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Related Experiment Video

Updated: Oct 5, 2025

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

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

Published on: October 27, 2019

Functional insight into LOAD-associated microglial response genes.

Lauren A Jonas^1,2, Tanya Jain^1,2, Yue-Ming Li^1,2

¹Weill Cornell, Weill Graduate School of Medical Sciences of Cornell University, New York, NY 10065, USA.

|January 26, 2022

Summary

This summary is machine-generated.

Neuroinflammation, particularly involving microglia, plays a key role in late-onset Alzheimer's disease (AD). This review explores major genes linked to microglia responses in AD development.

Keywords:

Alzheimer's LOAD TREM2 microglia

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Area of Science:

Neuroscience
Immunology
Genetics

Background:

Alzheimer's disease (AD) is pathologically defined by amyloid beta plaques and neurofibrillary tangles.
Recent genome-wide association studies (GWAS) highlight neuroinflammation's critical role in late-onset AD (LOAD).
The innate immune system, especially microglia, is increasingly recognized for its involvement in AD pathogenesis.

Purpose of the Study:

To review the function of major genes associated with microglia responses in LOAD.
To elucidate the role of immune and microglia-related gene variants in AD.
To highlight neuroinflammation as a therapeutic target for AD.

Main Methods:

Review of recent genome-wide association studies (GWAS) and whole-genome sequencing data.
Analysis of identified variants in immune and microglia-related genes.
Synthesis of current evidence on microglia function in AD.

Main Results:

Numerous variants in immune and microglia-related genes (e.g., TREM2, CD33, APOE) are linked to LOAD.
These genetic findings underscore the significance of neuroinflammation in AD.
Microglia are central players in the inflammatory processes contributing to AD.

Conclusions:

Neuroinflammation and microglia dysfunction are critical factors in LOAD.
Targeting microglia response genes presents a promising therapeutic strategy for AD.
Further research into these genes is essential for understanding and treating AD.