Neuroinflammation in the pathophysiology of Parkinson's disease: Evidence from animal models to human in vivo studies with [11C]‐PK11195 PET
Identifieur interne : 002D24 ( Main/Exploration ); précédent : 002D23; suivant : 002D25Neuroinflammation 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. Leenders [Pays-Bas]Source :
- Movement Disorders [ 0885-3185 ] ; 2007-10-15.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Animal model, Animals, Anti-Inflammatory Agents, Non-Steroidal (pharmacology), Brain (immunology), Brain (radionuclide imaging), COX‐2 inhibition, Cyclooxygenase 2 (blood), Cytokines (blood), Disease Models, Animal, Emission tomography, Human, Humans, Inflammation Mediators (blood), Isoquinolines (diagnostic use), Microglia, Microglia (immunology), Nerve Degeneration (immunology), Nerve Degeneration (radionuclide imaging), Nervous system diseases, Nitric Oxide Synthase Type II (blood), PK11195 PET, Parkinson disease, Parkinson's disease, Parkinsonian Disorders (immunology), Parkinsonian Disorders (radionuclide imaging), Pathophysiology, Positron, Positron emission tomography, Positron-Emission Tomography, Reactive Oxygen Species (immunology), microglia, neuroinflammation, neuroprotection.
- 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. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21552
Affiliations:
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Le document en format XML
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