Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Jul 9;10:202. doi: 10.3389/fnagi.2018.00202

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2018 Zhou, Ulland and Colonna.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Triggering receptor expressed on myeloid cells 2 (TREM2) maintains microglial metabolism through the mammalian target of rapamycin (mTOR) pathway in Alzheimer’s disease (AD). TREM2 pairs with DAP12 through charge interactions in the transmembrane domain. Upon TREM2 ligand binding, DAP12 gets phosphorylated and recruits spleen tyrosine kinase (SYK), which initiates a cascade of signaling events, including phosphoinositide 3-kinase (PI3K) activation, which is composed of p85 and p110. The recruitment of p85 requires DAP10. One of the PI3K downstream targets AKT then activates mammalian target of rapamycin complex 1 (mTORC1) and mTORC2, which inhibits autophagy. These signaling events maintain microglia at high energy states so that in AD models, microglia are able to cluster around amyloid plaques.