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Copper pathology in vulnerable brain regions in Parkinson’s disease

DOI: 10.1016/j.neurobiolaging.2013.09.034 DOI Help

Authors: Katherine M. Davies (Neuroscience Research Australia, Sydney, Australia) , Sylvain Bohic (Inserm, U836, Team 6, Rayonnement Synchrotron et Recherche Médicales, Grenoble Institut des Neurosciences, Grenoble, France) , Asunción Carmona (Centre National de la Recherche Scientifique, IN2P3, CENBG, UMR 5797, Gradignan, France) , Richard Ortega (CNRS) , Veronica Cottam (Neuroscience Research Australia, Sydney, Australia) , Dominic J. Hare (Elemental Bio-imaging Facility, University of Technology, Sydney, Australia) , John P.m. Finberg (Faculty of Medicine, Technion, Haifa, Israel) , Stefanie Reyes (Neuroscience Research Australia, Sydney, Australia) , Glenda M. Halliday (Neuroscience Research Australia, Sydney, Australia) , Julian F.b. Mercer (Centre for Cellular and Molecular Biology, Deakin University, Melbourne, Australia) , Kay L. Double (iscipline of Biomedical Science, School of Medical Sciences, Sydney Medical School, The University of Sydney, Australia)
Co-authored by industrial partner: No

Type: Journal Paper
Journal: Neurobiology Of Aging

State: Published (Approved)
Published: October 2013
Diamond Proposal Number(s): 7238

Abstract: 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 α-synuclein pathology, normal Cu, and limited cell loss. These data suggest that regions affected by α-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.

Journal Keywords: Copper; Copper Transporter 1 (Ctr1); Human Brain; Parkinson's Disease; Substantia Nigra; Superoxide Dismutase 1 (Sod1)

Subject Areas: Biology and Bio-materials, Medicine


Instruments: I18-Microfocus Spectroscopy

Other Facilities: ESRF

Added On: 07/10/2013 10:56

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