A tale on animal models of Parkinson's disease
Identifieur interne : 001B08 ( Main/Corpus ); précédent : 001B07; suivant : 001B09A tale on animal models of Parkinson's disease
Auteurs : Erwan Bezard ; Serge PrzedborskiSource :
- Movement Disorders [ 0885-3185 ] ; 2011-05.
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Abstract
Parkinson's disease is a neurodegenerative disorder whose cardinal manifestations are due primarily to a profound deficit in brain dopamine. Since the 1980s, several therapeutic strategies have been discovered to treat the symptoms of this neurological disorder, but as of yet, none halts or retards the neurodegenerative process. In an attempt to shed light on the neurobiology of Parkinson's disease, a number of experimental models have been developed, especially during the last 25 years. They come essentially in 3 flavors: pharmacological (eg, reserpine), toxic (eg, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine), and genetic (eg, transgenic synuclein mice). These models can also be recast as etiologic, pathogenic, and symptomatic/pathophysiologic, as each may contribute to our understanding of the cause, the mechanisms, and the treatment of Parkinson's disease. In this review, we will discuss the question of Parkinson's disease models, starting from the period when this journal was born to today. During this journey of 25 years, we will discuss both the significant contributions of the Parkinson's disease models and hurdles that remain to be overcome to one day cure this neurological disease. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23696
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ISTEX:8AE9E48366F7D98702E5A22CB84145106BC1C18DLe document en format XML
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Serge Przedborski is the Page and William Black Professor of Neurology.</note><note type="content">*Infrastructural support for this study was provided by the Université Victor‐Segalen Bordeaux 2 and the Centre National de la Recherche Scientifique.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">A tale on animal models of Parkinson's disease</title><author><persName><forename type="first">Erwan</forename><surname>Bezard</surname></persName><roleName type="degree">PhD</roleName><affiliation>Insitute of Neurodegenerative Diseases, Université Victor Ségalen‐Bordeaux II, Centre National de la Recherche Scientifique, Bordeaux, France</affiliation></author><author><persName><forename type="first">Serge</forename><surname>Przedborski</surname></persName><roleName type="degree">MD, PhD</roleName><note type="correspondence"><p>Correspondence: Center for Motor Neuron. 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In an attempt to shed light on the neurobiology of Parkinson's disease, a number of experimental models have been developed, especially during the last 25 years. They come essentially in 3 flavors: pharmacological (eg, reserpine), toxic (eg, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine), and genetic (eg, transgenic synuclein mice). These models can also be recast as etiologic, pathogenic, and symptomatic/pathophysiologic, as each may contribute to our understanding of the cause, the mechanisms, and the treatment of Parkinson's disease. In this review, we will discuss the question of Parkinson's disease models, starting from the period when this journal was born to today. During this journey of 25 years, we will discuss both the significant contributions of the Parkinson's disease models and hurdles that remain to be overcome to one day cure this neurological disease. © 2011 <i>Movement</i> Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p><b>Relevant conflicts of interest/financial disclosures:</b> Erwan Bezard is supported by Agence Nationale de la Recherche grants (ANR‐07‐JCJC‐0090, ANR‐08‐MNP‐018, ANR‐07‐MNP‐Trafinlid) and Serge Przedborski by NIH grants AG021617, NS042269, NS062180, NS064191, and NS38370; U.S. Department of Defense grants (W81XWH‐08‐1‐0522 and W81XWH‐08‐1‐0465); the Parkinson Disease Foundation (New York, NY); the Thomas Hartman Foundation for Parkinson's Research, and the MDA/Wings‐over‐Wall Street. Serge Przedborski is the Page and William Black Professor of Neurology.</p></note><note xml:id="fn2"><p>Infrastructural support for this study was provided by the Université Victor‐Segalen Bordeaux 2 and the Centre National de la Recherche Scientifique.</p></note><note xml:id="fn3"><p>Full financial disclosures and author roles may be found in the online version of this article.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>A tale on animal models of Parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Animal Models</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>A tale on animal models of Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Erwan</namePart><namePart type="family">Bezard</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Insitute of Neurodegenerative Diseases, Université Victor Ségalen‐Bordeaux II, Centre National de la Recherche Scientifique, Bordeaux, France</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Serge</namePart><namePart type="family">Przedborski</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Departments of Neurology, Pathology, and Cell Biology and the Center for Motor Neuron. Biology and Disease, Columbia University, New York, New York, USA</affiliation><description>Correspondence: Center for Motor Neuron. Biology and Disease, P&S 5‐420, Columbia University, 630 West 168th Street, New York, NY 10032, USA</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2011-05</dateIssued><dateCaptured encoding="w3cdtf">2010-10-05</dateCaptured><dateValid encoding="w3cdtf">2011-01-30</dateValid><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><extent unit="tables">1</extent><extent unit="references">112</extent><extent unit="words">8803</extent></physicalDescription><abstract lang="en">Parkinson's disease is a neurodegenerative disorder whose cardinal manifestations are due primarily to a profound deficit in brain dopamine. Since the 1980s, several therapeutic strategies have been discovered to treat the symptoms of this neurological disorder, but as of yet, none halts or retards the neurodegenerative process. In an attempt to shed light on the neurobiology of Parkinson's disease, a number of experimental models have been developed, especially during the last 25 years. They come essentially in 3 flavors: pharmacological (eg, reserpine), toxic (eg, 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine), and genetic (eg, transgenic synuclein mice). These models can also be recast as etiologic, pathogenic, and symptomatic/pathophysiologic, as each may contribute to our understanding of the cause, the mechanisms, and the treatment of Parkinson's disease. In this review, we will discuss the question of Parkinson's disease models, starting from the period when this journal was born to today. During this journey of 25 years, we will discuss both the significant contributions of the Parkinson's disease models and hurdles that remain to be overcome to one day cure this neurological disease. © 2011 Movement Disorder Society</abstract><note type="content">*Relevant conflicts of interest/financial disclosures: Erwan Bezard is supported by Agence Nationale de la Recherche grants (ANR‐07‐JCJC‐0090, ANR‐08‐MNP‐018, ANR‐07‐MNP‐Trafinlid) and Serge Przedborski by NIH grants AG021617, NS042269, NS062180, NS064191, and NS38370; U.S. Department of Defense grants (W81XWH‐08‐1‐0522 and W81XWH‐08‐1‐0465); the Parkinson Disease Foundation (New York, NY); the Thomas Hartman Foundation for Parkinson's Research, and the MDA/Wings‐over‐Wall Street. Serge Przedborski is the Page and William Black Professor of Neurology.</note><note type="content">*Infrastructural support for this study was provided by the Université Victor‐Segalen Bordeaux 2 and the Centre National de la Recherche Scientifique.</note><note type="content">*Full financial disclosures and author roles may be found in the online version of this article.</note><subject lang="en"><genre>Keywords</genre><topic>6‐hydroxydopamine (6‐OHDA)</topic><topic>1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP)</topic><topic>synuclein</topic><topic>LRRK2</topic><topic>rat</topic><topic>mouse</topic><topic>primate</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Review</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2011</date><detail type="title"><title>25th Anniversary</title></detail><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>993</start><end>1002</end><total>10</total></extent></part></relatedItem><identifier type="istex">8AE9E48366F7D98702E5A22CB84145106BC1C18D</identifier><identifier type="DOI">10.1002/mds.23696</identifier><identifier type="ArticleID">MDS23696</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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