Since we could experimentally reduce the level of Aβ in the presence of the NH2-terminal domain of PS-1, we decided to exploit the potential therapeutic significance of these results: to inquire whether isolated small soluble peptides from within the NH2-terminal domain of PS-1 exhibited enough of the inhibitory activity of the whole domain, such that when added to model systems of AD, they effectively reduced Aβ production. The gene discussed is PSEN1; the disease is Alzheimer disease.