TREM2, Microglia, and Neurodegenerative Diseases

Area of Science:

• Neuroscience
• Immunology
• Genetics

Background:

• Alzheimer's disease (AD) is a leading cause of death, characterized by amyloid-β plaques and tau tangles.
• Genetic variants in TREM2 (triggering receptor expressed on myeloid cells 2) significantly elevate AD risk.
• Microglia and the innate immune system are implicated in AD pathogenesis.

Purpose of the Study:

• To review recent advancements in TREM2 biology and microglial function in neurodegeneration.
• To explore TREM2's role in Alzheimer's disease progression.
• To identify novel therapeutic strategies targeting TREM2.

Main Methods:

• Review of recent scientific literature on TREM2, microglia, and Alzheimer's disease.
• Analysis of genetic studies linking TREM2 variants to AD risk.
• Synthesis of findings on TREM2's functions in amyloid plaque pathology and microglial responses.

Main Results:

• TREM2 plays critical roles in amyloid plaque maintenance and microglial envelopment of plaques.
• TREM2 signaling influences microglial viability and function in aging and diseased brains.
• Novel TREM2 ligands have been identified, expanding our understanding of its interactions.

Conclusions:

• TREM2 is a key player in Alzheimer's disease pathogenesis, linking innate immunity to AD.
• Targeting TREM2 and microglial pathways presents promising therapeutic avenues for AD.
• Further research into TREM2 biology may lead to interventions to delay or prevent AD progression.