[Objectives] To study the effect of PPARγ agonist DA on the cognitive function of AD mice as well as the mechanism.[Methods] 50 Kunming male mice were randomly divided into normal control group, model group and decanoic acid administration group, the AD mice model was established by subcutaneous injection of D-galactose for 8 weeks, and the treatment group was administered orally with different doses of decanoic acid (low dose of 50 mg/kg, middle dose of 100 mg/kg, high dose of 200 mg/kg).After 8 weeks, the Morris water maze was used to detect the learning and memory capability of mice;HE staining was used to observe the morphological change of hippocampal cells in brain tissue;Western-blot and immunohistochemistry technique were used to detect the expression of PPARγ and Aβ42 protein in brain tissue;the ELISA method was used for the determination of TNF-α and iNOS level in serum.[Results] Morris water maze results showed that DA could significantly improve the learning and memory function in AD mice (P<0.05);HE staining showed that DA could significantly reduce degeneration in hippocampal cells;Western-blot and immunohistochemistry results showed that DA could promote the expression of PPARγ and reduce the expression of Aβ42 in brain tissue (P<0.05);ELISA results showed that the TNF-α, iNOS levels decreased in AD mice serum after DA treatment (P<0.05).[Conclusions] DA could significantly improve the cognitive function of AD mice, improve the degeneration of hippocampal cells in brain tissue, and decrease the expression of Aβ42 in brain tissue.The mechanism might be related to activation of PPARγ protein and down-regulation of expression of relevant inflammatory factors.