Oxidative protein damage in cells engaged in beta-amyloidosis is related to apoE genotype

Neuroreport
Bozena Mazur-KoleckaDennis Dickson

Abstract

The epsilon4 allele of apolipoprotein E (apoE) is a risk factor for Alzheimer's disease. The reduced antioxidant defense in epsilon4 carriers is suggested to contribute to beta-amyloidosis. We found that oxidative stress induced by treatment with Fe2+ ions raised more protein carbonyls in vascular smooth muscle cells isolated from human brains with apoE genotype epsilon4/epsilon4 than with 3epsilon/epsilon3 and epsilon3/epsilon4. Antioxidant vitamin E prevented formation of carbonyls but not in cells with genotype epsilon4/epsilon4. Treatment with Fe2+ ions induced cellular accumulation of amyloid-beta protein (Abeta)-immunoreactive material that co-localized with heme oxygenase, a marker of oxidative stress, and apoE. We hypothesize that the damage caused by oxidation in epsilon4/epsilon4 carriers facilitates development of beta-amyloidosis.

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Citations

Feb 28, 2004·Brain Research·Janusz FrackowiakBozena Mazur-Kolecka
Dec 25, 2002·Neurobiology of Aging·Bozena Mazur-KoleckaAdam Golabek
Mar 29, 2006·Proceedings of the National Academy of Sciences of the United States of America·Robert W MahleyYadong Huang
Feb 15, 2005·Neurobiology of Aging·Mark A SmithGeorge Perry
Aug 18, 2005·Neurobiology of Aging·B Mazur-KoleckaJ Frackowiak
Jul 5, 2005·Neurobiology of Aging·Bozena Mazur-KoleckaJanusz Frackowiak
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Feb 18, 2005·Journal of Neuropathology and Experimental Neurology·Janusz FrackowiakBozena Mazur-Kolecka
Apr 21, 2009·Ageing Research Reviews·Francesca MangialaschePatrizia Mecocci

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