Neuroinflammatory processes in Parkinson's disease
Identifieur interne : 003126 ( Main/Exploration ); précédent : 003125; suivant : 003127Neuroinflammatory processes in Parkinson's disease
Auteurs : Stephane Hunot [France] ; E. C. Hirsch [France]Source :
- Annals of Neurology [ 0364-5134 ] ; 2003.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Antigens, CD (immunology), Apoptosis, Cell Death, Corpus Striatum (enzymology), Corpus Striatum (immunology), Corpus Striatum (pathology), Cyclooxygenase 2, Cytokine, Cytokines (immunology), Dopamine (immunology), Dopamine (metabolism), Dopaminergic neuron, Human, Humans, Inflammation, Interleukins (immunology), Isoenzymes (metabolism), Major Histocompatibility Complex (immunology), Membrane Proteins, Mesencephalon (pathology), Nerve Degeneration (pathology), Neuroglia, Neuroglia (immunology), Neuroglia (metabolism), Nitric Oxide Synthase (metabolism), Nitric-oxide synthase, Parkinson Disease (enzymology), Parkinson Disease (immunology), Parkinson Disease (pathology), Parkinson disease, Pathogenesis, Pathophysiology, Prostaglandin-Endoperoxide Synthases (metabolism), Prostaglandin-endoperoxide synthase.
- 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. Ann Neurol 2003;53 (suppl 3):S49–S60
Url:
DOI: 10.1002/ana.10481
Affiliations:
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<term>Corpus Striatum (immunology)</term>
<term>Corpus Striatum (pathology)</term>
<term>Cyclooxygenase 2</term>
<term>Cytokine</term>
<term>Cytokines (immunology)</term>
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<term>Isoenzymes (metabolism)</term>
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<term>Membrane Proteins</term>
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<term>Nitric-oxide synthase</term>
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<term>Parkinson Disease (pathology)</term>
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<term>Prostaglandin-Endoperoxide Synthases</term>
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<term>Parkinson Disease</term>
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<term>Cyclooxygenase 2</term>
<term>Humans</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. Ann Neurol 2003;53 (suppl 3):S49–S60</div>
</front>
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