Overproduction and accumulation of Aβcaused a strong downregulation of the activity of this enzyme in thebrain during Alzheimer’s disease.43,44 In addition, coimmunoprecipitation studies showed the interactionbetween neprilysin and serine phosphatase, as well as treatment ofprimary cultures with serine-phosphatase inhibitors, significantlyreduced cell-surface neprilysin activity.45 Therefore, enhanced neprilysin activity and reduced Aβ accumulationby our SST-scFv8D3 could probably explain the observed upregulatedlevels of this enzyme. This evidence concerns the gene MME and early-onset autosomal dominant Alzheimer disease.