Roles of TREM2 in Alzheimer's disease

Area of Science:

• Neuroscience
• Genetics
• Immunology

Background:

• Triggering receptor expressed on myeloid cells 2 (TREM2) gene variants increase risk for Alzheimer's disease (AD) and Nasu-Hakola disease.
• TREM2 is a type I transmembrane receptor primarily expressed on microglia in the central nervous system.
• TREM2 is critical in AD pathogenesis, regulating microglial inflammation, amyloid-β deposition, and tau pathology.

Purpose of the Study:

• To review the progress in understanding TREM2's role in Alzheimer's disease.
• To highlight the potential of TREM2 as a therapeutic target for neuroprotection.
• To identify areas for future research in TREM2-directed therapeutics.

Main Methods:

• Review of existing literature on TREM2 in Alzheimer's disease.
• Analysis of studies on TREM2 variants and their association with disease risk.
• Examination of research on soluble TREM2 (sTREM2) as a biomarker.
• Evaluation of novel mouse models and technological innovations for TREM2-based therapies.

Main Results:

• TREM2 variants are established risk factors for late-onset Alzheimer's disease.
• Soluble TREM2 (sTREM2) is a promising biomarker for AD clinical progression.
• Despite advances, the exact roles of membrane-bound TREM2 and sTREM2 in AD pathogenesis require further elucidation.
• Novel therapeutic strategies targeting TREM2 for neuroprotection are emerging.

Conclusions:

• TREM2 is a crucial factor in Alzheimer's disease pathogenesis and progression.
• TREM2 presents a significant therapeutic target for neurodegenerative diseases like AD.
• Further research is needed to fully understand TREM2's functions and develop effective TREM2-directed therapies.