Their studies showed that O-1602 mitigated cognitive impairment in Aβ1–42-induced neurotoxicity by reducing soluble Aβ1–42 levels in the hippocampus and frontal cortex, reversing GPR-55 downregulation, and decreasing levels of Ras homolog family member A (RhoA) and Rho-associated coiled-coil-containing protein kinase 2 (ROCK2) proteins. The gene discussed is RHOA; the disease is Cognitive impairment.