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, pioglitazone prevented MPTP-induced glial cell activation and loss of dopaminergic neurons. Mechanistically, neuronal death was prevented by inhibiting activation of the proinflammatory transcription factor NF-κB by (i) increasing Iκ-Bα expression and (ii) inhibiting nuclear translocation of p65. Pioglitazone also decreased the number of GFAP and iNOS positive cells in both the striatum and substantia nigra pars compacta [62].
