The lack of Cys residues in apoE4 has been hypothesized to contribute to the increased risk of developing AD, since the lipid peroxidation product HNE would not be able to be scavenged (unlike the case for apoE2 and apoE3) and thereby bind to and modify the structure and function of mitochondrial proteins in AD and MCI [33]. This evidence concerns the gene APOE and Alzheimer disease.