Inflammation and neurodegeneration in Parkinson's disease.
Identifieur interne : 002B78 ( Main/Exploration ); précédent : 002B77; suivant : 002B79Inflammation and neurodegeneration in Parkinson's disease.
Auteurs : Patrick L. Mcgeer [Canada] ; Edith G. McgeerSource :
- Parkinsonism & related disorders [ 1353-8020 ] ; 2004.
English descriptors
- KwdEn :
- MESH :
- metabolism : Inflammation, Nerve Degeneration, Parkinson Disease.
- pathology : Inflammation, Nerve Degeneration, Parkinson Disease.
- Animals, Humans.
Abstract
The immunohistochemical demonstration of reactive microglia and activated complement components suggests that chronic inflammation occurs in affected brain regions in Parkinson's disease (PD). Evidence from humans and monkeys exposed to MPTP indicates this inflammation may persist many years after the initial stimulus has disappeared. Chronic inflammation can damage host cells. Reports in the literature indicate that antiinflammatory agents inhibit dopaminergic cell death in animal models of PD, and there is one epidemiological report that their use significantly diminishes the risk of PD in humans. There is a marked elevation in the mRNA levels for complement proteins and markers of activated microglia in affected regions in PD. The upregulation appears greater than that found in inflamed arthritic joints. These data support the hypothesis that chronic inflammation may play an important role, if secondary, in the pathogenesis of PD.
DOI: 10.1016/j.parkreldis.2004.01.005
PubMed: 15109580
Affiliations:
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Le document en format XML
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Mcgeer</name><affiliation wicri:level="1"><nlm:affiliation>Kinsmen Laboratory of Neurological Research and the Pacific Parkinson's Research Centre, University of British Columbia, 2255 Westbrook Mall, Vancouver, BC, Canada V6T 1Z3. mcgeer@interchange.ubc.ca</nlm:affiliation><country>Canada</country><wicri:regionArea>Kinsmen Laboratory of Neurological Research and the Pacific Parkinson's Research Centre, University of British Columbia, 2255 Westbrook Mall, Vancouver, BC</wicri:regionArea><wicri:noRegion>BC</wicri:noRegion></affiliation></author><author><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. Mcgeer</name></author></analytic><series><title level="j">Parkinsonism & related disorders</title><idno type="ISSN">1353-8020</idno><imprint><date when="2004" type="published">2004</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Humans</term><term>Inflammation (metabolism)</term><term>Inflammation (pathology)</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (pathology)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Inflammation</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The immunohistochemical demonstration of reactive microglia and activated complement components suggests that chronic inflammation occurs in affected brain regions in Parkinson's disease (PD). Evidence from humans and monkeys exposed to MPTP indicates this inflammation may persist many years after the initial stimulus has disappeared. Chronic inflammation can damage host cells. Reports in the literature indicate that antiinflammatory agents inhibit dopaminergic cell death in animal models of PD, and there is one epidemiological report that their use significantly diminishes the risk of PD in humans. There is a marked elevation in the mRNA levels for complement proteins and markers of activated microglia in affected regions in PD. The upregulation appears greater than that found in inflamed arthritic joints. These data support the hypothesis that chronic inflammation may play an important role, if secondary, in the pathogenesis of PD.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G" last="Mcgeer">Edith G. Mcgeer</name></noCountry><country name="Canada"><noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L" last="Mcgeer">Patrick L. Mcgeer</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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