Together these observations indicate that LRP can participate in AD pathogenesis by altering the catabolism of LRP ligands (e.g., IGF-I, ApoE/lipoprotein/cholesterol, tPA, and α2M) and/or influencing Aβ metabolism and accumulation (Carro et al., 2002, 2005, 2006). Here, APOE is linked to Alzheimer disease.