The potential mechanism by which hypercholesterolemia causes Aβ formation was revealed by Jaya Prasanthi et al. (2008) in which they found that the hypercholesterolemia-induced production of Aβ was correlated with an increased level of β-site APP cleaving enzyme 1 (BACE1) and receptor for advanced glycation end products (RAGE), as well as a decreased level of insulin degrading enzyme (IDE) and low density lipoprotein receptor-related protein 1 (LRP-1). Here, BACE1 is linked to familial hypercholesterolemia.