TREM2 in Alzheimer’s Disease: Microglial Survival and Energy Metabolism

Frontiers in Aging Neuroscience

Yun-wu Zhang¹  Baoying Cheng¹  Xin Li¹  Yanfang Li²  Honghua Zheng²  Xiaofen Chen² 

[1] Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, Medical College, Xiamen University, Xiamen, China;Shenzhen Research Institute, Xiamen University, Shenzhen, China;

关键词: Alzheimer’s disease;    TREM2;    microglia;    survival;    metabolism;   

DOI  :  10.3389/fnagi.2018.00395

来源: DOAJ

【 摘 要 】

Alzheimer’s disease (AD) is the leading cause of age-related dementia among the elderly population. Recent genetic studies have identified rare variants of the gene encoding the triggering receptor expressed on myeloid cells-2 (TREM2) as significant genetic risk factors in late-onset AD (LOAD). TREM2 is specifically expressed in brain microglia and modulates microglial functions in response to key AD pathologies such as amyloid-β (Aβ) plaques and tau tangles. In this review article, we discuss recent research progress in our understanding on the role of TREM2 in microglia and its relevance to AD pathologies. In addition, we discuss evidence describing new TREM2 ligands and the role of TREM2 signaling in microglial survival and energy metabolism. A comprehensive understanding of TREM2 function in the pathogenesis of AD offers a unique opportunity to explore the potential of this microglial receptor as an alternative target in AD therapy.

【 授权许可】

Unknown