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Originally published In Press as doi:10.1074/jbc.C000165200 on May 8, 2000

J. Biol. Chem., Vol. 275, Issue 26, 19439-19442, June 30, 2000
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ACCELERATED PUBLICATION
Evidence that the beta -Amyloid Plaques of Alzheimer's Disease Represent the Redox-silencing and Entombment of Abeta by Zinc*

Math P. CuajungcoDagger §, Lee E. GoldsteinDagger , Akihiko Nunomura||**, Mark A. Smith||, James T. LimDagger , Craig S. AtwoodDagger ||, Xudong HuangDagger , Yasser W. FarragDagger , George Perry||, and Ashley I. BushDagger Dagger Dagger

From the Dagger  Laboratory for Oxidation Biology, Genetics and Aging Unit, Massachusetts General Hospital, Charlestown, Massachusetts 02129, the § Department of Psychiatry and Behavioral Science, University of Auckland School of Medicine, Auckland, New Zealand, the || Department of Pathology, Case Western Reserve University, Cleveland, Ohio 44106, and the ** Department of Psychiatry and Neurology, Asahikawa Medical College, Asahikawa 078-8510, Japan

Abeta binds Zn2+, Cu2+, and Fe3+ in vitro, and these metals are markedly elevated in the neocortex and especially enriched in amyloid plaque deposits of individuals with Alzheimer's disease (AD). Zn2+ precipitates Abeta in vitro, and Cu2+ interaction with Abeta promotes its neurotoxicity, correlating with metal reduction and the cell-free generation of H2O2 (Abeta 1-42 > Abeta 1-40 > ratAbeta 1-40). Because Zn2+ is redox-inert, we studied the possibility that it may play an inhibitory role in H2O2-mediated Abeta toxicity. In competition to the cytotoxic potentiation caused by coincubation with Cu2+, Zn2+ rescued primary cortical and human embryonic kidney 293 cells that were exposed to Abeta 1-42, correlating with the effect of Zn2+ in suppressing Cu2+-dependent H2O2 formation from Abeta 1-42. Since plaques contain exceptionally high concentrations of Zn2+, we examined the relationship between oxidation (8-OH guanosine) levels in AD-affected tissue and histological amyloid burden and found a significant negative correlation. These data suggest a protective role for Zn2+ in AD, where plaques form as the result of a more robust Zn2+ antioxidant response to the underlying oxidative attack.

* This work was supported by funds from the American Health Assistance Foundation, Prana Corp., Alzheimer's Association, by National Institute on Aging Grants R29-12686 and RO1-AG09287, and by the NH&MRC.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Recipient of the New Zealand Neurological Foundation Miller Postgraduate Scholarship.

Dagger Dagger To whom correspondence should be addressed: Director, Laboratory for Oxidation Biology, Massachusetts General Hospital, Bldg. 149, 13th St., Charlestown, MA 02129. Tel.: 617-726-8244; Fax: 617-724-9610; E-mail: bush@helix.mgh.harvard.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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