Related Experiment Video

Updated: Aug 16, 2025

Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain
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Immunofluorescence Staining Using IBA1 and TMEM119 for Microglial Density, Morphology and Peripheral Myeloid Cell Infiltration Analysis in Mouse Brain

Published on: October 27, 2019

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TREM2 dependent and independent functions of microglia in Alzheimer's disease

Jinchao Hou1, Yun Chen1,2, Gary Grajales-Reyes1

  • 1Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO, 63110, USA.

Molecular Neurodegeneration
|December 23, 2022
PubMed

Insights

Microglia, the brain's immune cells, are crucial in Alzheimer's disease (AD). This review highlights genetic and functional insights into microglial responses, particularly focusing on the TREM2 receptor and its role in AD pathology and potential therapies.

Area of Science:

  • Neuroscience
  • Immunology
  • Genetics

Background:

  • Microglia are key innate immune cells in the brain.
  • Alzheimer's disease (AD) research extensively studies microglial roles.
  • Genetic variants, especially in TREM2, significantly impact AD risk.

Purpose of the Study:

  • To review genetic and functional discoveries on microglial reactivity in AD.
  • To focus on the impact of TREM2 variants on microglial responses to AD pathologies.
  • To discuss therapeutic strategies informed by microglia and TREM2 biology.

Main Methods:

  • Literature review of genetic and functional studies.
  • Analysis of research on microglial responses to amyloid plaques, tauopathy, and demyelination.
  • Examination of studies in mouse models and human subjects.

Main Results:

  • Rare TREM2 variants are associated with increased AD risk.
  • TREM2 influences microglial activation and response to AD hallmarks.
  • Understanding TREM2's role provides insights into AD pathogenesis.

Conclusions:

  • Microglia and TREM2 are central to AD pathogenesis.
  • Targeting microglia and TREM2 pathways offers potential therapeutic avenues for AD.
Keywords:
APOEAlzheimer’s diseaseBeta-amyloid pathologyDemyelinationMicrogliaTREM2Tauopathy

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