The animals express mutant human amyloid precursor protein (APPsw) and presenilin-1 (PS1ΔE9) genes and exhibit Aβ plaque formation, hyperphosphorylation and aggregation of intracellular tau proteins, neurophysiological and behavioral abnormalities and signs of neurodegeneration that reflect AD patients’ pathology [12,13]. This evidence concerns the gene PSEN1 and Alzheimer disease.