Serveur d'exploration sur la maladie de Parkinson

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What causes cell death in Parkinson's disease?

Identifieur interne : 001996 ( Main/Corpus ); précédent : 001995; suivant : 001997

What causes cell death in Parkinson's disease?

Auteurs : Amitabh Gupta ; Valina L. Dawson ; Ted M. Dawson

Source :

RBID : ISTEX:48D8E7F0128E42858FDB877EE27C7757866B4EA5

Abstract

Currently, there is no proven neuroprotective or neurorestorative therapy for Parkinson's disease (PD). Several advances in the genetics of PD have created an opportunity to develop mechanistic‐based therapies that hold particular promise for identifying agents that slow and even halt the progression of PD, as well as restore function. Here we review many of the advances in the last decade regarding the identification of new targets for the treatment of PD based on understanding the molecular mechanisms of how mutations in genes linked to PD cause neurodegeneration. Ann Neurol 2008;64 (suppl):S3–S15

Url:
DOI: 10.1002/ana.21573

Links to Exploration step

ISTEX:48D8E7F0128E42858FDB877EE27C7757866B4EA5

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<placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2008-12</dateIssued>
<dateCaptured encoding="w3cdtf">2008-03-03</dateCaptured>
<dateValid encoding="w3cdtf">2008-10-03</dateValid>
<copyrightDate encoding="w3cdtf">2008</copyrightDate>
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<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<abstract lang="en">Currently, there is no proven neuroprotective or neurorestorative therapy for Parkinson's disease (PD). Several advances in the genetics of PD have created an opportunity to develop mechanistic‐based therapies that hold particular promise for identifying agents that slow and even halt the progression of PD, as well as restore function. Here we review many of the advances in the last decade regarding the identification of new targets for the treatment of PD based on understanding the molecular mechanisms of how mutations in genes linked to PD cause neurodegeneration. Ann Neurol 2008;64 (suppl):S3–S15</abstract>
<note type="content">*Potential conflicts of interest: This article is part of a supplement sponsored by Boehringer Ingelheim (BI). A.G. has received honorarium from BI. V.L.D. has no relationship with BI. T.M.D. is a paid contributor. T.M.D. has consulted for BI in the past, but reports no consulting agreements with pharmaceutical companies at the time of publication of this manuscript.</note>
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<titleInfo>
<title>Annals of Neurology</title>
<subTitle>Official Journal of the American Neurological Association and the Child Neurology Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated">
<title>Ann Neurol.</title>
</titleInfo>
<genre type="Journal">journal</genre>
<note type="content"> Additional Supporting Information may be found in the online version of this article.</note>
<subject>
<genre>article category</genre>
<topic>Basic Issues</topic>
</subject>
<identifier type="ISSN">0364-5134</identifier>
<identifier type="eISSN">1531-8249</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8249</identifier>
<identifier type="PublisherID">ANA</identifier>
<part>
<date>2008</date>
<detail type="volume">
<caption>vol.</caption>
<number>64</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>S2</number>
</detail>
<detail type="supplement">
<caption>Suppl. no.</caption>
<number>2</number>
</detail>
<extent unit="pages">
<start>S3</start>
<end>S15</end>
<total>13</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">48D8E7F0128E42858FDB877EE27C7757866B4EA5</identifier>
<identifier type="DOI">10.1002/ana.21573</identifier>
<identifier type="ArticleID">ANA21573</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 American Neurological Association</accessCondition>
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<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
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