It is of a substantial interest that all known mutation(s) or factors that protect from AD have the same underlying mode of operation: they all reduce the rate of AβPP-derived iAβ accumulation and prevent (or delay) the crossing of the T1 threshold by AβPP-derived iAβ within individual’s lifespan, whereas, as described below, all known FAD-causing mutations increase the rate of AβPP-derived iAβ accumulation and accelerate the crossing of the T1 threshold. This evidence concerns the gene PSEN1 and Alzheimer disease.