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Cu(II) Potentiation of Alzheimer Aβ Neurotoxicity
Journal article   Open access   Peer reviewed

Cu(II) Potentiation of Alzheimer Aβ Neurotoxicity

Xudong Huang, Math P. Cuajungco, Craig S. Atwood, Mariana A. Hartshorn, Joel D.A. Tyndall, Graeme R. Hanson, Karen C. Stokes, Michael Leopold, Gerd Multhaup, Lee E. Goldstein, …
The Journal of biological chemistry, v 274(52), pp 37111-37116
Dec 1999
DOI: https://doi.org/10.1074/jbc.274.52.37111
Featured in Collection :   UN Sustainable Development Goals @ Drexel
url
https://doi.org/10.1074/jbc.274.52.37111View
Published, Version of Record (VoR)CC BY V4.0,  Open

Abstract

Oxidative stress markers as well as high concentrations of copper are found in the vicinity of Aβ amyloid deposits in Alzheimer's disease. The neurotoxicity of Aβ in cell culture has been linked to H2O2generation by an unknown mechanism. We now report that Cu(II) markedly potentiates the neurotoxicity exhibited by Aβ in cell culture. The potentiation of toxicity is greatest for Aβ1–42 > Aβ1–40 ≫ mouse/rat Aβ1–40, corresponding to their relative capacities to reduce Cu(II) to Cu(I), form H2O2 in cell-free assays and to exhibit amyloid pathology. The copper complex of Aβ1–42 has a highly positive formal reduction potential (≈+500–550 mV versus Ag/AgCl) characteristic of strongly reducing cuproproteins. These findings suggest that certain redox active metal ions may be important in exacerbating and perhaps facilitating Aβ-mediated oxidative damage in Alzheimer's disease.

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Web of Science research areas
Biochemistry & Molecular Biology
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