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Immune receptor LAG3 regulates microglia function during Alzheimer's disease
Andrew T Perl1, Juan Wu2, John D Dong2
1Neurobiology Laboratory, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC 27709, United States; University of Virginia, Charlottesville, VA 22903, United States.
Deleting lymphocyte activation gene 3 (Lag3) in Alzheimer's disease (AD) models reduces neurodegeneration markers and improves behavior. This suggests Lag3 is a potential therapeutic target for AD treatment.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Alzheimer's Disease (AD) is the primary cause of dementia, with undefined etiology and lacking effective treatments.
- Immune dysregulation, particularly involving microglia, is implicated in AD pathogenesis.
Purpose of the Study:
- To investigate the role of lymphocyte activation gene 3 (Lag3) in a familial AD mouse model.
- To determine if targeting Lag3 can ameliorate AD-related pathologies and phenotypes.
Main Methods:
- Utilized the 5xFAD mouse model of familial AD.
- Administered Lag3 deletion and analyzed molecular, cellular, and behavioral outcomes.
- Performed transcriptional profiling of microglia.
Main Results:
- Lag3 deletion significantly reduced amyloidosis and microgliosis in 5xFAD mice.
- Behavioral deficits associated with neurodegeneration were attenuated.
- Lag3 deletion suppressed disease-associated microglia (DAM) gene expression, restoring homeostatic programs.
- Reduced CD8+ T cell infiltration in the brain was observed.
Conclusions:
- Lag3 plays a critical role in regulating microglia function in AD.
- Targeting Lag3 may offer a novel therapeutic strategy for Alzheimer's Disease.
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