4.6 Review

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

Journal

FRONTIERS IN AGING NEUROSCIENCE
Volume 10, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fnagi.2018.00395

Keywords

Alzheimer's disease; TREM2; microglia; survival; metabolism

Funding

  1. Natural Science Key Foundation of Fujian Educational Department of China [JZ160403]
  2. National Natural Science Foundation of China [81771164, 81870845]
  3. Natural Science Foundation of Guangdong Province of China [2016A030313821, 2017A030313604, 2018A030313158]
  4. Open Research Fund of State Key Laboratory of Cellular Stress Biology, Xiamen University [SKLCSB2018KF017]
  5. National Key Research and Development Program of China [2016YFC1305903]
  6. Fundamental Research Funds for the Central Universities [20720180049]

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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-beta (A beta) 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.

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