Impairments in brain insulin and insulin-like growth factor (IGF) signaling are core abnormalities in the pathogenesis of Alzheimer’s disease (AD) such that the molecular and biochemical consequences closely resemble the effects of both Type 1 and Type 2 diabetes mellitus [1,2-5], including deficits glucose utilization [6-8]. This evidence concerns the gene INS and early-onset autosomal dominant Alzheimer disease.