APOE and Alzheimer disease: However, both Cys residues of ApoE4 could be replaced by arginine (Arg) residues, resulting in no 4-HNE binding to neuron proteins and leading to a cascade of events such as Aβ fibril deposition, Aβ oligomer production, neurofibril tangle formation, neuronal death, decreased synaptic plasticity associated with learning and memory, asymmetric lipid bilayer composition, loss of lipid homeostasis, and oxidative stress, which collectively increases the risk of AD [71, 72].