CYP2D6‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy
Identifieur interne : 005925 ( Main/Exploration ); précédent : 005924; suivant : 005926CYP2D6‐debrisoquine hydroxylase gene polymorphism in multiple system atrophy
Auteurs : V. Planté-Bordeneuve [Royaume-Uni] ; O. Bandmann [Royaume-Uni] ; G. Wenning [Royaume-Uni] ; N. P. Quinn [Royaume-Uni] ; S. E. Daniel [Royaume-Uni] ; Harding [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1995-05.
English descriptors
- KwdEn :
- Alleles, Cytochrome P-450 CYP2D6, Cytochrome P-450 Enzyme System (genetics), Cytochrome P450, DNA Mutational Analysis, Gene Expression (physiology), Gene Frequency (genetics), Genotype, Humans, Mixed Function Oxygenases (genetics), Multiple system atrophy, Olivopontocerebellar Atrophies (genetics), Parkinson Disease (genetics), Parkinson's disease, Polymorphism, Genetic (genetics).
- MESH :
- chemical , genetics : Cytochrome P-450 Enzyme System, Mixed Function Oxygenases.
- chemical : Cytochrome P-450 CYP2D6.
- genetics : Gene Frequency, Olivopontocerebellar Atrophies, Parkinson Disease, Polymorphism, Genetic.
- physiology : Gene Expression.
- Alleles, DNA Mutational Analysis, Genotype, Humans.
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
Affiliations:
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Wenning</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N. P." last="Quinn">N. P. Quinn</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S. E." last="Daniel">S. E. Daniel</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London</wicri:cityArea></affiliation></author><author><name sortKey="Harding" sort="Harding" uniqKey="Harding" last="Harding">Harding</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology (Neurogenetics and Movement Disorders Sections and Parkinson's Disease Society Brain Bank), Institute of Neurology, London</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1995-05">1995-05</date><biblScope unit="vol">10</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="277">277</biblScope><biblScope unit="page" to="278">278</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">A74D2BAFCD624AC24D50C184996E977E8D1C8BCA</idno><idno type="DOI">10.1002/mds.870100307</idno><idno type="ArticleID">MDS870100307</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Alleles</term><term>Cytochrome P-450 CYP2D6</term><term>Cytochrome P-450 Enzyme System (genetics)</term><term>Cytochrome P450</term><term>DNA Mutational Analysis</term><term>Gene Expression (physiology)</term><term>Gene Frequency (genetics)</term><term>Genotype</term><term>Humans</term><term>Mixed Function Oxygenases (genetics)</term><term>Multiple system atrophy</term><term>Olivopontocerebellar Atrophies (genetics)</term><term>Parkinson Disease (genetics)</term><term>Parkinson's disease</term><term>Polymorphism, Genetic (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytochrome P-450 Enzyme System</term><term>Mixed Function Oxygenases</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Cytochrome P-450 CYP2D6</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Gene Frequency</term><term>Olivopontocerebellar Atrophies</term><term>Parkinson Disease</term><term>Polymorphism, Genetic</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Alleles</term><term>DNA Mutational Analysis</term><term>Genotype</term><term>Humans</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Plante Ordeneuve, V" sort="Plante Ordeneuve, V" uniqKey="Plante Ordeneuve V" first="V." last="Planté-Bordeneuve">V. Planté-Bordeneuve</name></region><name sortKey="Bandmann, O" sort="Bandmann, O" uniqKey="Bandmann O" first="O." last="Bandmann">O. Bandmann</name><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S. E." last="Daniel">S. E. Daniel</name><name sortKey="Harding" sort="Harding" uniqKey="Harding" last="Harding">Harding</name><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N. P." last="Quinn">N. P. Quinn</name><name sortKey="Wenning, G" sort="Wenning, G" uniqKey="Wenning G" first="G." last="Wenning">G. Wenning</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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