occlusion model of stroke reduces infarct size and lowers cyclin D1, a protein involved in programmed cell death (Pei et al., 2010). Additionally, PPARγ activation can stabilize mitochondria and protect neurons against apoptotic cell death and oxidative stress by upregulating the anti-apoptotic protein bcl-2 (Fuenzalida et al., 2007). At least part of the neuroprotective effects of PPARγ involves synergistic signaling with neurotrophins. For instance, NGF (nerve growth factor)-induced neuronal differentiation is mediated through activation of PPARγ in a TrkA-dependent manner. Further, PPARγ activation increases NGF and BDNF levels after SCI (Fuenzalida et al., 2005; Meng et al., 2011). Together these studies suggest that activation of PPARs, and in particular PPARγ, may be neuroprotective and promote neuronal survival.
