The isolated role of Aβ in the pathogenesis of AD has been examined in vivo without inhibition of the complex cascade in the processing of APP tg mice carrying the construct of murine Aβ under control of the NF-L promoter showed significant pathological changes with intraneuronal expression of Aβ, widespread apoptosis and reactive gliosis finally leading to death. This evidence concerns the gene APP and Alzheimer disease.