Null mutations in Vps26 and Vps35 in mice accelerate the production of β-amyloid (Aβ), a cleaved product of the amyloid precursor protein (APP) associated with AD pathogenesis [12] by increasing the resident time of APP within a given membrane compartment and enhancing APP β-cleavage by beta-secretase [26]. This evidence concerns the gene APP and Alzheimer disease.