Therefore, the AD animal model induced by BAPN was mainly caused by AoSMC metabolic dysfunction, and downregulation of RhoA/ROCK1/YAP/F-actin signaling with decreased AoSMC stiffness could result in increased elastin fragmentation, reduced collagen production, and dysfunction of the cell-ECM unit, thereby facilitating AD formation. The gene discussed is RHOA; the disease is Alzheimer disease.