Finally, inhibiting DPP-4, the primary inhibitory regulator of GLP-1, may be neuroprotective through activation of AMP-activated protein kinase (AMPK) in double transgenic AD mice expressing a chimeric mouse/human APP and a mutant human presenilin 1.86 Like GLP-1, DPP-4 is already approved for clinical treatment of T2DM and may be another promising “anti-insulin resistance” treatment for PD and AD (Fig. 3a). This evidence concerns the gene GLP1R and Alzheimer disease.