To recapitulate the pathogenesis of human AD, APP23 mouse model overexpresses human APP with the Swedish mutation under the murine Thy1 promoter [57], while deltaE9 mice express APP with the Swedish mutation controlled by mouse prion protein promoter elements together with mutant human PS1 lacking exon 9, which is associated with familial AD [29, 52]. The gene discussed is APP; the disease is Alzheimer disease.