An in vitro model of AD was established by PDGF-BB-mediated human aortic SMCs, and results showed that HIF1A-AS2 was obviously increased in human AD tissues and knockdown of HIF1A-AS2 suppressed the proliferation and migration, while promoted the phenotypic switching of SMCs through miR-33b/HMGA2 axis, which laid a theoretical foundation for understanding the development of AD and might provide novel strategies for AD therapy. This evidence concerns the gene HIF1A and Alzheimer disease.