Neuroinflammation in the pathophysiology of Parkinson's disease: evidence from animal models to human in vivo studies with [11C]-PK11195 PET.
Identifieur interne : 001D52 ( Ncbi/Checkpoint ); précédent : 001D51; suivant : 001D53Neuroinflammation in the pathophysiology of Parkinson's disease: evidence from animal models to human in vivo studies with [11C]-PK11195 PET.
Auteurs : Anna L. Bartels [Pays-Bas] ; Klaus L. LeendersSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Animals, Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Brain (immunology), Brain (radionuclide imaging), Cyclooxygenase 2 (blood), Cytokines (blood), Disease Models, Animal, Humans, Inflammation Mediators (blood), Isoquinolines (diagnostic use), Microglia (immunology), Nerve Degeneration (immunology), Nerve Degeneration (radionuclide imaging), Nitric Oxide Synthase Type II (blood), Parkinsonian Disorders (immunology), Parkinsonian Disorders (radionuclide imaging), Positron-Emission Tomography, Reactive Oxygen Species (immunology).
- MESH :
- chemical , blood : Cyclooxygenase 2, Cytokines, Inflammation Mediators, Nitric Oxide Synthase Type II.
- chemical , diagnostic use : Isoquinolines.
- chemical , immunology : Reactive Oxygen Species.
- chemical , pharmacology : Anti-Inflammatory Agents, Non-Steroidal.
- immunology : Brain, Microglia, Nerve Degeneration, Parkinsonian Disorders.
- radionuclide imaging : Brain, Nerve Degeneration, Parkinsonian Disorders.
- Animals, Disease Models, Animal, Humans, Positron-Emission Tomography.
Abstract
Increasing evidence suggests that neuroinflammation is an active process in Parkinson's disease (PD) that contributes to ongoing neurodegeneration. PD brains and experimental PD models show elevated cytokine levels and up-regulation of inflammatory-associated factors as cyclo-oxygenase-2 and inducible nitric oxide oxidase. Antiinflammatory treatment reduced neuronal degeneration in experimental models. In this review, we summarize the place of neuroinflammation in the pathophysiology of PD. In vivo PET studies are discussed. These methods provide a means to monitor in vivo potential clinical relevance of antiinflammatory treatment strategies in PD.
DOI: 10.1002/mds.21552
PubMed: 17592621
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Neuroinflammation in the pathophysiology of Parkinson's disease: evidence from animal models to human in vivo studies with [11C]-PK11195 PET.</title><author><name sortKey="Bartels, Anna L" sort="Bartels, Anna L" uniqKey="Bartels A" first="Anna L" last="Bartels">Anna L. Bartels</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, University Medical Centre Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands. a.l.bartels@neuro.umcg.nl</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, University Medical Centre Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen</wicri:regionArea><wicri:noRegion>9700 RB Groningen</wicri:noRegion></affiliation></author><author><name sortKey="Leenders, Klaus L" sort="Leenders, Klaus L" uniqKey="Leenders K" first="Klaus L" last="Leenders">Klaus L. Leenders</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2007">2007</date><idno type="doi">10.1002/mds.21552</idno><idno type="RBID">pubmed:17592621</idno><idno type="pmid">17592621</idno><idno type="wicri:Area/PubMed/Corpus">002607</idno><idno type="wicri:Area/PubMed/Curation">002607</idno><idno type="wicri:Area/PubMed/Checkpoint">002696</idno><idno type="wicri:Area/Ncbi/Merge">001D52</idno><idno type="wicri:Area/Ncbi/Curation">001D52</idno><idno type="wicri:Area/Ncbi/Checkpoint">001D52</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Neuroinflammation in the pathophysiology of Parkinson's disease: evidence from animal models to human in vivo studies with [11C]-PK11195 PET.</title><author><name sortKey="Bartels, Anna L" sort="Bartels, Anna L" uniqKey="Bartels A" first="Anna L" last="Bartels">Anna L. Bartels</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, University Medical Centre Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands. a.l.bartels@neuro.umcg.nl</nlm:affiliation><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Department of Neurology, University Medical Centre Groningen, University of Groningen, Hanzeplein 1, 9700 RB Groningen</wicri:regionArea><wicri:noRegion>9700 RB Groningen</wicri:noRegion></affiliation></author><author><name sortKey="Leenders, Klaus L" sort="Leenders, Klaus L" uniqKey="Leenders K" first="Klaus L" last="Leenders">Klaus L. Leenders</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2007" type="published">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anti-Inflammatory Agents, Non-Steroidal (pharmacology)</term><term>Brain (immunology)</term><term>Brain (radionuclide imaging)</term><term>Cyclooxygenase 2 (blood)</term><term>Cytokines (blood)</term><term>Disease Models, Animal</term><term>Humans</term><term>Inflammation Mediators (blood)</term><term>Isoquinolines (diagnostic use)</term><term>Microglia (immunology)</term><term>Nerve Degeneration (immunology)</term><term>Nerve Degeneration (radionuclide imaging)</term><term>Nitric Oxide Synthase Type II (blood)</term><term>Parkinsonian Disorders (immunology)</term><term>Parkinsonian Disorders (radionuclide imaging)</term><term>Positron-Emission Tomography</term><term>Reactive Oxygen Species (immunology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Cyclooxygenase 2</term><term>Cytokines</term><term>Inflammation Mediators</term><term>Nitric Oxide Synthase Type II</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Isoquinolines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Reactive Oxygen Species</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents, Non-Steroidal</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brain</term><term>Microglia</term><term>Nerve Degeneration</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Brain</term><term>Nerve Degeneration</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Positron-Emission Tomography</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Increasing evidence suggests that neuroinflammation is an active process in Parkinson's disease (PD) that contributes to ongoing neurodegeneration. PD brains and experimental PD models show elevated cytokine levels and up-regulation of inflammatory-associated factors as cyclo-oxygenase-2 and inducible nitric oxide oxidase. Antiinflammatory treatment reduced neuronal degeneration in experimental models. In this review, we summarize the place of neuroinflammation in the pathophysiology of PD. In vivo PET studies are discussed. These methods provide a means to monitor in vivo potential clinical relevance of antiinflammatory treatment strategies in PD.</div></front></TEI><affiliations><list><country><li>Pays-Bas</li></country></list><tree><noCountry><name sortKey="Leenders, Klaus L" sort="Leenders, Klaus L" uniqKey="Leenders K" first="Klaus L" last="Leenders">Klaus L. Leenders</name></noCountry><country name="Pays-Bas"><noRegion><name sortKey="Bartels, Anna L" sort="Bartels, Anna L" uniqKey="Bartels A" first="Anna L" last="Bartels">Anna L. 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