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 : 002B14 ( Main/Curation ); précédent : 002B13; suivant : 002B15Multiple 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.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Animals, Brain Chemistry (physiology), Cytokine, Cytokines (metabolism), Cytokines (physiology), Degeneration, Depression, Depressive Disorder (metabolism), Depressive Disorder (pathology), Depressive Disorder (physiopathology), Environment, Humans, Mechanism of action, Mental Disorders (metabolism), Mental Disorders (pathology), Mental Disorders (physiopathology), Microglia, Neurodegenerative Diseases (metabolism), Neurodegenerative Diseases (pathology), Neurodegenerative Diseases (physiopathology), Neurotoxin, Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson Disease (physiopathology), Parkinson disease, Pathogenesis, Review, Sensitization.
- MESH :
- chemical , metabolism : Cytokines.
- metabolism : Depressive Disorder, Mental Disorders, Neurodegenerative Diseases, Parkinson Disease.
- pathology : Depressive Disorder, Mental Disorders, Neurodegenerative Diseases, Parkinson Disease.
- physiology : Brain Chemistry, Cytokines.
- physiopathology : Depressive Disorder, Mental Disorders, Neurodegenerative Diseases, Parkinson Disease.
- Animals, Environment, Humans.
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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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>Animals</term><term>Brain Chemistry (physiology)</term><term>Cytokine</term><term>Cytokines (metabolism)</term><term>Cytokines (physiology)</term><term>Degeneration</term><term>Depression</term><term>Depressive Disorder (metabolism)</term><term>Depressive Disorder (pathology)</term><term>Depressive Disorder (physiopathology)</term><term>Environment</term><term>Humans</term><term>Mechanism of action</term><term>Mental Disorders (metabolism)</term><term>Mental Disorders (pathology)</term><term>Mental Disorders (physiopathology)</term><term>Microglia</term><term>Neurodegenerative Diseases (metabolism)</term><term>Neurodegenerative Diseases (pathology)</term><term>Neurodegenerative Diseases (physiopathology)</term><term>Neurotoxin</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Pathogenesis</term><term>Review</term><term>Sensitization</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Depressive Disorder</term><term>Mental Disorders</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Depressive Disorder</term><term>Mental Disorders</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Brain Chemistry</term><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Depressive Disorder</term><term>Mental Disorders</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Environment</term><term>Humans</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. 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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></INIST><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Multiple mechanisms of cytokine action in neurodegenerative and psychiatric states: neurochemical and molecular substrates.</title><author><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Neuroscience, Carleton University, Ottawa, Ontario, Canada. shayley@ccs.carleton.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Institute of Neuroscience, Carleton University, Ottawa, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15777246</idno><idno type="pmid">15777246</idno><idno type="wicri:Area/PubMed/Corpus">001297</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001297</idno><idno type="wicri:Area/PubMed/Curation">001297</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001297</idno><idno type="wicri:Area/PubMed/Checkpoint">001297</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001297</idno><idno type="wicri:Area/Ncbi/Merge">000516</idno><idno type="wicri:Area/Ncbi/Curation">000516</idno><idno type="wicri:Area/Ncbi/Checkpoint">000516</idno><idno type="wicri:doubleKey">1381-6128:2005:Hayley S:multiple:mechanisms:of</idno><idno type="wicri:Area/Main/Merge">002C88</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Multiple mechanisms of cytokine action in neurodegenerative and psychiatric states: neurochemical and molecular substrates.</title><author><name sortKey="Hayley, Shawn" sort="Hayley, Shawn" uniqKey="Hayley S" first="Shawn" last="Hayley">Shawn Hayley</name><affiliation wicri:level="1"><nlm:affiliation>Institute of Neuroscience, Carleton University, Ottawa, Ontario, Canada. shayley@ccs.carleton.ca</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Institute of Neuroscience, Carleton University, Ottawa, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Anisman, Hymie" sort="Anisman, Hymie" uniqKey="Anisman H" first="Hymie" last="Anisman">Hymie Anisman</name></author></analytic><series><title level="j">Current pharmaceutical design</title><idno type="ISSN">1381-6128</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brain Chemistry (physiology)</term><term>Cytokines (metabolism)</term><term>Cytokines (physiology)</term><term>Depressive Disorder (metabolism)</term><term>Depressive Disorder (pathology)</term><term>Depressive Disorder (physiopathology)</term><term>Environment</term><term>Humans</term><term>Mental Disorders (metabolism)</term><term>Mental Disorders (pathology)</term><term>Mental Disorders (physiopathology)</term><term>Neurodegenerative Diseases (metabolism)</term><term>Neurodegenerative Diseases (pathology)</term><term>Neurodegenerative Diseases (physiopathology)</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></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Depressive Disorder</term><term>Mental Disorders</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Depressive Disorder</term><term>Mental Disorders</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Brain Chemistry</term><term>Cytokines</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Depressive Disorder</term><term>Mental Disorders</term><term>Neurodegenerative Diseases</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Environment</term><term>Humans</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-alpha, 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></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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