The role of anti-inflammatory agents in Parkinson's disease
Identifieur interne : 002627 ( Main/Exploration ); précédent : 002626; suivant : 002628The role of anti-inflammatory agents in Parkinson's disease
Auteurs : Edith G. Mcgeer [Canada] ; Patrick L. Mcgeer [Canada]Source :
- CNS drugs [ 1172-7047 ] ; 2007.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- MESH :
- chemical , therapeutic use : Anti-Inflammatory Agents.
- drug therapy : Parkinson Disease.
- immunology : Complement Activation, Parkinson Disease.
- Animals, Humans, Models, Immunological.
Abstract
There is ample and increasing evidence, from studies of human pathology, animal models and tissue culture, that chronic inflammation occurs in the basal ganglia in patients with Parkinson's disease. In such inflammatory states, activated glia can produce large quantities of free radicals and other neurotoxic materials. Dopaminergic neurons appear to be particularly vulnerable to these neurotoxins. The anti-inflammatory drugs that are presently in wide use act on peripheral players in the inflammatory process. Many experiments are under way to find agents that inhibit more potent contributors, such as the activated microglia or terminal complement proteins. Whether such drugs will slow the process of Parkinson's disease or reduce the high risk of dementia in such patients remains to be determined in future work.
Affiliations:
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Le document en format XML
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Mcgeer</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Kinsmen Laboratory of Neurological Research, University of British Columbia</s1><s2>Vancouver, British Columbia</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, British Columbia</wicri:noRegion></affiliation></author><author><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Kinsmen Laboratory of Neurological Research, University of British Columbia</s1><s2>Vancouver, British Columbia</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, British Columbia</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">CNS drugs</title><title level="j" type="abbreviated">CNS drugs</title><idno type="ISSN">1172-7047</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">CNS drugs</title><title level="j" type="abbreviated">CNS drugs</title><idno type="ISSN">1172-7047</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Anti-Inflammatory Agents (therapeutic use)</term><term>Antiinflammatory agent</term><term>Complement Activation (immunology)</term><term>Human</term><term>Humans</term><term>Inflammation</term><term>Models, Immunological</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (immunology)</term><term>Parkinson disease</term><term>Review</term><term>Treatment</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anti-Inflammatory Agents</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Complement Activation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Models, Immunological</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Antiinflammatoire</term><term>Article synthèse</term><term>Homme</term><term>Inflammation</term><term>Parkinson maladie</term><term>Article synthèse</term><term>Traitement</term><term>Homme</term><term>Inflammation</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is ample and increasing evidence, from studies of human pathology, animal models and tissue culture, that chronic inflammation occurs in the basal ganglia in patients with Parkinson's disease. In such inflammatory states, activated glia can produce large quantities of free radicals and other neurotoxic materials. Dopaminergic neurons appear to be particularly vulnerable to these neurotoxins. The anti-inflammatory drugs that are presently in wide use act on peripheral players in the inflammatory process. Many experiments are under way to find agents that inhibit more potent contributors, such as the activated microglia or terminal complement proteins. Whether such drugs will slow the process of Parkinson's disease or reduce the high risk of dementia in such patients remains to be determined in future work.</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Mcgeer, Edith G" sort="Mcgeer, Edith G" uniqKey="Mcgeer E" first="Edith G." last="Mcgeer">Edith G. Mcgeer</name></noRegion><name sortKey="Mcgeer, Patrick L" sort="Mcgeer, Patrick L" uniqKey="Mcgeer P" first="Patrick L." last="Mcgeer">Patrick L. Mcgeer</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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