In vivo studies document that agonists for different PPAR isoforms typically improve outcomes in pre-clinical models of CNS injury or disease. For instance, in EAE (experimental autoimmune encephalomyelitis, an animal model of MS), several PPAR agonists have proven effective in delaying the onset and progression of disease (Niino et al., 2001; Diab et al., 2002, 2004; Feinstein et al., 2002; Gocke et al., 2009). PPARδ and PPARγ agonists also have shown benefits in experimental models of SCI, TBI and stroke (McTigue et al., 2007; Yi et al., 2008; Allahtavakoli et al., 2009; Sauerbeck et al., 2011; Thal et al., 2011; Villapol et al., 2012). Activation of these receptors attenuated inflammation and apoptosis, reduced lesion size and improved functional recovery; they also promoted oligodendrogenesis and differentiation (McTigue et al., 2007; Park et al., 2007; Yi et al., 2008; Allahtavakoli et al., 2009; Paterniti et al., 2010; Meng et al., 2011; Sauerbeck et al., 2011; Thal et al., 2011; Villapol et al., 2012). Neuropathology was exacerbated after CNS injury in mice deficient in PPARα, suggesting that endogenous PPAR ligands may limit neuropathology
