One of the reasons for the excessive buildup of the AβOs-forming Aβ42 is the loss, early in the spread of AD pathology, of the production of the neprilysin-promoting SST (somatostatin) by SST-producing cells in the dentate gyral hilus and the hippocampal CA1-CA3 fields [75,76] (Figure 3). This evidence concerns the gene SST and Alzheimer disease.