However, it is doubtful that treatment with PPAR-γ agonists should be the single or dominant form of insulin sensitizer therapy in AD because: 1) the brain expresses predominantly PPAR-δ followed by PPAR-γ, which have overlapping but non-identical functions [29]; and 2) the L165,041 PPAR-δ agonist was shown to be superior to F-L-Leu PPAR-γ agonist in rescuing neurodegeneration and deficits in spatial learning and memory in the i.c. STZ model of sporadic AD [28]. The gene discussed is PPARD; the disease is Alzheimer disease.