The primary role of amyloid beta peptide (Aβ) in the aetiology of Alzheimer's disease (AD) is supported by a wealth of genetic and biochemical data (Hardy and Selkoe, 2002; Walsh et al., 2002): not only is familial AD known to be caused by mutations that favour aggregation-prone isoforms of Aβ (Goate et al., 1991; Levy-Lahad et al., 1995; Li et al., 1995; Rogaev et al., 1995; Sherrington et al., 1995; Suzuki et al., 1994) but also, conversely, disease risk is reduced by a mutation that slows peptide generation (Jonsson et al., 2012). Here, APP is linked to Alzheimer disease.