which can be advantageous since similarly acting drugs can be combined for more potent effects (Diab et al., 2004). Furthermore, attenuating inflammatory signals reduces disease severity in models of MS, even after the onset of clinical symptoms (Diab et al., 2002, 2004). Notably, these beneficial effects can occur through PPAR-dependent and PPAR-independent mechanisms. For example, pioglitazone reduced intraspinal astrocyte activation in a receptor dependent manner in the sciatic nerve transection model (Jia et al., 2013), while 15d-PGJ2, another PPARγ agonist, promoted astrocyte-mediated neuroprotection independent of PPARγ (Giri et al., 2004; Haskew-Layton et al., 2013).
