Pathogenic role of glial cells in Parkinson's disease
Identifieur interne : 004007 ( Main/Exploration ); précédent : 004006; suivant : 004008Pathogenic role of glial cells in Parkinson's disease
Auteurs : Peter Teismann [États-Unis] ; Kim Tieu [États-Unis] ; Oren Cohen [États-Unis] ; Dong-Kug Choi [États-Unis] ; Du Chu Wu [États-Unis] ; Daniel Marks [États-Unis] ; Miquel Vila [États-Unis] ; Vernice Jackson-Lewis [États-Unis] ; Serge Przedborski [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2003-02.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects), Adrenergic Agents (adverse effects), Animals, Astrocytes (drug effects), Astrocytes (pathology), Dopamine Agents (adverse effects), Glial Cell Line-Derived Neurotrophic Factor, Glial cell, Human, IL‐1β, MPTP, Mice, Microglia (drug effects), Microglia (pathology), Nerve Growth Factors (administration & dosage), Nerve Growth Factors (pharmacology), Neuroprotective Agents (administration & dosage), Neuroprotective Agents (pharmacology), Oxidopamine (adverse effects), Parkinson disease, Parkinson's disease, Parkinsonian Disorders (chemically induced), Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Pathogenesis, Pathology, Reactive Oxygen Species (metabolism), Review, Substantia Nigra (drug effects), Substantia Nigra (metabolism), Substantia Nigra (pathology), astrocyte, gliosis, iNOS, microglia, neurodegeneration.
- MESH :
- chemical , administration & dosage : Nerve Growth Factors, Neuroprotective Agents.
- chemical , adverse effects : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Adrenergic Agents, Dopamine Agents, Oxidopamine.
- chemically induced : Parkinsonian Disorders.
- drug effects : Astrocytes, Microglia, Substantia Nigra.
- metabolism : Parkinsonian Disorders, Reactive Oxygen Species, Substantia Nigra.
- pathology : Astrocytes, Microglia, Parkinsonian Disorders, Substantia Nigra.
- chemical , pharmacology : Nerve Growth Factors, Neuroprotective Agents.
- Animals, Glial Cell Line-Derived Neurotrophic Factor, Mice.
Abstract
An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;19:119). Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). The loss of these neurons is associated with a glial response composed mainly of activated microglial cells and, to a lesser extent, of reactive astrocytes. This glial response may be the source of trophic factors and can protect against reactive oxygen species and glutamate. Alternatively, this glial response can also mediate a variety of deleterious events related to the production of pro‐oxidant reactive species, and pro‐inflammatory prostaglandin and cytokines. We discuss the potential protective and deleterious effects of glial cells in the SNpc of PD and examine how those factors may contribute to the pathogenesis of this disease. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10332
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2003-02">2003-02</date><biblScope unit="vol">18</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="121">121</biblScope><biblScope unit="page" to="129">129</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">DAA156CA42ADF35B3BD37D6F27F3D07C934D0495</idno><idno type="DOI">10.1002/mds.10332</idno><idno type="ArticleID">MDS10332</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (adverse effects)</term><term>Adrenergic Agents (adverse effects)</term><term>Animals</term><term>Astrocytes (drug effects)</term><term>Astrocytes (pathology)</term><term>Dopamine Agents (adverse effects)</term><term>Glial Cell Line-Derived Neurotrophic Factor</term><term>Glial cell</term><term>Human</term><term>IL‐1β</term><term>MPTP</term><term>Mice</term><term>Microglia (drug effects)</term><term>Microglia (pathology)</term><term>Nerve Growth Factors (administration & dosage)</term><term>Nerve Growth Factors (pharmacology)</term><term>Neuroprotective Agents (administration & dosage)</term><term>Neuroprotective Agents (pharmacology)</term><term>Oxidopamine (adverse effects)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Parkinsonian Disorders (chemically induced)</term><term>Parkinsonian Disorders (metabolism)</term><term>Parkinsonian Disorders (pathology)</term><term>Pathogenesis</term><term>Pathology</term><term>Reactive Oxygen Species (metabolism)</term><term>Review</term><term>Substantia Nigra (drug effects)</term><term>Substantia Nigra (metabolism)</term><term>Substantia Nigra (pathology)</term><term>astrocyte</term><term>gliosis</term><term>iNOS</term><term>microglia</term><term>neurodegeneration</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Nerve Growth Factors</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Adrenergic Agents</term><term>Dopamine Agents</term><term>Oxidopamine</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Astrocytes</term><term>Microglia</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinsonian Disorders</term><term>Reactive Oxygen Species</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Astrocytes</term><term>Microglia</term><term>Parkinsonian Disorders</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Nerve Growth Factors</term><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Glial Cell Line-Derived Neurotrophic Factor</term><term>Mice</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Anatomopathologie</term><term>Article synthèse</term><term>Cellule gliale</term><term>Homme</term><term>Parkinson maladie</term><term>Pathogénie</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">An erratum for this article appears in the January, 2004 issue of Movement Disorders (Mov Disord 2004;19:119). Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the progressive loss of the dopaminergic neurons in the substantia nigra pars compacta (SNpc). The loss of these neurons is associated with a glial response composed mainly of activated microglial cells and, to a lesser extent, of reactive astrocytes. This glial response may be the source of trophic factors and can protect against reactive oxygen species and glutamate. Alternatively, this glial response can also mediate a variety of deleterious events related to the production of pro‐oxidant reactive species, and pro‐inflammatory prostaglandin and cytokines. We discuss the potential protective and deleterious effects of glial cells in the SNpc of PD and examine how those factors may contribute to the pathogenesis of this disease. © 2002 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region><settlement><li>New York</li></settlement><orgName><li>Université Columbia</li></orgName></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Teismann, Peter" sort="Teismann, Peter" uniqKey="Teismann P" first="Peter" last="Teismann">Peter Teismann</name></region><name sortKey="Choi, Dong Ug" sort="Choi, Dong Ug" uniqKey="Choi D" first="Dong-Kug" last="Choi">Dong-Kug Choi</name><name sortKey="Cohen, Oren" sort="Cohen, Oren" uniqKey="Cohen O" first="Oren" last="Cohen">Oren Cohen</name><name sortKey="Jackson Ewis, Vernice" sort="Jackson Ewis, Vernice" uniqKey="Jackson Ewis V" first="Vernice" last="Jackson-Lewis">Vernice Jackson-Lewis</name><name sortKey="Marks, Daniel" sort="Marks, Daniel" uniqKey="Marks D" first="Daniel" last="Marks">Daniel Marks</name><name sortKey="Przedborski, Serge" sort="Przedborski, Serge" uniqKey="Przedborski S" first="Serge" last="Przedborski">Serge Przedborski</name><name sortKey="Przedborski, Serge" sort="Przedborski, Serge" uniqKey="Przedborski S" first="Serge" last="Przedborski">Serge Przedborski</name><name sortKey="Tieu, Kim" sort="Tieu, Kim" uniqKey="Tieu K" first="Kim" last="Tieu">Kim Tieu</name><name sortKey="Vila, Miquel" sort="Vila, Miquel" uniqKey="Vila M" first="Miquel" last="Vila">Miquel Vila</name><name sortKey="Wu, Du Chu" sort="Wu, Du Chu" uniqKey="Wu D" first="Du Chu" last="Wu">Du Chu Wu</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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