Neuroinflammatory processes in Parkinson's disease.
Identifieur interne : 000F48 ( PubMed/Corpus ); précédent : 000F47; suivant : 000F49Neuroinflammatory processes in Parkinson's disease.
Auteurs : Etienne C. Hirsch ; Stéphane Hunot ; Andreas HartmannSource :
- Parkinsonism & related disorders [ 1353-8020 ] ; 2005.
English descriptors
- KwdEn :
- 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:15885630Le 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>
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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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<author><name sortKey="Hunot, Stephane" sort="Hunot, Stephane" uniqKey="Hunot S" first="Stéphane" last="Hunot">Stéphane Hunot</name>
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<term>Parkinson Disease (immunology)</term>
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<term>Neuroimmunomodulation</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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<Title>Parkinsonism & related disorders</Title>
<ISOAbbreviation>Parkinsonism Relat. Disord.</ISOAbbreviation>
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<ArticleTitle>Neuroinflammatory processes in Parkinson's disease.</ArticleTitle>
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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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