The role of glial reaction and inflammation in Parkinson's disease.
Identifieur interne : 001099 ( PubMed/Corpus ); précédent : 001098; suivant : 001100The role of glial reaction and inflammation in Parkinson's disease.
Auteurs : E C Hirsch ; T. Breidert ; E. Rousselet ; S. Hunot ; A. Hartmann ; P P MichelSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2003.
English descriptors
- KwdEn :
- Animals, Anti-Inflammatory Agents (therapeutic use), Cytokines (metabolism), Dopamine (metabolism), Humans, Inflammation (etiology), Nerve Degeneration (physiopathology), Neuroglia, Neurons (metabolism), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (physiopathology).
- MESH :
- chemical , metabolism : Cytokines, Dopamine.
- chemical , therapeutic use : Anti-Inflammatory Agents.
- etiology : Inflammation.
- metabolism : Neurons, Parkinson Disease.
- pathology : Parkinson Disease.
- physiopathology : Nerve Degeneration, Parkinson Disease.
- Animals, Humans, Neuroglia.
Abstract
The glial reaction is generally considered to be a consequence of neuronal death in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and Parkinson's disease. In Parkinson's disease, postmortem examination reveals a loss of dopaminergic neurons in the substantia nigra associated with a massive astrogliosis and the presence of activated microglial cells. Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, suggesting that toxic substances released by the glial cells may be involved in the propagation and perpetuation of neuronal degeneration. Glial cells can release deleterious compounds such as proinflammatory cytokines (TNF-alpha, Il-1beta, IFN-gamma), which may act by stimulating nitric oxide production in glial cells, or which may exert a more direct deleterious effect on dopaminergic neurons by activating receptors that contain intracytoplasmic death domains involved in apoptosis. In line with this possibility, an activation of proteases such as caspase-3 and caspase-8, which are known effectors of apoptosis, has been reported in Parkinson's disease. Yet, caspase inhibitors or invalidation of TNF-alpha receptors does not protect dopaminergic neurons against degeneration in experimental models of the disease, suggesting that manipulation of a single signaling pathway may not be sufficient to protect dopaminergic neurons. In contrast, the antiinflammatory drugs pioglitazone, a PPAR-gamma agonist, and the tetracycline derivative minocycline have been shown to reduce glial activation and protect the substantia nigra in an animal model of the disease. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in Parkinson's disease.
PubMed: 12846989
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Hartmann</name></author><author><name sortKey="Michel, P P" sort="Michel, P P" uniqKey="Michel P" first="P P" last="Michel">P P Michel</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2003">2003</date><idno type="RBID">pubmed:12846989</idno><idno type="pmid">12846989</idno><idno type="wicri:Area/PubMed/Corpus">001099</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001099</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">The role of glial reaction and inflammation in Parkinson's disease.</title><author><name sortKey="Hirsch, E C" sort="Hirsch, E C" uniqKey="Hirsch E" first="E C" last="Hirsch">E C Hirsch</name><affiliation><nlm:affiliation>INSERM U289, Experimental Neurology and Therapeutics, Hôpital de la Salpêtrière, 75651 Paris Cedex 13, France. hirsch@ccr.jussieu.fr</nlm:affiliation></affiliation></author><author><name sortKey="Breidert, T" sort="Breidert, T" uniqKey="Breidert T" first="T" last="Breidert">T. Breidert</name></author><author><name sortKey="Rousselet, E" sort="Rousselet, E" uniqKey="Rousselet E" first="E" last="Rousselet">E. Rousselet</name></author><author><name sortKey="Hunot, S" sort="Hunot, S" uniqKey="Hunot S" first="S" last="Hunot">S. Hunot</name></author><author><name sortKey="Hartmann, A" sort="Hartmann, A" uniqKey="Hartmann A" first="A" last="Hartmann">A. Hartmann</name></author><author><name sortKey="Michel, P P" sort="Michel, P P" uniqKey="Michel P" first="P P" last="Michel">P P Michel</name></author></analytic><series><title level="j">Annals of the New York Academy of Sciences</title><idno type="ISSN">0077-8923</idno><imprint><date when="2003" type="published">2003</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anti-Inflammatory Agents (therapeutic use)</term><term>Cytokines (metabolism)</term><term>Dopamine (metabolism)</term><term>Humans</term><term>Inflammation (etiology)</term><term>Nerve Degeneration (physiopathology)</term><term>Neuroglia</term><term>Neurons (metabolism)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Dopamine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Inflammation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Neuroglia</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The glial reaction is generally considered to be a consequence of neuronal death in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and Parkinson's disease. In Parkinson's disease, postmortem examination reveals a loss of dopaminergic neurons in the substantia nigra associated with a massive astrogliosis and the presence of activated microglial cells. Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, suggesting that toxic substances released by the glial cells may be involved in the propagation and perpetuation of neuronal degeneration. Glial cells can release deleterious compounds such as proinflammatory cytokines (TNF-alpha, Il-1beta, IFN-gamma), which may act by stimulating nitric oxide production in glial cells, or which may exert a more direct deleterious effect on dopaminergic neurons by activating receptors that contain intracytoplasmic death domains involved in apoptosis. In line with this possibility, an activation of proteases such as caspase-3 and caspase-8, which are known effectors of apoptosis, has been reported in Parkinson's disease. Yet, caspase inhibitors or invalidation of TNF-alpha receptors does not protect dopaminergic neurons against degeneration in experimental models of the disease, suggesting that manipulation of a single signaling pathway may not be sufficient to protect dopaminergic neurons. In contrast, the antiinflammatory drugs pioglitazone, a PPAR-gamma agonist, and the tetracycline derivative minocycline have been shown to reduce glial activation and protect the substantia nigra in an animal model of the disease. Inhibition of the glial reaction and the inflammatory processes may thus represent a therapeutic target to reduce neuronal degeneration in Parkinson's disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">12846989</PMID><DateCreated><Year>2003</Year><Month>07</Month><Day>08</Day></DateCreated><DateCompleted><Year>2003</Year><Month>08</Month><Day>04</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0077-8923</ISSN><JournalIssue CitedMedium="Print"><Volume>991</Volume><PubDate><Year>2003</Year><Month>Jun</Month></PubDate></JournalIssue><Title>Annals of the New York Academy of Sciences</Title><ISOAbbreviation>Ann. N. Y. Acad. Sci.</ISOAbbreviation></Journal><ArticleTitle>The role of glial reaction and inflammation in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>214-28</MedlinePgn></Pagination><Abstract><AbstractText>The glial reaction is generally considered to be a consequence of neuronal death in neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and Parkinson's disease. In Parkinson's disease, postmortem examination reveals a loss of dopaminergic neurons in the substantia nigra associated with a massive astrogliosis and the presence of activated microglial cells. Recent evidence suggests that the disease may progress even when the initial cause of neuronal degeneration has disappeared, suggesting that toxic substances released by the glial cells may be involved in the propagation and perpetuation of neuronal degeneration. Glial cells can release deleterious compounds such as proinflammatory cytokines (TNF-alpha, Il-1beta, IFN-gamma), which may act by stimulating nitric oxide production in glial cells, or which may exert a more direct deleterious effect on dopaminergic neurons by activating receptors that contain intracytoplasmic death domains involved in apoptosis. In line with this possibility, an activation of proteases such as caspase-3 and caspase-8, which are known effectors of apoptosis, has been reported in Parkinson's disease. Yet, caspase inhibitors or invalidation of TNF-alpha receptors does not protect dopaminergic neurons against degeneration in experimental models of the disease, suggesting that manipulation of a single signaling pathway may not be sufficient to protect dopaminergic neurons. In contrast, the antiinflammatory drugs pioglitazone, a PPAR-gamma agonist, and the tetracycline derivative minocycline have been shown to reduce glial activation and protect the substantia nigra in an animal model of the disease. 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