APOLIPOPROTEIN E TRONG CHUYỂN HÓA LIPID VÀ BỆNH ALZHEIMER

Abstract

Alzheimer's disease (AD) has an unclear etiology. The best known pathogenesis is the beta-amyloid pathway and the tau phosphorylation pathway. Dysregulation of lipid metabolism has emerged as a central feature of many neurodegenerative diseases, possibly as a mechanism for AD. Isoforms of a lipid transport protein, apolipoprotein E (APOE), have the potential to alter the risk and recovery of several neurodegenerative diseases, including late-onset Alzheimer's disease (LOAD). Allelic variants of the APOE gene alter cellular and tissue lipid metabolism in different cell types and systems. Aiming to understand the metabolic relevance of APOE, we examine the molecular changes in lipid metabolism resulting from different APOE isoforms. These changes in lipid metabolism may shed light on the pathogenic mechanisms and modulate the risk of developing and recovering from neurodegenerative diseases. Several methods for identifying genetic polymorphisms APOE are also discussed.