Overproduction of Aβ may arise, for example, as a consequence of familial AD-causing mutations in the APP or presenilin genes or by an inflammation-induced increase in APP translation [44,45], whereas an increased conversion of the Aβ peptide to toxic oligomers is promoted by the catalytic activity of apolipoprotein-E, especially the apoE4 variant [46]. The gene discussed is APOE; the disease is Alzheimer disease.