The APPswe/PS1dE9 mouse model (APP/PS1), co-expressed Swedish, mutated human APP695 and human mutated presenilin 1 (PS1) in which exon 9 is deleted [17], exhibit AD-like pathological and behavioral changes, including accumulation of amyloid plaques in brain, degeneration of cholinergic system, and impaired exploratory behavior and spatial memory [18]. This evidence concerns the gene APP and Alzheimer disease.