This discrepancy could be due to posttranscriptional changes in the control of gene expression at the RNA level, but more likely could be the result of differences in brain organisation between humans and mice, because the APP/PS1 model does not develop neurofibrillary tangles, other typical pathologic alterations observed in AD human patients, or because the stages of AD in the patients were more severe than the AD neuropathology suffered by mice at 12 months of age. Here, PSEN1 is linked to Alzheimer disease.