K670N- M671L)2576) [10] and the double transgenic APP Swedish PS1 dE9 mouse model, in which mice are expressing APP and PS1 mutations associated with early-onset AD forms, i.e. a chimeric mouse/human amyloid precursor protein (Mo/HuAPP695swe) and a mutant human presenilin 1 (PS1-dE9) both directed to CNS neurons under the prion protein promoter [11, 12]. This evidence concerns the gene APP and Alzheimer disease.