Copper pathology in vulnerable brain regions in Parkinson's disease.
DAVIES, Katherine
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
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Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
DAVIES, Katherine
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
REYES, Stefanie
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
HALLIDAY, Glenda
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
DOUBLE, Kay
Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
Discipline of Biomedical Sciences
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Neuroscience Research Australia [NeuRA]
School of Medical Sciences, Faculty of Medicine
Discipline of Biomedical Sciences
Langue
en
Article de revue
Ce document a été publié dans
Neurobiol Aging. 2014-04, vol. 35, n° 4, p. 858-66
Résumé en anglais
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 ...Lire la suite >
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.< Réduire
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