Copper pathology in vulnerable brain regions in Parkinson's disease.
Identifieur interne : 000585 ( PubMed/Corpus ); précédent : 000584; suivant : 000586Copper pathology in vulnerable brain regions in Parkinson's disease.
Auteurs : Katherine M. Davies ; Sylvain Bohic ; Asunci N Carmona ; Richard Ortega ; Veronica Cottam ; Dominic J. Hare ; John P M. Finberg ; Stefanie Reyes ; Glenda M. Halliday ; Julian F B. Mercer ; Kay L. DoubleSource :
- Neurobiology of aging [ 1558-1497 ] ; 2014.
English descriptors
- KwdEn :
- Cation Transport Proteins (metabolism), Copper (metabolism), Gyrus Cinguli (enzymology), Humans, Locus Coeruleus (cytology), Locus Coeruleus (metabolism), Molecular Targeted Therapy, Neurons (metabolism), Parkinson Disease (drug therapy), Parkinson Disease (genetics), Parkinson Disease (metabolism), Substantia Nigra (cytology), Substantia Nigra (metabolism), Superoxide Dismutase (metabolism), Superoxide Dismutase-1, alpha-Synuclein.
- MESH :
- chemical , metabolism : Cation Transport Proteins, Copper, Superoxide Dismutase.
- cytology : Locus Coeruleus, Substantia Nigra.
- drug therapy : Parkinson Disease.
- enzymology : Gyrus Cinguli.
- genetics : Parkinson Disease.
- metabolism : Locus Coeruleus, Neurons, Parkinson Disease, Substantia Nigra.
- Humans, Molecular Targeted Therapy, Superoxide Dismutase-1, alpha-Synuclein.
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.
DOI: 10.1016/j.neurobiolaging.2013.09.034
PubMed: 24176624
Links to Exploration step
pubmed:24176624Le document en format XML
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<term>Humans</term>
<term>Locus Coeruleus (cytology)</term>
<term>Locus Coeruleus (metabolism)</term>
<term>Molecular Targeted Therapy</term>
<term>Neurons (metabolism)</term>
<term>Parkinson Disease (drug therapy)</term>
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<front><div type="abstract" xml:lang="en">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.</div>
</front>
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<Abstract><AbstractText>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.</AbstractText>
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<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Davies</LastName>
<ForeName>Katherine M</ForeName>
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<AffiliationInfo><Affiliation>Inserm, U836, Team 6, Rayonnement Synchrotron et Recherche Médicales, Grenoble Institut des Neurosciences, Grenoble, France; European Synchrotron Radiation Facility, BP220, Grenoble, France; Université Joseph Fourier 1, Grenoble Institut des Neurosciences, Grenoble, France. Electronic address: bohic@esrf.fr.</Affiliation>
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