that PPARδ agonists may be efficacious antioxidant agents to ameliorate oxidative stress associated with AD. Interestingly, the actions of L-160,043 were more pronounced than the PPARα agonist, GW7647, or partial PPARγ agonist, F-L-Leu [15]. It is important to note that the PPARδ agonist was administered the same day as STZ. Future studies should assess whether PPARδ activation at later stages of AD progression can also halt AD development.
