ParkinsonFranceV1, PubMed, Corpus, bibRecord, 000F48

Neuroinflammatory processes in Parkinson's disease.

Identifieur interne : 000F48 ( PubMed/Corpus ); précédent : 000F47; suivant : 000F49

Neuroinflammatory processes in Parkinson's disease.

Auteurs : Etienne C. Hirsch ; Stéphane Hunot ; Andreas Hartmann

Source :

Parkinsonism & related disorders [ 1353-8020 ] ; 2005.

RBID : pubmed:15885630

English descriptors

KwdEn :
- Encephalitis (immunology), Encephalitis (pathology), Humans, Neuroimmunomodulation (immunology), Parkinson Disease (immunology), Parkinson Disease (pathology).
MESH :
- immunology : Encephalitis, Neuroimmunomodulation, Parkinson Disease.
- pathology : Encephalitis, Parkinson Disease.
- Humans.

Abstract

In Parkinson's disease (PD), post-mortem examination reveals a loss of dopaminergic (DA) neurons in the substantia nigra (SN) associated with a massive astrogliosis and the presence of activated microglial cells. Similarly, microglial activation has also been reported to be associated with the loss of DA neurons in animal models of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, annonacine and lipopolysaccharide (LPS). Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, raising the possibility that toxic substances released by glial cells could be involved in the propagation of neuronal degeneration. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in PD.

DOI: 10.1016/j.parkreldis.2004.10.013
PubMed: 15885630

Links to Exploration step

pubmed:15885630

Le document en format XML

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<author><name sortKey="Hirsch, Etienne C" sort="Hirsch, Etienne C" uniqKey="Hirsch E" first="Etienne C" last="Hirsch">Etienne C. Hirsch</name>
<affiliation><nlm:affiliation>INSERM U675, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, Paris, France. hirsch@ccr.jussieu.fr</nlm:affiliation>
</affiliation>
</author>
<author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name>
</author>
<author><name sortKey="Hartmann, Andreas" sort="Hartmann, Andreas" uniqKey="Hartmann A" first="Andreas" last="Hartmann">Andreas Hartmann</name>
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<author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name>
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<author><name sortKey="Hartmann, Andreas" sort="Hartmann, Andreas" uniqKey="Hartmann A" first="Andreas" last="Hartmann">Andreas Hartmann</name>
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<series><title level="j">Parkinsonism & related disorders</title>
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<term>Parkinson Disease (immunology)</term>
<term>Parkinson Disease (pathology)</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Encephalitis</term>
<term>Neuroimmunomodulation</term>
<term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Encephalitis</term>
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<front><div type="abstract" xml:lang="en">In Parkinson's disease (PD), post-mortem examination reveals a loss of dopaminergic (DA) neurons in the substantia nigra (SN) associated with a massive astrogliosis and the presence of activated microglial cells. Similarly, microglial activation has also been reported to be associated with the loss of DA neurons in animal models of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, annonacine and lipopolysaccharide (LPS). Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, raising the possibility that toxic substances released by glial cells could be involved in the propagation of neuronal degeneration. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in PD.</div>
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<JournalIssue CitedMedium="Print"><Volume>11 Suppl 1</Volume>
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<Month>Jun</Month>
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<Title>Parkinsonism & related disorders</Title>
<ISOAbbreviation>Parkinsonism Relat. Disord.</ISOAbbreviation>
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<ArticleTitle>Neuroinflammatory processes in Parkinson's disease.</ArticleTitle>
<Pagination><MedlinePgn>S9-S15</MedlinePgn>
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<Abstract><AbstractText>In Parkinson's disease (PD), post-mortem examination reveals a loss of dopaminergic (DA) neurons in the substantia nigra (SN) associated with a massive astrogliosis and the presence of activated microglial cells. Similarly, microglial activation has also been reported to be associated with the loss of DA neurons in animal models of PD induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, annonacine and lipopolysaccharide (LPS). Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, raising the possibility that toxic substances released by glial cells could be involved in the propagation of neuronal degeneration. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in PD.</AbstractText>
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<NumberOfReferences>78</NumberOfReferences>
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Neuroinflammatory processes in Parkinson's disease.

Neuroinflammatory processes in Parkinson's disease.

Source :

English descriptors

Abstract

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki