Perspectives on recent advances in the understanding and treatment of Parkinson’s disease
Identifieur interne : 000200 ( Main/Corpus ); précédent : 000199; suivant : 000201Perspectives on recent advances in the understanding and treatment of Parkinson’s disease
Auteurs : A. H. Schapira ; Y. Agid ; P. Barone ; P. Jenner ; M. R. Lemke ; W. Poewe ; O. Rascol ; H. Reichmann ; E. TolosaSource :
- European Journal of Neurology [ 1351-5101 ] ; 2009-10.
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- KwdEn :
Abstract
There have been numerous important recent advances in our understanding of the causes of Parkinson’s disease (PD), the treatments available and how these are best applied for the long‐term management of patients. Novel genes causing familial PD have been discovered and mechanisms leading to cell dysfunction and death identified. The PD prodrome is now a subject of great interest and clinical markers are being defined that may in future, together with biochemical markers, support an early, pre‐motor diagnosis of PD. This will become important as new therapies are developed to modify disease progression. In the interim, the optimization of existing therapies remains an important priority. The value of existing and novel continuous drug delivery systems in PD is seen as providing simplified regimens, maintenance of motor control, reduction in motor complications and improved patient adherence to drug use.
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DOI: 10.1111/j.1468-1331.2009.02793.x
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ISTEX:D88BCA9904F670DD3121DAAB11B4163D17FFBE3ELe document en format XML
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Novel genes causing familial PD have been discovered and mechanisms leading to cell dysfunction and death identified. The PD prodrome is now a subject of great interest and clinical markers are being defined that may in future, together with biochemical markers, support an early, pre‐motor diagnosis of PD. This will become important as new therapies are developed to modify disease progression. In the interim, the optimization of existing therapies remains an important priority. 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Journal compilation © 2009 EFNS</copyright><eventGroup><event type="firstOnline" date="2009-08-30"></event><event type="publishedOnlineFinalForm" date="2009-09-14"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-06"></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="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1090">1090</numbering><numbering type="pageLast" number="1099">1099</numbering></numberingGroup><correspondenceTo>A. Schapira, Department of Clinical Neurosciences, Institute of Neurology, UCL, Rowland Hill Street, London NW3 2PF, UK (tel.: 020 7830 2012; fax: 020 7472 6829; e‐mail: <email>a.schapira@medsch.ucl.ac.uk</email>).</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ENE.ENE2793.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 23 June 2009 Accepted 29 July 2009</unparsedEditorialHistory><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="3"></count></countGroup><titleGroup><title type="main">Perspectives on recent advances in the understanding and treatment of Parkinson’s disease</title><title type="shortAuthors">A. H. Schapira <i>et al.</i></title><title type="short">Perspectives in Parkinson’s disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>A. H.</givenNames><familyName>Schapira</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>Y.</givenNames><familyName>Agid</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a3"><personName><givenNames>P.</givenNames><familyName>Barone</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a4"><personName><givenNames>P.</givenNames><familyName>Jenner</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a5"><personName><givenNames>M. R.</givenNames><familyName>Lemke</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a6"><personName><givenNames>W.</givenNames><familyName>Poewe</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a7"><personName><givenNames>O.</givenNames><familyName>Rascol</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a8"><personName><givenNames>H.</givenNames><familyName>Reichmann</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a9"><personName><givenNames>E.</givenNames><familyName>Tolosa</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Clinical Neurosciences, Institute of Neurology, University College London, Queen Square, London</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="FR"><unparsedAffiliation>Institute of the Brain and Spine, INSERM, Pierre et Marie Curie University, Assistance Publique‐Hôpitaux de Paris, Paris, France</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="IT"><unparsedAffiliation>Department of Neurological Sciences, University of Naples, Napoli, Italy</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="GB"><unparsedAffiliation>Neurodegenerative Diseases Research Group, School of Biomedical and Health Sciences, King’s College London, London, UK</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="DE"><unparsedAffiliation>Department of Psychiatry, University of Kiel, Kliniken Alsterdorf, Hamburg, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a6" countryCode="AT"><unparsedAffiliation>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</unparsedAffiliation></affiliation><affiliation xml:id="a7" countryCode="FR"><unparsedAffiliation>Departments of Clinical Pharmacology and Neurosciences, INSERM CIC‐9302 and UMR‐825, Toulouse University Hospital, Toulouse, France</unparsedAffiliation></affiliation><affiliation xml:id="a8" countryCode="DE"><unparsedAffiliation>Universitätsklinikum Carl Gustav Carus, an der Technischen Universität Dresden, Dresden, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a9" countryCode="ES"><unparsedAffiliation>Neurology Service, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, IDIBAPS, Universitat de Barcelona, Spain</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">autophagy</keyword><keyword xml:id="k2">depression</keyword><keyword xml:id="k3">dopamine agonist</keyword><keyword xml:id="k4">levodopa</keyword><keyword xml:id="k5">mitochondrial</keyword><keyword xml:id="k6">neuroprotection</keyword><keyword xml:id="k7">non‐motor</keyword><keyword xml:id="k8">Parkinson’s disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>There have been numerous important recent advances in our understanding of the causes of Parkinson’s disease (PD), the treatments available and how these are best applied for the long‐term management of patients. Novel genes causing familial PD have been discovered and mechanisms leading to cell dysfunction and death identified. The PD prodrome is now a subject of great interest and clinical markers are being defined that may in future, together with biochemical markers, support an early, pre‐motor diagnosis of PD. This will become important as new therapies are developed to modify disease progression. In the interim, the optimization of existing therapies remains an important priority. The value of existing and novel continuous drug delivery systems in PD is seen as providing simplified regimens, maintenance of motor control, reduction in motor complications and improved patient adherence to drug use.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Perspectives on recent advances in the understanding and treatment of Parkinson’s disease</title></titleInfo><titleInfo type="abbreviated"><title>Perspectives in Parkinson’s disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Perspectives on recent advances in the understanding and treatment of Parkinson’s disease</title></titleInfo><name type="personal"><namePart type="given">A. H.</namePart><namePart type="family">Schapira</namePart><affiliation>Department of Clinical Neurosciences, Institute of Neurology, University College London, Queen Square, London</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Y.</namePart><namePart type="family">Agid</namePart><affiliation>Institute of the Brain and Spine, INSERM, Pierre et Marie Curie University, Assistance Publique‐Hôpitaux de Paris, Paris, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Barone</namePart><affiliation>Department of Neurological Sciences, University of Naples, Napoli, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Jenner</namePart><affiliation>Neurodegenerative Diseases Research Group, School of Biomedical and Health Sciences, King’s College London, London, UK</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. R.</namePart><namePart type="family">Lemke</namePart><affiliation>Department of Psychiatry, University of Kiel, Kliniken Alsterdorf, Hamburg, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">W.</namePart><namePart type="family">Poewe</namePart><affiliation>Department of Neurology, Innsbruck Medical University, Innsbruck, Austria</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O.</namePart><namePart type="family">Rascol</namePart><affiliation>Departments of Clinical Pharmacology and Neurosciences, INSERM CIC‐9302 and UMR‐825, Toulouse University Hospital, Toulouse, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Reichmann</namePart><affiliation>Universitätsklinikum Carl Gustav Carus, an der Technischen Universität Dresden, Dresden, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">E.</namePart><namePart type="family">Tolosa</namePart><affiliation>Neurology Service, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Hospital Clínic, IDIBAPS, Universitat de Barcelona, Spain</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">2009-10</dateIssued><edition>Received 23 June 2009 Accepted 29 July 2009</edition><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">3</extent></physicalDescription><abstract lang="en">There have been numerous important recent advances in our understanding of the causes of Parkinson’s disease (PD), the treatments available and how these are best applied for the long‐term management of patients. Novel genes causing familial PD have been discovered and mechanisms leading to cell dysfunction and death identified. The PD prodrome is now a subject of great interest and clinical markers are being defined that may in future, together with biochemical markers, support an early, pre‐motor diagnosis of PD. This will become important as new therapies are developed to modify disease progression. In the interim, the optimization of existing therapies remains an important priority. The value of existing and novel continuous drug delivery systems in PD is seen as providing simplified regimens, maintenance of motor control, reduction in motor complications and improved patient adherence to drug use.</abstract><subject lang="en"><genre>Keywords</genre><topic>autophagy</topic><topic>depression</topic><topic>dopamine agonist</topic><topic>levodopa</topic><topic>mitochondrial</topic><topic>neuroprotection</topic><topic>non‐motor</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>2009</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>1090</start><end>1099</end><total>10</total></extent></part></relatedItem><identifier type="istex">D88BCA9904F670DD3121DAAB11B4163D17FFBE3E</identifier><identifier type="DOI">10.1111/j.1468-1331.2009.02793.x</identifier><identifier type="ArticleID">ENE2793</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2009 The Author(s). 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