Vascular dementia (VD), which accounts for around 15% of dementia cases, is a major threat to the health and productivity of the global population (O’Brien and Thomas, 2015) as it is associated with high morbidity and reduced cognitive function. White matter lesions (WMLs) and neuroinflammation are pathologic features of VD (Saggu et al., 2016; Hase et al., 2018). Moreover, the latter accelerates the apoptosis of oligodendrocytes, leading to demyelination and WMLs (Gouw et al., 2011). Myelin repair is critical for cognitive recovery (Li et al., 2017). Remyelination—which is often defective in demyelinating diseases including VD (Fancy et al., 2009; Jiang et al., 2017)—depends on the proliferation and differentiation of oligodendrocyte progenitor cells (OPCs; Franklin and Ffrench-Constant, 2008). Thus, therapeutic strategies that suppress inflammation and stimulate OPC differentiation into oligodendrocytes can alleviate cognitive impairment associated with VD by stimulating remyelination (Jiang et al., 2017; Figlia et al., 2018).