This is thought to increase the levels of β-amyloid (Aβ), a cleavage product of APP that aggregates upon misfolding, accumulates in plaques in the brains of people with Alzheimer disease (AD) and DS (Braak and Braak, 1994), and in turn is assumed to underlie the development of early-onset, highly penetrant, AD-like pathology in individuals with DS (Decourt et al., 2013). The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.