文献类型：期刊文献

英文题名：The immunometabolic reprogramming of microglia in Alzheimer's disease

作者：Chen, Hongli[1];Guo, Zichen[1];Sun, Yaxuan[1];Dai, Xueling[1]

第一作者：Chen, Hongli

通讯作者：Dai, XL[1]

机构：[1]Beijing Union Univ, Coll Biochem Engn, Beijing Key Lab Bioact Subst & Funct Food, Beijing 100023, Peoples R China

第一机构：北京联合大学应用文理学院|北京联合大学生物化学工程学院

通讯机构：[1]corresponding author), Beijing Union Univ, Coll Biochem Engn, Beijing Key Lab Bioact Subst & Funct Food, Beijing 100023, Peoples R China.|[1141726]北京联合大学生物化学工程学院;[11417]北京联合大学;[114172]北京联合大学应用文理学院;

年份：2023

卷号：171

外文期刊名：NEUROCHEMISTRY INTERNATIONAL

收录：;Scopus(收录号：2-s2.0-85173512173);WOS:【SCI-EXPANDED(收录号:WOS:001099602500001)】；

基金：This research was supported by grants from the Beijing Natural Science Foundation (6164030) , Beijing Key Laboratory of Bioactive Substances and Functional Foods Research Project, the Academic Research Projects of Beijing Union University (ZK80202102) , and Education Reform Project of Beijing Union University (JY2023Y008) .

语种：英文

外文关键词：Microglia; Immunometabolism; Reprogramming; Neuroinflammation; Alzheimer's disease

摘要：Alzheimer's disease (AD) is an age-related neurodegenerative disorder (NDD). In the central nervous system (CNS), immune cells like microglia could reprogram intracellular metabolism to alter or exert cellular immune functions in response to environmental stimuli. In AD, microglia could be activated and differentiated into pro-inflammatory or anti-inflammatory phenotypes, and these differences in cellular phenotypes resulted in variance in cellular energy metabolism. Considering the enormous energy requirement of microglia for immune functions, the changes in mitochondria-centered energy metabolism and substrates of microglia are crucial for the cellular regulation of immune responses. Here we reviewed the mechanisms of microglial metabolic reprogramming by analyzing their flexible metabolic patterns and changes that occurred in their metabolism during the development of AD. Further, we summarized the role of drugs in modulating immunometabolic reprogramming to prevent neuroinflammation, which may shed light on a new research direction for AD treatment.