INS and Alzheimer disease: These early impediments in the neuronal insulin and glucose metabolism have been proposed to trigger a detrimental bioenergetic shift from glucose to alternative and less efficient energy substrates (reviewed in Neth and Craft, 2017) and have been suggested to precede any other pathological alteration, including even mitochondrial dysfunction, in AD patients (Zilberter and Zilberter, 2017; Holscher, 2019).