GEO series
Immune Receptor Lag3 Deletion Alleviates Neurodegeneration Phenotypes in a Mouse Model of Alzheimer’s Disease
GSE307127
Mus musculus
Expression profiling by high throughput sequencing
36 samples
2025/09/10
GPL19057
Summary
Alzheimer’s disease (AD) is the leading cause of dementia, but effective treatments remail unavailable. Using the 5xFAD familial AD mouse model, we show that deletion of the immune checkpoint receptor Lymphocyte activation gene 3 (Lag3) reduces amyloidosis, microgliosis, and neurodegeneration-related behavioral deficits. Transcriptional profiling revealed that Lag3 deletion reverses aberrant expression of disease-associated microglia (DAM) genes and decreased CD8+ T cells infiltration in the brain. These findings suggest that Lag3 regulates microglia function and may represent a potential therapeutic target for AD.
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Paper (PMID 42182406) ↗
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