APP and Alzheimer disease: It follows that the “normal” kinetics of accumulation of iAβ in the healthy individual are not uniformly linear (as depicted in Panel A of Figure 24) but composed of the linear portions of AβPP-derived iAβ accumulation interspersed by dozens of micro-steps, each resulting from the transient unconventional activation (“microburst”) of the AβPP-independent C99/iAβ production pathway; as long as the levels of iAβ do not cross the T1 threshold, no AD occurs.