PPARδ agonists may exert therapeutic benefits in patients with Parkinson's disease (PD), a neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. Progression of PD has been attributed to reactive oxygen species (ROS) and oxidized dopamine, which are toxic to dopaminergic neurons [61]. This disease manifests itself in motor dysfunctions and tremors. The synthetic opiate 1-methyl-4-phenyl-1,2,3,6-tetrahydrodropyridine (MPTP) induces PD in drug-addicted individuals. In mice, administration of GW501516 or L-165041 48 h before the first injection of MPTP significantly ameliorated depletion of striatal dopamine and its metabolites. As mentioned above, these PPARδ agonists also protected human neuroblastoma cells, SH-SY5Y, from cell death induced by the dopaminergic neurotoxin MPP+. This protection was associated with a significant reduction of caspase-3 and may contribute to the neuroprotective efficacy of GW501516 and L-165041 in experimental models of PD [12]. The protective role of PPARδ in PD has not been adequately explored, and it is unclear if, similar to the PPARγ agonist pioglitazone, PPARδ agonists can modulate oxidative stress and inflammatory processes associated with PD. In particular, in a mouse model of PD,
