A Review of the Effects of ApoE3 and the Principle of Treating Alzheimer’s Disease

Abstract

The onset of Alzheimer ’s disease is related to genetics, abnormal deposition of beta amyloid (Aβ), hyperphosphorylation of Tau protein, neuroinflammation, oxidative stress, neurotransmitter disorders, age and other factors. In recent years, the global population aging has intensified, and the prevalence of Alzheimer’s disease has continued to rise. It is estimated that the number of patients around the world will reach 78 million by 2030. This paper starts with the polymorphism of the genetic pathogenic gene of Alzheimer’s disease, apolipoprotein E (ApoE), breaks the previous research inertia that focused solely on the “pathogenic mechanism” of ApoE4, and discusses some pathogenic genes in Alzheimer’s disease by focusing on the specific blocking effect of ApoE3 R136S mutation on tau pathology. From molecular mechanisms, cellular models, and animal experiments to clinical translation, this paper demonstrates that the ApoE3 R136S mutation exerts a neuroprotective effect against AD through multiple pathways, including inhibiting tau propagation, regulating immune responses, and promoting tau degradation.