Progress in neuroprotection in Parkinson’s disease
Identifieur interne : 000070 ( Main/Corpus ); précédent : 000069; suivant : 000071Progress in neuroprotection in Parkinson’s disease
Auteurs : A. H. V. SchapiraSource :
- European Journal of Neurology [ 1351-5101 ] ; 2008-04.
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Abstract
Slowing or aborting the progress of neurodegeneration in Parkinson’s disease (PD) remains the most important unmet need of this disorder. There are several recent developments in trial design and also in drugs under investigation for possible neuroprotective effect. Emphasis has been placed on clinical as opposed to imaging end‐points and these include change in a clinical rating scale, e.g. United Parkinson's disease Rating Scale (UPDRS), or time to additional therapy. The introduction of the delayed‐start, or wash‐in, trial design adds an additional dimension to drug evaluation for neuroprotection. Compounds that have been recently tested in clinical trial include the monoamine oxidase‐B inhibitor rasagiline, the anti‐apoptotic agents TCH346 and CEP1347, and the promitochondrial agent creatine. The dopamine agonists have been evaluated for a neuroprotective effect using imaging end‐points. Perhaps the most important and simplest concept for neuroprotection has been the theory that early dopaminergic support for the degenerating dopaminergic system per se provides significant long‐term clinical benefit for PD patients.
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DOI: 10.1111/j.1468-1331.2008.02055.x
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ISTEX:BB0EFA6AB8B6D39793D0E17620E44A128BBC9AC0Le document en format XML
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Schapira, University Department of Clinical Neurosciences, University College London, Rowland Hill Street, London NW3 2PF, UK (tel.: +44 20 7830 2012; fax: +44 20 7472 6829; e‐mail: <email>a.schapira@medsch.ucl.ac.uk</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE2055.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 29 November 2007 Accepted 10 December 2007</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Progress in neuroprotection in Parkinson’s disease</title><title type="shortAuthors">A. H. V. Schapira</title><title type="short">Progress in neuroprotection in Parkinson’s disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#aff-1-1"><personName><givenNames>A. H. V.</givenNames><familyName>Schapira</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="aff-1-1" countryCode="GB"><unparsedAffiliation>University Department of Clinical Neurosciences, Institute of Neurology, University College London, London, UK</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">apoptosis</keyword><keyword xml:id="k2">dopamine agonists</keyword><keyword xml:id="k3">monoamine oxidase inhibitors</keyword><keyword xml:id="k4">neuroprotection</keyword><keyword xml:id="k5">Parkinson’s disease</keyword><keyword xml:id="k6">propargylamines</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Slowing or aborting the progress of neurodegeneration in Parkinson’s disease (PD) remains the most important unmet need of this disorder. There are several recent developments in trial design and also in drugs under investigation for possible neuroprotective effect. Emphasis has been placed on clinical as opposed to imaging end‐points and these include change in a clinical rating scale, e.g. United Parkinson's disease Rating Scale (UPDRS), or time to additional therapy. The introduction of the delayed‐start, or wash‐in, trial design adds an additional dimension to drug evaluation for neuroprotection. Compounds that have been recently tested in clinical trial include the monoamine oxidase‐B inhibitor rasagiline, the anti‐apoptotic agents TCH346 and CEP1347, and the promitochondrial agent creatine. The dopamine agonists have been evaluated for a neuroprotective effect using imaging end‐points. Perhaps the most important and simplest concept for neuroprotection has been the theory that early dopaminergic support for the degenerating dopaminergic system <i>per se</i> provides significant long‐term clinical benefit for PD patients.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Progress in neuroprotection in Parkinson’s disease</title></titleInfo><titleInfo type="abbreviated"><title>Progress in neuroprotection in Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Progress in neuroprotection in Parkinson’s disease</title></titleInfo><name type="personal"><namePart type="given">A. H. V.</namePart><namePart type="family">Schapira</namePart><affiliation>University Department of Clinical Neurosciences, Institute of Neurology, University College London, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2008-04</dateIssued><edition>Received 29 November 2007 Accepted 10 December 2007</edition><copyrightDate encoding="w3cdtf">2008</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Slowing or aborting the progress of neurodegeneration in Parkinson’s disease (PD) remains the most important unmet need of this disorder. 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Perhaps the most important and simplest concept for neuroprotection has been the theory that early dopaminergic support for the degenerating dopaminergic system per se provides significant long‐term clinical benefit for PD patients.</abstract><subject lang="en"><genre>Keywords</genre><topic>apoptosis</topic><topic>dopamine agonists</topic><topic>monoamine oxidase inhibitors</topic><topic>neuroprotection</topic><topic>Parkinson’s disease</topic><topic>propargylamines</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2008</date><detail type="title"><title>The Scientific and Clinical Basis for Future Therapies in Parkinson’s Disease</title></detail><detail type="volume"><caption>vol.</caption><number>15</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s1</number></detail><extent unit="pages"><start>5</start><end>13</end><total>9</total></extent></part></relatedItem><identifier type="istex">BB0EFA6AB8B6D39793D0E17620E44A128BBC9AC0</identifier><identifier type="DOI">10.1111/j.1468-1331.2008.02055.x</identifier><identifier type="ArticleID">ENE2055</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2008 The Author</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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