Combining lipidomics analysis results, it was shown that VLCFAs accumulated and phosphatidylserine was greatly reduced in the AD model group, so it was hypothesized that PPARγ may promote peroxisome proliferation, increase the decomposition of VLCFAs and the synthesis of phosphatidylserine (PEs and POs), thereby alleviating long-chain fatty acid accumulation and increasing the level of phosphatidylserine in the brain, thereby improving the cognitive function of AD. The gene discussed is PPARG; the disease is Alzheimer disease.