Two observations support significant commonalities between these two forms of disease, suggesting that factors important for early-onset and familial cases will also be important for late-onset and sporadic AD: first, the APOE Ɛ4 allele not only modulates the AAO of AD in a sporadic setting, but also in carriers of presenilin mutations, and second, the identification of the protective effect of APP p.A673T in the Icelandic population showed that amyloid β has crucial roles in both early- and late-onset AD [10]. The gene discussed is APOE; the disease is Alzheimer disease.