Movement Disorders (revue)

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CYP2D6‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy

Identifieur interne : 003989 ( Istex/Corpus ); précédent : 003988; suivant : 003990

CYP2D6‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy

Auteurs : V. Planté-Bordeneuve ; O. Bandmann ; G. Wenning ; N. P. Quinn ; S. E. Daniel ; Harding

Source :

RBID : ISTEX:A74D2BAFCD624AC24D50C184996E977E8D1C8BCA

English descriptors

Abstract

Molecular genetic studies of the cytochrome P450 system enzyme CYP2D6, which hydroxylates debrisoquine, have indicated an excess of mutant alleles in large series of patients with Parkinosn's disease (PD) when compared with controls. We have investigated CYP2D6 polymorphism in 91 patients with multiple system atrophy (MSA) in order to determine if this finding is specific to PD or if there is similar evidence of genetic susceptibility to neurotoxicity in MSA. The distribution of CYP2D6 alleles was not significantly different between MSA patients and controls, and there were fewer poor metabolisers in the MSA group than in the control group.

Url:
DOI: 10.1002/mds.870100307

Links to Exploration step

ISTEX:A74D2BAFCD624AC24D50C184996E977E8D1C8BCA

Le document en format XML

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<title>CYP2D6‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy</title>
</titleInfo>
<titleInfo type="abbreviated" lang="en">
<title>POLYMORPHISM IN MULTIPLE SYSTEM ATROPHY</title>
</titleInfo>
<titleInfo type="alternative" contentType="CDATA" lang="en">
<title>‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy</title>
</titleInfo>
<name type="personal">
<namePart type="given">V.</namePart>
<namePart type="family">Planté‐Bordeneuve</namePart>
<affiliation>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London, England</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">O.</namePart>
<namePart type="family">Bandmann</namePart>
<affiliation>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London, England</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">G.</namePart>
<namePart type="family">Wenning</namePart>
<affiliation>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London, England</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">N. P.</namePart>
<namePart type="family">Quinn</namePart>
<affiliation>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London, England</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="given">S. E.</namePart>
<namePart type="family">Daniel</namePart>
<affiliation>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London, England</affiliation>
<role>
<roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal">
<namePart type="termsOfAddress">Prof.</namePart>
<namePart type="family">Harding</namePart>
<affiliation>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London, England</affiliation>
<description>Correspondence: University Department of Clinical Neurology (Neurogenetics Section), Institute of Neurology, Queen Square, London WC1N 3BG, U.K.</description>
<role>
<roleTerm type="text">author</roleTerm>
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<typeOfResource>text</typeOfResource>
<genre authority="originalCategForm">article</genre>
<originInfo>
<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place>
<placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">1995-05</dateIssued>
<dateValid encoding="w3cdtf">1994-09-08</dateValid>
<copyrightDate encoding="w3cdtf">1995</copyrightDate>
</originInfo>
<language>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
</language>
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<internetMediaType>text/html</internetMediaType>
<extent unit="tables">1</extent>
<extent unit="references">10</extent>
</physicalDescription>
<abstract lang="en">Molecular genetic studies of the cytochrome P450 system enzyme CYP2D6, which hydroxylates debrisoquine, have indicated an excess of mutant alleles in large series of patients with Parkinosn's disease (PD) when compared with controls. We have investigated CYP2D6 polymorphism in 91 patients with multiple system atrophy (MSA) in order to determine if this finding is specific to PD or if there is similar evidence of genetic susceptibility to neurotoxicity in MSA. The distribution of CYP2D6 alleles was not significantly different between MSA patients and controls, and there were fewer poor metabolisers in the MSA group than in the control group.</abstract>
<subject lang="en">
<genre>Keywords</genre>
<topic>Multiple system atrophy</topic>
<topic>Cytochrome P450</topic>
<topic>Parkinson's disease</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<subject>
<genre>article category</genre>
<topic>Article</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>1995</date>
<detail type="volume">
<caption>vol.</caption>
<number>10</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>3</number>
</detail>
<extent unit="pages">
<start>277</start>
<end>278</end>
<total>2</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">A74D2BAFCD624AC24D50C184996E977E8D1C8BCA</identifier>
<identifier type="DOI">10.1002/mds.870100307</identifier>
<identifier type="ArticleID">MDS870100307</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 1995 Movement Disorder Society</accessCondition>
<recordInfo>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
<recordContentSource>WILEY</recordContentSource>
</recordInfo>
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</metadata>
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