Multiple mechanisms of cytokine action in neurodegenerative and psychiatric states: Neurochemical and molecular substrates : The role of cytokines in neurodegeneration and psychiatric conditions: Multiple mechanisms of action
Identifieur interne : 002E50 ( Main/Merge ); précédent : 002E49; suivant : 002E51Multiple mechanisms of cytokine action in neurodegenerative and psychiatric states: Neurochemical and molecular substrates : The role of cytokines in neurodegeneration and psychiatric conditions: Multiple mechanisms of action
Auteurs : Shawn Hayley [Canada] ; Hymie Anisman [Canada]Source :
- Current pharmaceutical design [ 1381-6128 ] ; 2005.
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- Pascal (Inist)
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Abstract
Neuroinflammatory processes appear to play a fundamental role in the pathology associated with a number of neurodegenerative and psychiatric conditions. In this respect, the immunocompetent brain microglia and peripheral macrophages release a host of proinflammatory cytokines that not only modulate immunological processes but also influence neuronal functioning and even survival. For instance, alterations of the cytokines, tumor necrosis factor-a, as well as several of the interferons and interleukins have been associated with Parkinson's disease (PD) and clinical depression. Importantly, anti-inflammatory treatments that block these cytokines may impart protection against behavioural pathology and neuronal damage in animal models of PD and depression involving exposure to environmental toxins and stressors, respectively. The present review highlights the involvement of inflammatory cells and cytokines in depression and PD and explores some of the potential cellular and molecular mechanisms through which the immunotransmitters affect neuronal functioning. Attention is also devoted to the possibility that cytokines may sensitize neuroinflammatory pathways that, in turn, favour long-term pathology.
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Pascal:05-0396238Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en" level="a">Multiple mechanisms of cytokine action in neurodegenerative and psychiatric states: Neurochemical and molecular substrates : The role of cytokines in neurodegeneration and psychiatric conditions: Multiple mechanisms of action</title><author><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Institute of Neuroscience, Carleton University</s1><s2>Ottawa, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Ottawa, Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Institute of Neuroscience, Carleton University</s1><s2>Ottawa, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Ottawa, Ontario</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">05-0396238</idno><date when="2005">2005</date><idno type="stanalyst">PASCAL 05-0396238 INIST</idno><idno type="RBID">Pascal:05-0396238</idno><idno type="wicri:Area/PascalFrancis/Corpus">000891</idno><idno type="wicri:Area/PascalFrancis/Curation">000432</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000782</idno><idno type="wicri:explorRef" wicri:stream="PascalFrancis" wicri:step="Checkpoint">000782</idno><idno type="wicri:doubleKey">1381-6128:2005:Hayley S:multiple:mechanisms:of</idno><idno type="wicri:Area/Main/Merge">002E50</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Multiple mechanisms of cytokine action in neurodegenerative and psychiatric states: Neurochemical and molecular substrates : The role of cytokines in neurodegeneration and psychiatric conditions: Multiple mechanisms of action</title><author><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Institute of Neuroscience, Carleton University</s1><s2>Ottawa, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Ottawa, Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Institute of Neuroscience, Carleton University</s1><s2>Ottawa, Ontario</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Ottawa, Ontario</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Current pharmaceutical design</title><title level="j" type="abbreviated">Curr. pharm. des.</title><idno type="ISSN">1381-6128</idno><imprint><date when="2005">2005</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Current pharmaceutical design</title><title level="j" type="abbreviated">Curr. pharm. des.</title><idno type="ISSN">1381-6128</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cytokine</term><term>Degeneration</term><term>Depression</term><term>Mechanism of action</term><term>Microglia</term><term>Neurotoxin</term><term>Parkinson disease</term><term>Pathogenesis</term><term>Review</term><term>Sensitization</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Mécanisme action</term><term>Cytokine</term><term>Sensibilisation</term><term>Etat dépressif</term><term>Parkinson maladie</term><term>Dégénérescence</term><term>Microglie</term><term>Neurotoxine</term><term>Article synthèse</term><term>Pathogénie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neuroinflammatory processes appear to play a fundamental role in the pathology associated with a number of neurodegenerative and psychiatric conditions. In this respect, the immunocompetent brain microglia and peripheral macrophages release a host of proinflammatory cytokines that not only modulate immunological processes but also influence neuronal functioning and even survival. For instance, alterations of the cytokines, tumor necrosis factor-a, as well as several of the interferons and interleukins have been associated with Parkinson's disease (PD) and clinical depression. Importantly, anti-inflammatory treatments that block these cytokines may impart protection against behavioural pathology and neuronal damage in animal models of PD and depression involving exposure to environmental toxins and stressors, respectively. The present review highlights the involvement of inflammatory cells and cytokines in depression and PD and explores some of the potential cellular and molecular mechanisms through which the immunotransmitters affect neuronal functioning. Attention is also devoted to the possibility that cytokines may sensitize neuroinflammatory pathways that, in turn, favour long-term pathology.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name></noRegion><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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