Compared with WT mice, in smAT2 mice, there were no significant changes in NADPH oxidase activity, superoxide anion production, expressions of inflammatory mediators and NADPH oxidase subunits, RAGE and Aβ1-40 level, and neuronal degeneration markers among all groups, indicating that the potential inhibitory effect of AT2 receptor activation on the cognitive deficit in our mouse model might be due to attenuation of amplified oxidative stress and inflammation, improvement of RAGE-mediated Aβ clearance system, downregulation of Aβ level, and reduction of neuronal degeneration. The gene discussed is AGTR2; the disease is Cognitive impairment.