Patients with AD (hereinafter ADs) have very complex brain metabolic alterations, including insulin and insulin growth factor 1 (IGF-1) resistances [2,3], reduced glucose transporters (Glut 1, Glut 3) [4], abnormal glycolysis pathway [5,6,7,8], oxidative stress [9,10,11,12] mitochondrial dysfunction [13,14] and altered mitochondrial enzyme activities [15,16,17,18,19,20], and disruption of Ca2+ homeostasis [21], all of which are factors leading to reduced brain glucose breakdown and utilization (Cerebral glucose hypometabolism: CGH), responsible for low energy generation (ATP). Here, INS is linked to Alzheimer disease.