APP and Alzheimer disease: In sharp contrast, the protective Icelandic mutation reduces the rate of accumulation of AβPP-derived iAβ, resulting in the delay or prevention of the threshold crossing, of the activation of the AβPP-independent iAβ generation pathway, and, consequently, of the commencement of symptomatic AD [4]; it also delays or prevents the crossing of the AACD-triggering threshold and thus protects from this condition as well [2,4].