Challenges to the development of disease‐modifying therapies in Parkinson’s disease
Identifieur interne : 000412 ( Main/Corpus ); précédent : 000411; suivant : 000413Challenges to the development of disease‐modifying therapies in Parkinson’s disease
Auteurs : A. H. V. SchapiraSource :
- European Journal of Neurology [ 1351-5101 ] ; 2011-03.
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Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder that involves the neurones of multiple transmitter pathways. The dopaminergic neuronal degeneration determines the main early clinical characteristics of the disease. There have been many recent valuable insights into the pathogenesis of PD, driven primarily by research of the genetic causes of the disease. These now provide a clearer view of the pathways that lead to neuronal dysfunction and death. Perhaps surprisingly, the same pathways initiated by gene mutations causing familial PD are those already identified to be involved in idiopathic sporadic PD, namely mitochondrial dysfunction, oxidative stress and protein misfolding and aggregation. Novel therapies designed to slow PD progression are likely to intervene in one or more of these pathways. Some candidates have been tested based upon this hypothesis, albeit with varying results. Significant developments in this area face several challenges including effective disease‐modelling systems and clinical trial designs that can enable a true positive result to be obtained in a relatively short period.
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DOI: 10.1111/j.1468-1331.2010.03324.x
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ISTEX:7726EEE24BD30E1DF19CBC016DE3A920C367D414Le document en format XML
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European Journal of Neurology © 2011 EFNS</copyright><eventGroup><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.4.4 mode:FullText" date="2011-01-24"></event><event type="firstOnline" date="2011-01-24"></event><event type="publishedOnlineFinalForm" date="2011-01-24"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-24"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-17"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="16">16</numbering><numbering type="pageLast" number="21">21</numbering></numberingGroup><correspondenceTo>Prof. A. 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.ENE3324.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 29 November 2010 Accepted 23 December 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="0"></count></countGroup><titleGroup><title type="main">Challenges to the development of disease‐modifying therapies in Parkinson’s disease</title><title type="shortAuthors">A. H. V. Schapira</title><title type="short">Development of disease‐modifying therapies 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>Department of Clinical Neurosciences, Institute of Neurology, University College London, London, UK</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">autophagy</keyword><keyword xml:id="k2">genes</keyword><keyword xml:id="k3">mitochondria</keyword><keyword xml:id="k4">neuroprotection</keyword><keyword xml:id="k5">Parkinson’s disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Parkinson’s disease (PD) is a progressive neurodegenerative disorder that involves the neurones of multiple transmitter pathways. The dopaminergic neuronal degeneration determines the main early clinical characteristics of the disease. There have been many recent valuable insights into the pathogenesis of PD, driven primarily by research of the genetic causes of the disease. These now provide a clearer view of the pathways that lead to neuronal dysfunction and death. Perhaps surprisingly, the same pathways initiated by gene mutations causing familial PD are those already identified to be involved in idiopathic sporadic PD, namely mitochondrial dysfunction, oxidative stress and protein misfolding and aggregation. Novel therapies designed to slow PD progression are likely to intervene in one or more of these pathways. Some candidates have been tested based upon this hypothesis, albeit with varying results. Significant developments in this area face several challenges including effective disease‐modelling systems and clinical trial designs that can enable a true positive result to be obtained in a relatively short period.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Challenges to the development of disease‐modifying therapies in Parkinson’s disease</title></titleInfo><titleInfo type="abbreviated"><title>Development of disease‐modifying therapies in Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Challenges to the development of disease‐modifying therapies in Parkinson’s disease</title></titleInfo><name type="personal"><namePart type="given">A. H. V.</namePart><namePart type="family">Schapira</namePart><affiliation>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="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2011-03</dateIssued><edition>Received 29 November 2010 Accepted 23 December 2010</edition><copyrightDate encoding="w3cdtf">2011</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">Parkinson’s disease (PD) is a progressive neurodegenerative disorder that involves the neurones of multiple transmitter pathways. The dopaminergic neuronal degeneration determines the main early clinical characteristics of the disease. There have been many recent valuable insights into the pathogenesis of PD, driven primarily by research of the genetic causes of the disease. These now provide a clearer view of the pathways that lead to neuronal dysfunction and death. Perhaps surprisingly, the same pathways initiated by gene mutations causing familial PD are those already identified to be involved in idiopathic sporadic PD, namely mitochondrial dysfunction, oxidative stress and protein misfolding and aggregation. Novel therapies designed to slow PD progression are likely to intervene in one or more of these pathways. Some candidates have been tested based upon this hypothesis, albeit with varying results. Significant developments in this area face several challenges including effective disease‐modelling systems and clinical trial designs that can enable a true positive result to be obtained in a relatively short period.</abstract><subject lang="en"><genre>Keywords</genre><topic>autophagy</topic><topic>genes</topic><topic>mitochondria</topic><topic>neuroprotection</topic><topic>Parkinson’s disease</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>2011</date><detail type="title"><title>The Management of Parkinson’s Disease – What is New?</title></detail><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="supplement"><caption>Suppl. no.</caption><number>s1</number></detail><extent unit="pages"><start>16</start><end>21</end><total>6</total></extent></part></relatedItem><identifier type="istex">7726EEE24BD30E1DF19CBC016DE3A920C367D414</identifier><identifier type="DOI">10.1111/j.1468-1331.2010.03324.x</identifier><identifier type="ArticleID">ENE3324</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2011 The Author(s). 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