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Immune receptor LAG3 regulates microglia function during Alzheimer's disease
Andrew T Perl1,2, Juan Wu1, John D Dong1
1Neurobiology Laboratory, National Institute of Environmental Health Sciences, NIH, DHHS, Research Triangle Park, NC 27709.
Deleting the immune checkpoint receptor, lymphocyte activation gene 3 (Lag3), improves Alzheimer's disease (AD) symptoms in mice. This approach reduces amyloid plaques and inflammation, offering a potential new therapy for AD.
Area of Science:
- Neuroimmunology
- Neurodegenerative Diseases
- Molecular Biology
Background:
- Alzheimer's Disease (AD) is a leading cause of dementia with undefined etiology and limited treatments.
- The role of immune checkpoints in AD pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the impact of lymphocyte activation gene 3 (Lag3) deletion on AD phenotypes in a mouse model.
- To explore Lag3 as a potential therapeutic target for Alzheimer's Disease.
Main Methods:
- Utilized the 5xFAD mouse model of familial Alzheimer's Disease.
- Performed genetic deletion of the Lag3 immune checkpoint receptor.
- Assessed molecular (amyloidosis, microgliosis), cellular (DAM gene expression), and behavioral phenotypes.
- Analyzed CD8+ T cell infiltration in the brain.
Main Results:
- Lag3 deletion significantly reduced amyloidosis and microgliosis in 5xFAD mice.
- Behavioral deficits associated with neurodegeneration were attenuated.
- Suppressed aberrant expression of disease-associated microglia (DAM) genes, restoring microglial homeostasis.
- Observed reduced CD8+ T cell infiltration in the brain.
Conclusions:
- Lag3 plays a critical role in regulating microglia function in the context of AD.
- Targeting Lag3 may offer a novel therapeutic strategy for Alzheimer's Disease by modulating neuroinflammation and microglial activation.
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