It notably reduces both the incidence and mortality rates of AD and suppresses the aortic dilation; (2) Set reversed phenotypic switching of VSMCs by upregulating the expression of GPX4 and further inhibiting ferroptosis; (3) Set enhanced the transcriptional activity of GPX4 through the activation of the PGC-1α/NRF2 pathway-mediated mitochondrial biogenesis. This evidence concerns the gene PPARGC1A and Alzheimer disease.