Abstract:The effects and mechanisms of Astragalus polysaccharides （APS） on Alzheimer′s disease （AD）mouse model were investigated. Following enzymatic extraction，the total glucose，protein，and glucuronic acid content of APS was determined，and Fourier transform-infrared （FT-IR） spectroscopy analysis was conducted. The mouse model of AD was induced by AlCl3 combined with D-galactose. APS was administered by gavage，and Morris water maze test was carried out to examine mouse behavior. The superoxide dismutase（SOD） and malondialdehyde （MDA） levels in mouse brain tissue were measured by enzyme-linked immunosorbent assay （ELISA）. Pathological changes in the brain tissue were revealed by hematoxylin and eosin stain（HE） staining and Nissl staining. The expression of Kelch-like ECH-associated protein 1 （Keap1），nuclear factor erythroid 2-related factor 2 （Nrf2），and amyloid-beta （Aβ） was determined by Western blot. The results indicated that APS exhibited the sugar content of （55.76±1.88）%，the protein content of （4.87±0.42）%，and the glucuronic acid content of （5.85±0.34）%. The FT-IR spectroscopy results revealed characteristic absorption peaks indicative of polysaccharides in APS. APS effectively alleviated memory impairment and improved memory function in AD mice. Moreover，it reduced brain tissue damage by inhibiting MDA secretion and enhancing SOD activity. From a mechanism perspective，APS downregulated the expression of Keap1 and Aβ，while upregulating the expression of Nrf2 in the brain tissue. In conclusion，APS possessed potential effects in alleviating AD by activating the Keap1/Nrf2/Aβ pathway.