Format

Send to

Choose Destination
Nat Rev Neurosci. 2016 Apr;17(4):201-7. doi: 10.1038/nrn.2016.7. Epub 2016 Feb 25.

TREM2 variants: new keys to decipher Alzheimer disease pathogenesis.

Author information

1
Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63108, USA.
2
Eli Lilly and Company, Lilly Corporate Center, Indianapolis, Indiana 46285, USA.

Abstract

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-β (Aβ) plaques and that TREM2 variants may have an impact on such a function. We discuss how TREM2 may control the microglial response to Aβ 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.

PMID:
26911435
DOI:
10.1038/nrn.2016.7
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center