Recently found signs of early neurodegeneration, cognitive decline, Aβ deposits, and increased tau phosphorylation in rats of the OXYS strain [11–14] along with the absence of specific for the early familial forms of AD mutations in App, Psen1, and Psen2 genes in the OXYS genome [12] lend themselves to be a faithful model of sporadic AD. The gene discussed is APP; the disease is Mental deterioration.