APOE and Alzheimer disease: The finding of unexpectedly large proportions of C-terminal APOE in β-amyloid plaques of ε4/ε4 homozygous AD subjects leads to the hypothesis that the partially folded protein is highly sensitive to proteolysis [46,47,48,49,50] and this prevents APOE in helping Aβ clearance, favoring instead its deposition [81].