This can be due to genetic factors [e.g., mutations in ApoE ε2 or ε4 allele, presenilin 1 (PS1), α1-antichymotrypsin (ACT), neprilysin, low-density lipoprotein-receptor related protein (LRP-1), angiotensin-converting enzyme (ACE)], as well as non-genetic factors (e.g., hypertension) where dysfunctional receptor system, RAGE/LPR1, causes reduced clearance of amyloid, leading to increase Aβ accumulation (Xiong et al., 2009; Carrano et al., 2011; Viggars et al., 2011; Hartz et al., 2012). This evidence concerns the gene ACE and Hypertension.