This study was therefore designed to investigate whether AS mitigates Alzheimer's disease (AD) progression by targeting PLA2G4A to restore lysosomal homeostasis.<h4>Methods</h4>The therapeutic potential of AS was investigated in APP/PS1 mice by analyzing cognitive function, β-amyloid (Aβ) load, and lysosomal integrity, with its mechanism of action further explored in N2a-sw cells.<h4>Results</h4>AS treatment reduced GSK3α/β expression in both APP/PS1 mice and N2a-sw cells. The gene discussed is PLA2G4A; the disease is Alzheimer disease.