In Alzheimer’s disease (AD), diabetes-related oxidative stress in the brain promotes the accumulation of neurotoxic Aβ in synaptic mitochondria, inhibiting mitochondrial respiration and biogenesis, impairing mitochondrial electron transport chain function, and resulting in the overproduction of ROS, which, in turn, increases the processing of the amyloid-beta precursor protein (APP) for Aβ deposition [116]. This evidence concerns the gene APP and diabetes mellitus.