TREM2 and Amyloid Beta: A Love-Hate Relationship

Joe Udeochu; Faten A Sayed; Li Gan

doi:10.1016/j.neuron.2018.02.018

TREM2 and Amyloid Beta: A Love-Hate Relationship

Neuron. 2018 Mar 7;97(5):991-993. doi: 10.1016/j.neuron.2018.02.018.

Authors

Joe Udeochu¹, Faten A Sayed², Li Gan³

Affiliations

¹ Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA.
² Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA, USA; Neuroscience Graduate Program, University of California, San Francisco, San Francisco, CA, USA.
³ Gladstone Institute of Neurological Disease, University of California, San Francisco, San Francisco, CA, USA; Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco, San Francisco, CA, USA; Neuroscience Graduate Program, University of California, San Francisco, San Francisco, CA, USA. Electronic address: lgan@gladstone.ucsf.edu.

PMID: 29518360
DOI: 10.1016/j.neuron.2018.02.018

Abstract

Mutations in TREM2 increase risk for late-onset AD. In this issue of Neuron, Zhao et al. (2018) show that TREM2 binds Aβ to enhance its clearance and Lee et al. (2018) demonstrate that human TREM2 expression in AD mice ameliorates Aβ-associated deficits.

Publication types

Research Support, N.I.H., Extramural
Comment

MeSH terms

Alzheimer Disease / genetics*
Amyloid beta-Peptides / genetics
Animals
Gene Dosage
Humans
Membrane Glycoproteins / genetics
Mice
Microglia
Phenotype
Receptors, Immunologic / genetics

Substances

Amyloid beta-Peptides
Membrane Glycoproteins
Receptors, Immunologic
TREM2 protein, human
Trem2 protein, mouse

Grants and funding

K12 GM081266/GM/NIGMS NIH HHS/United States