Importantly, when removing the neuroprotective nature of Aβ40 on Glu neurotransmission (by fixing the maximal effect δ at 0), the model generates outcomes that are incompatible with clinical observations such as the ADAS-Cog average values for MCI subjects, the differential sensitivity of Aβ– vs Aβ + MCI subjects to scopolamine and the impact of APOE on slopes of cognitive worsening in untreated AD patients. This evidence concerns the gene APOE and Alzheimer disease.