These discrepancies could be likely due to differences in brain organisation between humans and mice [45], to the fact that the APP/PS1 model does not develop neurofibrillary tangles, a typical pathologic alteration observed in AD patients [46], or simply because the age of 12 months old used here, as well as by other laboratories, is still too short to detect gross changes. This evidence concerns the gene PSEN1 and Alzheimer disease.