ABCA7 and Alzheimer disease: An independent study using the same Abca7 null (Abca7−/−) mouse line but crossed with the TgCRND8 AD mouse model revealed an increase in the area of dense plaques at 18 weeks of age that the authors concluded was likely to be a reflection of the increased production of Aβ in the TgCRND8-Abca7−/− mice [13].