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Updated: Jan 23, 2026

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

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TREM2 function impedes tau seeding in neuritic plaques

Cheryl E G Leyns1,2,3, Maud Gratuze1,2,3, Sneha Narasimhan4

  • 1Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA.

Nature Neuroscience
|June 26, 2019
PubMed

Insights

Genetic variants in triggering receptor expressed on myeloid cells 2 (TREM2) are linked to Alzheimer's disease risk. TREM2 deficiency worsens tau pathology by reducing microgliosis around amyloid plaques, indicating TREM2's role in limiting tau spread.

Area of Science:

  • Neuroscience
  • Genetics
  • Immunology

Background:

  • Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) are associated with an increased risk of developing sporadic, late-onset Alzheimer's disease.
  • Microglia, the brain's immune cells, play a crucial role in Alzheimer's disease pathogenesis.

Purpose of the Study:

  • To investigate the functional impact of TREM2 variants on microglial response to amyloid-β plaques.
  • To determine the role of TREM2 in the seeding and spreading of tau aggregates in Alzheimer's disease.

Main Methods:

  • Utilized germline knockout mouse models for Trem2.
  • Introduced the TREM2R47H variant into mouse models.
  • Analyzed microgliosis surrounding amyloid-β plaques and quantified tau aggregate seeding and spreading.

Main Results:

  • Germline knockout of Trem2 or the presence of the TREM2R47H variant significantly reduced microgliosis around amyloid-β plaques.
  • Reduced microgliosis correlated with facilitated seeding and spreading of neuritic plaque tau aggregates.
  • TREM2 deficiency promoted the development of peri-plaque tau pathologies.

Conclusions:

  • TREM2 and microglia are critical in controlling the accumulation and spread of tau pathology around amyloid plaques.
  • Impaired TREM2 function exacerbates tau seeding and spreading, contributing to Alzheimer's disease progression.
  • These findings highlight TREM2 as a potential therapeutic target for mitigating tau pathology in Alzheimer's disease.

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