APP and Alzheimer disease: The principal pathological hallmarks of brain in AD have been well described, i.e., extraneuronal deposits of fibrillar amyloid beta-peptide (Aβ) and dystrophic neurites (senile plaques, SP), intracellular accumulations of neurotoxic Aβ oligomers, intracellular deposits of hyperphosphorylated tau (neurofibrillary tangles, NFT), with tau being a key microtubule stabilizing protein, and synapse loss [2,3,4].