Finally, it should be noted that our data refer to the APPPS1 mice which co-express mutations of both APP and PS1 genes associated with the familial forms of AD and which promote overproduction of Aβ accelerating cerebral amyloidosis in these mice, but do not model the tau pathology and robust neurodegeneration observed in AD [5, 41]. This evidence concerns the gene PSEN1 and Alzheimer disease.