Likewise, the ratio of Aβ42:APP/Aβ plaque load was greater in DS compared to AD suggesting an accelerated production of Aβ42 or higher levels of Aβ N-terminal truncation that precludes recognition by the APP/Aβ 6E10 antibody (Kummer and Heneka, 2014; Thal et al., 2015) a major Aβ component in the cerebellum in DS (Lalowski et al., 1996). The gene discussed is APP; the disease is Alzheimer disease.