Brain insulin/IGF resistance and the reduction in glucose consumption found in AD patients have been reported to have a broad range of molecular implications among which are the disruption of signaling pathways that regulate neuronal survival, impairments in energy production, reduced neuronal plasticity, increased activity of kinases that aberrantly phosphorylate tau, together with mitochondria dysfunctions and generation of ROS [71]. This evidence concerns the gene IGF1 and Alzheimer disease.