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Published on: June 14, 2020
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Basic Science and Pathogenesis
Deniz Ghaffari1, Jennifer K Griffin1, Ye Zhou1
1University of Toronto, Toronto, ON, Canada.
Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
Summary
Microglia TREM2 signaling differs between mouse strains, impacting Alzheimer's disease (AD) pathology. ABI3 deletion effects in AD models may depend on these TREM2 pathway variations.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Alzheimer's disease (AD) is a leading cause of dementia with no effective treatments.
- Microglia, immune cells in the brain, are implicated in AD pathogenesis due to associated genetic variants.
- Conflicting results exist regarding the role of ABI3 deletion in AD mouse models, suggesting underlying biological differences.
Purpose of the Study:
- To investigate the impact of genetic background differences on TREM2 signaling in microglia.
- To explore how altered TREM2 signaling in different microglial populations may explain discrepancies in ABI3 deletion studies for AD.
- To identify potential therapeutic targets by understanding the interplay between TREM2 and ABI3 in AD.
Main Methods:
- Primary microglia from C57 and SJL mice were used.
- TREM2 cleavage was measured by ELISA.
- TREM2 signaling pathway components (SYK, PLCG2) were analyzed via western blotting after anti-TREM2 antibody stimulation.
- Amyloid-beta phagocytosis by microglia was assessed using live imaging.
Main Results:
- SJL microglia exhibited significantly lower TREM2 cleavage compared to C57 microglia.
- Stimulation of SJL microglia with an anti-TREM2 antibody resulted in attenuated SYK and PLCG2 phosphorylation.
- SJL microglia showed reduced amyloid-beta phagocytosis compared to C57 microglia, indicating impaired TREM2 function.
Conclusions:
- TREM2 signaling and AD-related functions are significantly altered in SJL microglia.
- Differences in TREM2 signaling between microglial populations may explain conflicting AD phenotypes observed in ABI3-deficient mouse models.
- Further research aims to elucidate the molecular link between TREM2 and ABI3 to develop novel AD therapeutics.
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