CYP2D6‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy
Identifieur interne : 003989 ( Istex/Corpus ); précédent : 003988; suivant : 003990CYP2D6‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy
Auteurs : V. Planté-Bordeneuve ; O. Bandmann ; G. Wenning ; N. P. Quinn ; S. E. Daniel ; HardingSource :
- Movement Disorders [ 0885-3185 ] ; 1995-05.
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.
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DOI: 10.1002/mds.870100307
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<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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</name>
<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>
<physicalDescription><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>
</mods>
</metadata>
<serie></serie>
</istex>
</record>
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