Since human apolipoprotein E4 (APOE4) [30] is the strongest genetic risk factor for sporadic AD, testing proceeded to the E4FAD AD mouse model that incorporates targeted replacement of mouse APOE with hAPOE4. Oxidative stress is a primary driving force in AD pathogenesis [31, 32], linked to the lipid peroxidation product 4-hydroxynonenal (HNE) that accumulates in the brains of late-stage and presymptomatic AD patients, and is linked to apoE4 negative function [33, 34]. Here, APOE is linked to Alzheimer disease.