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

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)....

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Bibliographic Details
Published in:Frontiers in aging neuroscience 2018-11, Vol.10, p.395-395
Main Authors: Zheng, Honghua, Cheng, Baoying, Li, Yanfang, Li, Xin, Chen, Xiaofen, Zhang, Yun-Wu
Format: Article
Language:English
Subjects:
Age
Aging
Alzheimer's disease
Amyloid
Brain research
Dementia
Dementia disorders
Disease
Energy metabolism
Geriatrics
Metabolism
Microglia
Myeloid cells
Neuroscience
Pathogenesis
Pathology
Peptides
Population genetics
Population studies
Proteins
Risk factors
Roles
Senile plaques
survival
Tau protein
TREM2
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Summary: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.
ISSN:1663-4365
1663-4365
DOI:10.3389/fnagi.2018.00395