In our investigations of the mechanisms by which aneuploidy arises in Alzheimer’s disease, we discovered that Aβ-42, either added exogenously or produced endogenously due to APP overexpression or due to expression of familial Alzheimer’s disease-causing mutant forms of the APP or presenilin genes, directly induces mitotic spindle abnormalities, chromosome mis-segregation, and aneuploidy both in mouse and cell culture models of Alzheimer’s disease [27,28]. The gene discussed is APP; the disease is Alzheimer disease.