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J. Lipid Res.
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Originally published In Press as doi:10.1194/jlr.R800069-JLR200 on December 22, 2008

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Journal of Lipid Research, Vol. 50, S183-S188, April 2009
Copyright © 2009 by American Society for Biochemistry and Molecular Biology

Lipoprotein Metabolism

Apolipoprotein E: structure determines function, from atherosclerosis to Alzheimer's disease to AIDS

Robert W. Mahley1,*,{dagger},§,**,{dagger}{dagger}, Karl H. Weisgraber*,{dagger},**,{dagger}{dagger} and Yadong Huang*,{dagger},**

* Gladstone Institute of Neurological Disease, San Francisco, CA 94158
{dagger} Gladstone Institute of Cardiovascular Disease, San Francisco, CA 94158
§ Department of Medicine, University of California, San Francisco, CA 94143
** Department of Pathology, University of California, San Francisco, CA 94143
{dagger}{dagger} Cardiovascular Research Institute, University of California, San Francisco, CA 94143

This work was supported in part by grant R01 AG028793 and program project grant 2P01AG02207 from the National Institutes of Health.

Published, JLR Papers in Press, December 22, 2008.

1 To whom correspondence should be addressed. e-mail: rmahley{at}gladstone.ucsf.edu


ABSTRACT

Apolipoprotein (apo) E has roles beyond lipoprotein metabolism. The detrimental effects of apoE4 in cardiovascular, neurological, and infectious diseases correlate with its structural features (e.g., domain interaction) that distinguish it from apoE3 and apoE2. Structure/function studies revealed that apoE2 is severely defective in LDL receptor binding because of a structural difference that alters the receptor binding region and helped unravel the mechanism of type III hyperlipoproteinemia. ApoE4 is the major genetic risk factor for Alzheimer's disease and sets the stage for neuropathological disorders precipitated by genetic, metabolic, and environmental stressors. ApoE also influences susceptibility to parasitic, bacterial, and viral infections. In HIV-positive patients, apoE4 homozygosity hastens progression to AIDS and death and increases susceptibility to opportunistic infections. The next phase in our understanding of apoE will be characterized by clinical intervention to prevent or reverse the detrimental effects of apoE4 by modulating its structure or blocking the pathological processes it mediates.

Supplementary key words cholesterol • neurodegeneration • HIV • coronary heart disease • LDL receptor • dysbetalipoproteinemia • heparan sulfate proteoglycans • infectious diseases • evolution

Abbreviations: Aβ, amyloid β; AD, Alzheimer's disease; apo, apolipoprotein; HLP, hyperlipoproteinemia; HSPG, heparan sulfate proteoglycans; HSV, herpes simplex virus


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JLR 50th Anniversary Collections
Anniversary Collection::Lipoprotein Metabolism

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