Journal
NATURE REVIEWS NEUROSCIENCE
Volume 17, Issue 4, Pages 201-207Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nrn.2016.7
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Funding
- US National Institutes of Health (NIH) [1RF1AG051485-01]
- Cure Alzheimer disease Fund
- Lilly Innovation Fellowship Award (Eli Lilly and Company)
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Genome-wide association studies have identified rare variants of the gene that encodes triggering receptor expressed on myeloid cells 2 (TREM2)-an immune receptor that is found in brain microglia-as risk factors for non-familial Alzheimer disease (AD). Furthermore, animal studies have indicated that microglia have an important role in the brain response to amyloid-beta(A beta) plaques and that TREM2 variants may have an impact on such a function. We discuss how TREM2 may control the microglial response to A beta and its impact on microglial senescence, as well as the interaction of TREM2 with other molecules that are encoded by gene variants associated with AD and the hypothetical consequences of the cleavage of TREM2 from the cell surface.
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