Cheng Xuehua, Wei Yong, Qian Zijun, Han Li
Department of TCM Geriatrics, Huadong Hospital Affiliated to Fudan University, Shanghai, 200040, People's Republic of China.
GeneScience Pharmaceuticals CoLtd., Changchun, 130012, People's Republic of China.
Cell Mol Neurobiol. 2023 May;43(4):1537-1549. doi: 10.1007/s10571-022-01269-6. Epub 2022 Aug 12.
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.
自噬是一个高度进化保守的过程,它降解胞质大分子或受损细胞器(如线粒体)以及细胞内病原体以获取能量和维持生存。自噬功能障碍与阿尔茨海默病(AD)的病理过程相关,包括Aβ斑块和神经原纤维缠结。最近,大脑中持续免疫反应的存在被认为是AD的一种新的核心病理。越来越多的证据表明,在临床试验和临床前研究中,自噬激活可能通过降解炎性小体或促炎细胞因子以及改善免疫系统功能来抑制炎症反应。本综述概述了AD中自噬、炎症及其潜在介质的最新信息。总之,我们认为了解自噬与炎症之间的关系将为AD未来的治疗意义提供有见地的知识。