INS and Alzheimer disease: Thus, it is not surprising that aberrant insulin signaling and brain glucose hypometabolism are considered as components of the pathogenesis of Alzheimer’s disease and progression of physiological aging: these metabolic phenomena trigger a cascade of pathological events, namely mitochondrial dysfunction, oxidative stress, excitotoxicity, apoptosis, and activation of pro-inflammatory cytokines [81,82,83,84] (Figure 1).