Indeed, defects in APP intracellular trafficking and processing leading to Aβ production in neurons, as well as defects in PrP metabolism, are likely the most common cause of AD and prion diseases, respectively; thus, understanding how APP and PrP are targeted to a selected destination inside the cells and identifying the molecular mechanisms controlling the Aβ /prions generation is a key for new therapies. This evidence concerns the gene PRNP and Alzheimer disease.