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TREM2 variants: new keys to decipher Alzheimer disease pathogenesis
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TREM2 variants: new keys to decipher Alzheimer disease pathogenesis
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Journal Article
TREM2 variants: new keys to decipher Alzheimer disease pathogenesis
2016
Overview
A series of genetic studies has implicated the microglial immune receptor TREM2 in the pathogenesis of Alzheimer disease (AD). Here, Colonna and Wang describe recent studies that have begun to unpick the mechanisms by which TREM2 is involved in AD and discuss unanswered questions in the field.
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.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 45/43
/ 64/110
/ Alzheimer Disease - genetics
/ Alzheimer Disease - pathology
/ Alzheimer Disease - physiopathology
/ Analysis
/ Animal Genetics and Genomics
/ Animals
/ Dementia
/ Genetic Variation - genetics
/ Genome-wide association studies
/ Genome-Wide Association Study
/ Genomes
/ Humans
/ Kinases
/ Ligands
/ Membrane Glycoproteins - genetics
/ Membrane Glycoproteins - metabolism
/ Mutation
/ progress
/ Proteins
/ Receptors, Immunologic - genetics
