While Aβ exposure decreased LRP1 levels in endothelial cells in a dose-dependent manner (Deane et al., 2004), hypoxia or reactive oxygen species, conditions often detected in AD (Fanelli et al., 2013; Swerdlow et al., 2013), reduced LRP1 expression in vascular smooth muscle cells (Bell et al., 2009; Kanekiyo et al., 2012). This evidence concerns the gene LRP1 and Alzheimer disease.