AKT1 and Alzheimer disease: In the postmortem brains of both T2D and sporadic AD patients, central resistance to insulin was documented by attenuated insulin signaling, namely via a decreased phosphorylation of the insulin cascade kinases PDK1 (3-phosphoinositide-dependent protein kinase-1), Akt (protein kinase B, PKB), and GSK-3β (glycogen synthase kinase 3β), and this effect was more pronounced in patients with both T2D and AD [3].