期刊
NEUROBIOLOGY OF AGING
卷 35, 期 4, 页码 858-866出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2013.09.034
关键词
Copper; Copper transporter 1 (Ctr1); Human brain; Parkinson's disease; Substantia nigra; Superoxide dismutase 1 (SOD1)
资金
- National Health and Medical Research Council of Australia
- Schizophrenia Research Institute
- National Institute of Alcohol Abuse and Alcoholism (National Institutes of Health) [R24AA012725]
- Sydney Brain Bank
- Neuroscience Research Australia
- University of New South Wales
- Partenariats Hubert Curien (PHC)-FAST
- Australian Department of Innovation, Industry, Science and Research International Science Linkage FAST programs
- Parkinson's New South Wales
- Parkinson's Australia Capital Territory
- 36th District of Quota International
- AMP
- Australian Postgraduate Award
Synchrotron-based x-ray fluorescence microscopy, immunofluorescence, and Western blotting were used to investigate changes in copper (Cu) and Cu-associated pathways in the vulnerable substantia nigra (SN) and locus coeruleus (LC) and in nondegenerating brain regions in cases of Parkinson's disease (PD) and appropriate healthy and disease controls. In PD and incidental Lewy body disease, levels of Cu and Cu transporter protein 1, were significantly reduced in surviving neurons in the SN and LC. Specific activity of the cuproprotein superoxide dismutase 1 was unchanged in the SN in PD but was enhanced in the parkinsonian anterior cingulate cortex, a region with a-synuclein pathology, normal Cu, and limited cell loss. These data suggest that regions affected by a-synuclein pathology may display enhanced vulnerability and cell loss if Cu-dependent protective mechanisms are compromised. Additional investigation of copper pathology in PD may identify novel targets for the development of protective therapies for this disorder. (C) 2014 Elsevier Inc. All rights reserved.
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