserved process that degrades cytosolic macromolecules or damaged organelles (e.g., mitochondria), as well as intracellular pathogens for energy and survival. Dysfunction of autophagy has been associated with the pathologies of Alzheimer’s disease (AD), including Aβ plaques and neurofibrillary tangles. Recently, the presence of sustained immune response in the brain has been considered a new core pathology in AD. Accumulating evidence suggests that autophagy activation may suppress inflammation response through degrading inflammasomes or pro-inflammatory cytokines and improving immune system function in both clinical trials and preclinical studies. This review provides an overview of updated information on autophagy and inflammation and their potential mediators in AD. In summary, we believe that understanding the relationship between autophagy and inflammation will provide insightful knowledge for future therapeutic implications in AD.
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