APOE and Alzheimer disease: Despite minimal differences in the primary structures (i. e., mutations of R158C in ApoE2, and C112R in ApoE4 with respect to most common ApoE3 isoform (Table 1)), the three ApoE variants show extremely divergent physiological (i. e., lipid binding [3,4,6,7]) and pathological (i. e., onset of AD [39,40]) behavior.