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The triggering receptor expressed on myeloid cells 2: "TREM-ming" the inflammatory component associated with

Troy T Rohn1

  • 1Department of Biological Sciences, Boise State University, Boise, ID 83725, USA. trohn@boisestate.edu

Oxidative Medicine and Cellular Longevity
|March 28, 2013
PubMed

Insights

New Alzheimer's disease (AD) research highlights the triggering receptor expressed on myeloid cells 2 (TREM2) gene. Variants in TREM2 significantly increase the risk of late-onset AD, emphasizing inflammation's role.

Area of Science:

  • Neurodegenerative Disorders
  • Neuroinflammation
  • Genetics of Alzheimer's Disease

Background:

  • Alzheimer's disease (AD) involves progressive memory and cognitive decline.
  • While senile plaques and neurofibrillary tangles are studied, inflammation's role in AD etiology is increasingly recognized.
  • A novel TREM2 gene variant significantly elevates the risk for late-onset AD.

Purpose of the Study:

  • To discuss recent developments concerning TREM2 and its role in AD.
  • To explore how TREM2 loss-of-function may contribute to AD pathogenesis.
  • To provide an overview of pathways linking beta-amyloid, NFTs, oxidative stress, and inflammation in AD.

Main Methods:

  • Review of recent genetic and molecular findings related to TREM2.
  • Discussion of TREM2 function on microglial cells.
  • Analysis of pathways involving beta-amyloid, NFTs, oxidative stress, and inflammation.

Main Results:

  • TREM2 variants triple the risk of developing late-onset AD.
  • TREM2 is expressed on microglial cells, modulating phagocytosis and inflammation.
  • Loss of TREM2 function may enhance CNS oxidative stress and inflammation.

Conclusions:

  • TREM2 plays a critical role in regulating neuroinflammation.
  • Dysfunctional TREM2 is a significant risk factor for Alzheimer's disease.
  • Understanding TREM2 pathways is crucial for developing novel AD therapeutics.

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