Cilostazol has a wide variety of pleiotropic effects capable of inducing neurogenesis (Lee et al., 2009; Tanaka et al., 2010), promoting oligodendrocyte precursor cell differentiation (Miyamoto et al., 2013), preventing lipid peroxidation (Hiramatsu et al., 2010; Kurtoglu et al., 2014), enhancing cholesterol efflux from macrophages (Nakaya et al., 2010), ameliorating insulin resistance (Wada et al., 2013), reducing inflammatory burden (Otsuki et al., 2001; Tsai et al., 2008; Hattori et al., 2009), and improving systemic lymphatic function by inducing proliferation and stabilization of lymphatic endothelial cells (Kimura et al., 2014). In a clinical setting, cilostazol is currently used as an anti-platelet drug (Gotoh et al., 2000; Shinohara et al., 2010), and may be used to prevent ischemic events in patients with CAA. Major manifestations of CAA include lobar hemorrhage and cortical microhemorrhage, as well as CMI. As most CAA patients are elderly (Zhang-Nunes et al., 2006), this necessitates the use of anti-platelet drugs with little risk of hemorrhage (Charidimou et al., 2012). The second Cilostazol Stroke Prevention Study (CSPS2) for patients with cerebral infarction showed that the hemorrhagic stroke was significantly
