Within the CNS, NG2+ OPCs (oligodendrocyte precursor cells) can differentiate into mature myelinating oligodendrocytes following injury or demyelination (McTigue and Tripathi, 2008). However, the mechanisms that regulate these processes after injury or insult are not well understood (McTigue et al., 1998; McTigue and Tripathi, 2008; Whittaker et al., 2012). In models of MS, clinical symptoms and demyelination are exacerbated in PPARγ heterozygous mice (Natarajan et al., 2003). Work by De Nuccio et al. (2011) points to a potential mechanism; they show that PPARγ agonists promote OPC differentiation by inducing mitochondrial respiratory chain activity and oscillatory Ca2+ waves, which are crucial for oligodendrocyte differentiation. Furthermore, PPARγ activation directly promotes differentiation of rat OPCs into mature oligodendrocytes (Bernardo et al., 2009). Since myelin is composed mostly of lipid and since PPARs play a major role in lipid metabolism, it is not surprising that PPARs regulate the differentiation and function of oligodendrocytes (Saluja et al., 2001; Leisewitz et al., 2008; Kanakasabai et al., 2012). Statins (cholesterol-reducing drugs) also promote oligodendrocyte maturation by inducing PPARγ, an effect that is blocked by PPARγ antagonism (Sim
