In an amyloid-beta 1-42 (Aβ<sub>42</sub>)-induced Alzheimer's disease (AD) model, PS treatment reduced cytotoxicity and countered the Aβ<sub>42</sub>-induced downregulation of SIRT1 and PGC-1α, particularly at 70% and 80% PS purity, indicating PS's role in preserving neuronal viability and combating AD-like pathology. Here, PPARGC1A is linked to Alzheimer disease.