It has been found that neuronal ApoE4 mediates the pathophysiology of AD may include: prevents lipid excretion; induces inflammation of microglia to damage neurons; participation in the occurrence of Tau pathology, etc.; and studies have confirmed that selective removal of ApoE4 from neurons significantly reduce Tau pathology, glial proliferation, neurodegeneration, neuronal hyperexcitability, and myelin deficiency (Koutsodendris et al., 2023). This evidence concerns the gene MAPT and Alzheimer disease.