Journal article

Elevated labile Cu is associated with oxidative pathology in Alzheimer disease

SA James, I Volitakis, PA Adlard, JA Duce, CL Masters, RA Cherny, AI Bush

Free Radical Biology and Medicine | Published : 2012

Abstract

Oxidative stress is implicated in Alzheimer disease (AD) pathogenesis, for which evidence indicates that radical species are generated by the redox-active biometal Cu. The contribution of labile Cu to the oxidative stress observed in AD has not been evaluated. The Cu content of postmortem cortical tissue from nondemented elderly controls and AD cases was measured using inductively coupled plasma mass spectroscopy, and the proportion of labile Cu was assessed using the Cu-phenanthroline assay. Further, the capacity of the tissue to stabilize Cu 2+ was evaluated using immobilized metal-affinity chromatography, and the level of tissue oxidative damage was determined by the presence of thiobarbi..

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University of Melbourne Researchers

Grants

Funding Acknowledgements

We thank Fairlie Hinton and Dr. Catriona McLean for the provision of neuropathologically characterized human brain samples (through the NNTRC) and Monica Lind and Dr. Alan Rembach for useful discussions and assistance with laboratory studies. This work was supported by funds from the Australian Research Council and the National Health and Medical Research Council, Operational Infrastructure Support from the Victoria state government, the Alzheimer's Association, and the CSIRO OCE Postdoctoral Fellowship Program. A.I.B. is a paid consultant to Adeona Pharmaceuticals, a shareholder of Brighton Biotech, and has received speaker payments from Amgen. C.L.M., R.A.C., and A.I.B. are shareholders in and paid consultants to Prana Biotechnology Ltd.