The successive processing of APP by BACE1 and γ-secretase indeed leads to the production of Aβ peptides (a causative agent in the pathogenesis of Alzheimer's disease (AD)), and APP-intracellular domains (AICDs) which, following association with the adaptor protein Fe65 and nuclear translocation, are able to suppress the expression of the major Apolipoprotein ε (ApoE)/lipoprotein receptor LRP1 by binding directly to its promoter [11]. This evidence concerns the gene APOE and early-onset autosomal dominant Alzheimer disease.