Building on the role of aneuploidy in AD, Rao and Yamada and colleagues hypothesized that SGO1 heterozygous knockout mice may serve as a potential model of sporadic late-onset AD, and they indeed discovered some AD-related pathology as the mice aged, which was associated with prolonged mitosis and spindle checkpoint activation (Rao et al., 2018a; Rao et al., 2018b). This evidence concerns the gene SGO1 and Alzheimer disease.