As for AACD, its definition as the extended segment of the first AD stage, commencing with the crossing of the T0 threshold by AβPP-derived iAβ, provides the explanation for how the Icelandic mutation protects from aging-associated cognitive decline: in exactly the same manner that it renders protection from AD, namely by lowering the rate of AβPP-derived iAβ accumulation with the result that iAβ levels do not reach the T0 threshold within the lifetime of a mutation carrier (or reach it at a substantially later age than in wild-type AβPP carriers). The gene discussed is APP; the disease is Alzheimer disease.