Thus, any anticipation that the ablation of endogenous Sst would by itself profoundly affect amyloid plaque formation in APPNL-F/NL-F mice needs to be tempered by the recognition that Aβ deposition in this model depends on Aβ1–42 production that far exceeds physiological Aβ production in human AD brains. Here, SST is linked to Alzheimer disease.