Neuroinflammatory processes in Parkinson's disease.
Identifieur interne : 001130 ( PubMed/Corpus ); précédent : 001129; suivant : 001131Neuroinflammatory processes in Parkinson's disease.
Auteurs : Stephane Hunot ; E C HirschSource :
- Annals of neurology [ 0364-5134 ] ; 2003.
English descriptors
- KwdEn :
- Antigens, CD (immunology), Cell Death, Corpus Striatum (enzymology), Corpus Striatum (immunology), Corpus Striatum (pathology), Cyclooxygenase 2, Cytokines (immunology), Dopamine (immunology), Dopamine (metabolism), Humans, Interleukins (immunology), Isoenzymes (metabolism), Major Histocompatibility Complex (immunology), Membrane Proteins, Mesencephalon (pathology), Nerve Degeneration (pathology), Neuroglia (immunology), Neuroglia (metabolism), Nitric Oxide Synthase (metabolism), Parkinson Disease (enzymology), Parkinson Disease (immunology), Parkinson Disease (pathology), Prostaglandin-Endoperoxide Synthases (metabolism).
- MESH :
- chemical , immunology : Antigens, CD, Cytokines, Dopamine, Interleukins.
- enzymology : Corpus Striatum, Parkinson Disease.
- immunology : Corpus Striatum, Major Histocompatibility Complex, Neuroglia, Parkinson Disease.
- chemical , metabolism : Dopamine, Isoenzymes, Neuroglia, Nitric Oxide Synthase, Prostaglandin-Endoperoxide Synthases.
- pathology : Corpus Striatum, Mesencephalon, Nerve Degeneration, Parkinson Disease.
- Cell Death, Cyclooxygenase 2, Humans, Membrane Proteins.
Abstract
Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory-associated factors such as cyclooxygenase-2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD.
DOI: 10.1002/ana.10481
PubMed: 12666098
Links to Exploration step
pubmed:12666098Le document en format XML
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<author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name>
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<term>Corpus Striatum (pathology)</term>
<term>Cyclooxygenase 2</term>
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<term>Isoenzymes (metabolism)</term>
<term>Major Histocompatibility Complex (immunology)</term>
<term>Membrane Proteins</term>
<term>Mesencephalon (pathology)</term>
<term>Nerve Degeneration (pathology)</term>
<term>Neuroglia (immunology)</term>
<term>Neuroglia (metabolism)</term>
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<term>Parkinson Disease (enzymology)</term>
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<term>Parkinson Disease (pathology)</term>
<term>Prostaglandin-Endoperoxide Synthases (metabolism)</term>
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<term>Mesencephalon</term>
<term>Nerve Degeneration</term>
<term>Parkinson Disease</term>
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory-associated factors such as cyclooxygenase-2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD.</div>
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<Abstract><AbstractText>Parkinson's disease (PD) is a movement disorder characterized by the progressive degeneration of dopaminergic neurons in the midbrain. To date, its cause remains unknown and the mechanism of nerve cell death uncertain. Apart from the massive loss of dopaminergic neurons, PD brains also show a conspicuous glial reaction together with signs of a neuroinflammatory reaction manifested by elevated cytokine levels and upregulation of inflammatory-associated factors such as cyclooxygenase-2 and inducible nitric oxide synthase. Mounting evidence also suggests a possible deleterious effect of these neuroinflammatory processes in experimental models of the disease. We propose that, in PD, neuroinflammation plays a role in the cascade of events leading to nerve cell death, thus propagating the neurodegenerative process. In this review, we summarize and discuss the latest findings regarding neuroinflammatory aspects in PD.</AbstractText>
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