Recent research has identified gene variants encoding ubiquilin1 (UBQLN1) [16] and sortilin1 (SORL1) [17] as risk factors, and GWAS approaches have identified a number of variants (CLU, PICALM and CRI) associated with AD [18], [19], which may also contribute to abnormal APP processing and Aβ accumulation. The gene discussed is APP; the disease is Alzheimer disease.