The role of LDLR in AD pathology remains somewhat unclear because LDLR knockout appeared not to affect disease development in one AD model [107] whereas there was a significant increase in Aβ deposition in other APPADLdlr−/− mice [108], as confirmed [109], and, unlike APOE, elimination of LDLR appears to increase the severity of both AD and ATH in the relevant mouse models. Here, APOE is linked to Alzheimer disease.