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Role of ApoE in conformation-prone diseases and atherosclerosis

A D Dergunov1

  • 1National Research Center for Preventive Medicine, Moscow, 101990, Russia. dergunov@img.ras.ru

Biochemistry. Biokhimiia
|August 15, 2006
PubMed

Insights

Apolipoprotein E (apoE) isoforms influence Alzheimer's disease (AD) and atherosclerosis. ApoE4 is linked to higher AD risk, and its interaction with beta-amyloid (Abeta) aggregates is a key factor in AD development.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Cardiovascular Science

Background:

  • Three human plasma apolipoprotein E (apoE) isoforms act as ligands for lipoprotein receptors, differentially affecting pro-atherogenic lipoprotein metabolism.
  • The apoE4 isoform is specifically associated with increased risks of atherosclerosis and Alzheimer's disease (AD).
  • Conformational changes in beta-amyloid (Abeta) peptides, modulated by apoE and serum amyloid P (SAP), are critical in AD pathogenesis, particularly the accumulation of soluble Abeta oligomers.

Purpose of the Study:

  • To explore the role of apoE isoforms as pathological chaperones in Abeta aggregation and AD development.
  • To investigate the structural variations among apoE isoforms and their impact on lipoprotein distribution.
  • To identify molecular targets for AD intervention based on apoE pathways.

Main Methods:

  • The study involves analyzing the structural properties and self-association of apoE isoforms in solution.
  • Investigating the differential interactions of apoE isoforms with Abeta and SAP.
  • Considering the metabolic pathways involving apoE in relation to AD and atherosclerosis.

Main Results:

  • ApoE isoforms act as "pathological" chaperones, influencing Abeta aggregation differently.
  • Distinct self-associated structures exist for each apoE isoform, affecting their distribution in plasma lipoproteins.
  • The apoE pathway presents four potential molecular targets for AD therapeutic strategies.

Conclusions:

  • Structural variations in apoE isoforms contribute to their differential roles in AD and atherosclerosis.
  • Targeting apoE-Abeta interactions and apoE metabolism offers potential therapeutic avenues for AD.
  • Strategies include inhibiting Abeta oligomer formation, apoE synthesis, apoE-Abeta binding, and enhancing ABCA1 expression.

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