The interaction between ApoE and Aβ, particularly the influence of ApoE lipidation on this process, sheds light on how disruptions in lipid homeostasis may contribute to AD progression, with delipidated apoE4 particularly prone to accelerating fibril formation (Lin et al., 2018; Wildsmith et al., 2013; Sanan et al., 1994; Pillot et al., 1999). This evidence concerns the gene APOE and Alzheimer disease.