Transgenic mice that express mutant human APP (e.g. double mutant K670N, M671L; V717F) develop senile plaques, but not neurofibrillary tangles or neuronal loss (Games et al., 1995; Hsiao et al., 1996; LaFerla and Green, 2012), and this was also the case when APP mutations were combined with PSEN1 mutations (Takeuchi et al., 2000), indicating that mice are not suitable to model AD. This evidence concerns the gene APP and Alzheimer disease.