tracers is significantly enhanced in cilostazol-treated CAA model mice, thereby resulting in maintenance of vascular integrity, amelioration of Aβ deposits (Figure 4), and prevention of cognitive decline (Maki et al., 2014). Memory-preserving activity of cilostazol has been demonstrated in aged wild-type mice (Yanai et al., 2014) and a rat model of chronic cerebral hypoperfusion (Watanabe et al., 2006), suggesting that cilostazol could be a potential disease modifying therapy of AD and other dementing disorders.
