TREM2: Keeping Microglia Fit during Good Times and Bad

Soyon Hong; Beth Stevens

doi:10.1016/j.cmet.2017.09.010

TREM2: Keeping Microglia Fit during Good Times and Bad

Cell Metab. 2017 Oct 3;26(4):590-591. doi: 10.1016/j.cmet.2017.09.010.

Authors

Soyon Hong¹, Beth Stevens²

Affiliations

¹ F.M. Kirby Neurobiology Center, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA.
² F.M. Kirby Neurobiology Center, Boston Children's Hospital and Harvard Medical School, Boston, MA 02115, USA; Stanley Center for Psychiatric Research, Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA. Electronic address: beth.stevens@childrens.harvard.edu.

PMID: 28978423
DOI: 10.1016/j.cmet.2017.09.010

Abstract

Microglia are the macrophages of the brain and play an important role in Alzheimer's disease (AD). In Cell, Ulland et al. (2017) recently reported that mutations in TREM2, a protein implicated in AD, disrupt microglial energy state and function, thus sabotaging the microglia's ability to defend the brain against amyloid plaques.

MeSH terms

Alzheimer Disease / genetics*
Alzheimer Disease / metabolism
Alzheimer Disease / pathology
Animals
Disease Models, Animal
Gene Deletion
Gene Expression Regulation
Humans
Membrane Glycoproteins / genetics*
Membrane Glycoproteins / metabolism
Mice
Microglia / metabolism
Microglia / pathology*
Mutation
Plaque, Amyloid / genetics
Plaque, Amyloid / metabolism
Plaque, Amyloid / pathology
Receptors, Immunologic / genetics*
Receptors, Immunologic / metabolism
Signal Transduction
TOR Serine-Threonine Kinases / metabolism

Substances

Membrane Glycoproteins
Receptors, Immunologic
TREM2 protein, human
Trem2 protein, mouse
TOR Serine-Threonine Kinases