CYP2D6 Polymorphism and Parkinson's disease susceptibility
Identifieur interne : 004D95 ( Main/Curation ); précédent : 004D94; suivant : 004D96CYP2D6 Polymorphism and Parkinson's disease susceptibility
Auteurs : Nada Sabbagh [France] ; Alexis Brice [France] ; Delphine Marez [France] ; Alexandra Dürr [France] ; Maryline Legrand [France] ; Jean-Marc Lo Guidice [France] ; Alain Destée [France] ; Yves Agid [France] ; Franck Broly [France]Source :
- Movement Disorders [ 0885-3185 ] ; 1999-03.
Descripteurs français
- Pascal (Inist)
- Wicri :
English descriptors
- KwdEn :
- Aged, CYP2D6 polymorphism, Case-Control Studies, Chi-Square Distribution, Cytochrome P-450 CYP2D6 (genetics), Cytochrome P450, Exploration, Family Health, Female, France, Gene, Gene Dosage, Genetic Predisposition to Disease (genetics), Genotype, Human, Humans, Male, Middle Aged, Parkinson Disease (genetics), Parkinson disease, Parkinson's disease, Phenotype, Polymerase chain reaction, Polymorphism, Genetic (genetics), Restriction fragment length polymorphism, SSCP, Single strand conformation polymorphism.
- MESH :
- chemical , genetics : Cytochrome P-450 CYP2D6.
- geographic : France.
- genetics : Genetic Predisposition to Disease, Parkinson Disease, Polymorphism, Genetic.
- Aged, Case-Control Studies, Chi-Square Distribution, Family Health, Female, Gene Dosage, Genotype, Humans, Male, Middle Aged, Phenotype.
Abstract
Following the recent identification of multiple novel mutations and alleles of the cytochrome P450 CYP2D6 gene which cause decreased, increased, or absent enzyme activity, we re‐examined the controversial hypothesis of a role of the CYP2D6 polymorphism in Parkinson's disease (PD) susceptibility. For this purpose, a strategy based on PCR‐SSCP and RFLP analyses allowing the detection of all known CYP2D6 alleles was performed in DNA from 109 patients with sporadic PD. This strategy was also applied to DNA from 68 members of PD families including 18 affected and 50 unaffected members. Seventeen mutations occurring alone or in various combination on 14 alleles of CYP2D6 have been identified in patients with sporadic PD. Moreover, 12 mutations and nine alleles of the gene have been characterized in members of PD families. No significant difference was observed when the distribution of mutations and alleles of CYP2D6 was compared between the PD patients and 514 control subjects previously analyzed using the same strategy. There was also no difference in the distribution of phenotypes predicted from genotypes between both groups. In addition, when the distribution of CYP2D6 genotypes was compared, no difference between affected and unaffected members of PD families was observed. These data indicate that CYP2D6 polymorphism is not a susceptibility factor to PD.
Url:
DOI: 10.1002/1531-8257(199903)14:2<230::AID-MDS1005>3.0.CO;2-6
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<term>Chi-Square Distribution</term>
<term>Cytochrome P-450 CYP2D6 (genetics)</term>
<term>Cytochrome P450</term>
<term>Exploration</term>
<term>Family Health</term>
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<term>Genotype</term>
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<term>Humans</term>
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<term>Middle Aged</term>
<term>Parkinson Disease (genetics)</term>
<term>Parkinson disease</term>
<term>Parkinson's disease</term>
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<term>Restriction fragment length polymorphism</term>
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<term>Single strand conformation polymorphism</term>
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<front><div type="abstract" xml:lang="en">Following the recent identification of multiple novel mutations and alleles of the cytochrome P450 CYP2D6 gene which cause decreased, increased, or absent enzyme activity, we re‐examined the controversial hypothesis of a role of the CYP2D6 polymorphism in Parkinson's disease (PD) susceptibility. For this purpose, a strategy based on PCR‐SSCP and RFLP analyses allowing the detection of all known CYP2D6 alleles was performed in DNA from 109 patients with sporadic PD. This strategy was also applied to DNA from 68 members of PD families including 18 affected and 50 unaffected members. Seventeen mutations occurring alone or in various combination on 14 alleles of CYP2D6 have been identified in patients with sporadic PD. Moreover, 12 mutations and nine alleles of the gene have been characterized in members of PD families. No significant difference was observed when the distribution of mutations and alleles of CYP2D6 was compared between the PD patients and 514 control subjects previously analyzed using the same strategy. There was also no difference in the distribution of phenotypes predicted from genotypes between both groups. In addition, when the distribution of CYP2D6 genotypes was compared, no difference between affected and unaffected members of PD families was observed. These data indicate that CYP2D6 polymorphism is not a susceptibility factor to PD.</div>
</front>
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<term>Human</term>
<term>Parkinson disease</term>
<term>Polymerase chain reaction</term>
<term>Restriction fragment length polymorphism</term>
<term>Single strand conformation polymorphism</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Parkinson maladie</term>
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<term>Polymorphisme conformation simple brin</term>
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<ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">CYP2D6 Polymorphism and Parkinson's disease susceptibility</title>
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</author>
<author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name>
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<placeName><settlement type="city">Paris</settlement>
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</placeName>
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<author><name sortKey="Broly, Franck" sort="Broly, Franck" uniqKey="Broly F" first="Franck" last="Broly">Franck Broly</name>
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<author><name sortKey="Brice, Alexis" sort="Brice, Alexis" uniqKey="Brice A" first="Alexis" last="Brice">Alexis Brice</name>
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<author><name sortKey="Legrand, Maryline" sort="Legrand, Maryline" uniqKey="Legrand M" first="Maryline" last="Legrand">Maryline Legrand</name>
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</affiliation>
</author>
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</author>
<author><name sortKey="Agid, Yves" sort="Agid, Yves" uniqKey="Agid Y" first="Yves" last="Agid">Yves Agid</name>
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<placeName><settlement type="city">Paris</settlement>
</placeName>
<placeName><settlement type="city">Paris</settlement>
<region type="region" nuts="2">Île-de-France</region>
</placeName>
<orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName>
</affiliation>
</author>
<author><name sortKey="Broly, Franck" sort="Broly, Franck" uniqKey="Broly F" first="Franck" last="Broly">Franck Broly</name>
<affiliation wicri:level="1"><country xml:lang="fr">France</country>
<wicri:regionArea>Laboratoire de Biochimie & Biologie Moléculaire de l'Hôpital Calmette, Lille</wicri:regionArea>
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<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>John Wiley & Sons, Inc.</publisher>
<pubPlace>New York</pubPlace>
<date type="published" when="1999-03">1999-03</date>
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<front><div type="abstract" xml:lang="en">Following the recent identification of multiple novel mutations and alleles of the cytochrome P450 CYP2D6 gene which cause decreased, increased, or absent enzyme activity, we re‐examined the controversial hypothesis of a role of the CYP2D6 polymorphism in Parkinson's disease (PD) susceptibility. For this purpose, a strategy based on PCR‐SSCP and RFLP analyses allowing the detection of all known CYP2D6 alleles was performed in DNA from 109 patients with sporadic PD. This strategy was also applied to DNA from 68 members of PD families including 18 affected and 50 unaffected members. Seventeen mutations occurring alone or in various combination on 14 alleles of CYP2D6 have been identified in patients with sporadic PD. Moreover, 12 mutations and nine alleles of the gene have been characterized in members of PD families. No significant difference was observed when the distribution of mutations and alleles of CYP2D6 was compared between the PD patients and 514 control subjects previously analyzed using the same strategy. There was also no difference in the distribution of phenotypes predicted from genotypes between both groups. In addition, when the distribution of CYP2D6 genotypes was compared, no difference between affected and unaffected members of PD families was observed. These data indicate that CYP2D6 polymorphism is not a susceptibility factor to PD.</div>
</front>
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</author>
<author><name sortKey="Legrand, M" sort="Legrand, M" uniqKey="Legrand M" first="M" last="Legrand">M. Legrand</name>
</author>
<author><name sortKey="Lo Guidice, J M" sort="Lo Guidice, J M" uniqKey="Lo Guidice J" first="J M" last="Lo Guidice">J M Lo Guidice</name>
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</author>
<author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name>
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<placeName><settlement type="city">Paris</settlement>
<region type="region" nuts="2">Île-de-France</region>
</placeName>
<orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName>
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<author><name sortKey="Broly, F" sort="Broly, F" uniqKey="Broly F" first="F" last="Broly">F. Broly</name>
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<country xml:lang="fr">France</country>
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<author><name sortKey="Brice, A" sort="Brice, A" uniqKey="Brice A" first="A" last="Brice">A. Brice</name>
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<author><name sortKey="Durr, A" sort="Durr, A" uniqKey="Durr A" first="A" last="Dürr">A. Dürr</name>
</author>
<author><name sortKey="Legrand, M" sort="Legrand, M" uniqKey="Legrand M" first="M" last="Legrand">M. Legrand</name>
</author>
<author><name sortKey="Lo Guidice, J M" sort="Lo Guidice, J M" uniqKey="Lo Guidice J" first="J M" last="Lo Guidice">J M Lo Guidice</name>
</author>
<author><name sortKey="Destee, A" sort="Destee, A" uniqKey="Destee A" first="A" last="Destée">A. Destée</name>
</author>
<author><name sortKey="Agid, Y" sort="Agid, Y" uniqKey="Agid Y" first="Y" last="Agid">Yves Agid</name>
<affiliation><country>France</country>
<placeName><settlement type="city">Paris</settlement>
<region type="region" nuts="2">Île-de-France</region>
</placeName>
<orgName type="hospital" n="4">Hôpital de la Salpêtrière</orgName>
</affiliation>
</author>
<author><name sortKey="Broly, F" sort="Broly, F" uniqKey="Broly F" first="F" last="Broly">F. Broly</name>
</author>
</analytic>
<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="1999" type="published">1999</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term>
<term>Case-Control Studies</term>
<term>Chi-Square Distribution</term>
<term>Cytochrome P-450 CYP2D6 (genetics)</term>
<term>Family Health</term>
<term>Female</term>
<term>France</term>
<term>Gene Dosage</term>
<term>Genetic Predisposition to Disease (genetics)</term>
<term>Genotype</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Parkinson Disease (genetics)</term>
<term>Phenotype</term>
<term>Polymorphism, Genetic (genetics)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytochrome P-450 CYP2D6</term>
</keywords>
<keywords scheme="MESH" type="geographic" xml:lang="en"><term>France</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Genetic Predisposition to Disease</term>
<term>Parkinson Disease</term>
<term>Polymorphism, Genetic</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Case-Control Studies</term>
<term>Chi-Square Distribution</term>
<term>Family Health</term>
<term>Female</term>
<term>Gene Dosage</term>
<term>Genotype</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Phenotype</term>
</keywords>
<keywords scheme="Wicri" type="geographic" xml:lang="fr"><term>France</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Following the recent identification of multiple novel mutations and alleles of the cytochrome P450 CYP2D6 gene which cause decreased, increased, or absent enzyme activity, we re-examined the controversial hypothesis of a role of the CYP2D6 polymorphism in Parkinson's disease (PD) susceptibility. For this purpose, a strategy based on PCR-SSCP and RFLP analyses allowing the detection of all known CYP2D6 alleles was performed in DNA from 109 patients with sporadic PD. This strategy was also applied to DNA from 68 members of PD families including 18 affected and 50 unaffected members. Seventeen mutations occurring alone or in various combination on 14 alleles of CYP2D6 have been identified in patients with sporadic PD. Moreover, 12 mutations and nine alleles of the gene have been characterized in members of PD families. No significant difference was observed when the distribution of mutations and alleles of CYP2D6 was compared between the PD patients and 514 control subjects previously analyzed using the same strategy. There was also no difference in the distribution of phenotypes predicted from genotypes between both groups. In addition, when the distribution of CYP2D6 genotypes was compared, no difference between affected and unaffected members of PD families was observed. These data indicate that CYP2D6 polymorphism is not a susceptibility factor to PD.</div>
</front>
</TEI>
</PubMed>
</double>
</record>
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