P450 enzymes and Parkinson's disease: The story so far
Identifieur interne : 004F37 ( Main/Exploration ); précédent : 004F36; suivant : 004F38P450 enzymes and Parkinson's disease: The story so far
Auteurs : Andrew G. Riedl [Royaume-Uni] ; Paul M. Watts [Royaume-Uni] ; Jenner [Royaume-Uni] ; C. David Marsden [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 1998-03.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Animals, CYP2D6, Cell Death (genetics), Cytochrome P-450 CYP1A1 (genetics), Cytochrome P-450 CYP2D6 (genetics), Cytochrome P-450 Enzyme System (genetics), Cytochrome P450, DNA Mutational Analysis, Debrisoquine, Gene Expression Regulation, Enzymologic (physiology), Gene expression, Genetic determinism, Genotype, Human, Humans, Mutation, P450, Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson disease, Parkinson's disease, Phenotype, Polymorphism, Polymorphism, Genetic (genetics), Polymorphisms, Review, Risk factor, Substantia Nigra (pathology), Young‐onset Parkinson's disease.
- MESH :
- chemical , genetics : Cytochrome P-450 CYP1A1, Cytochrome P-450 CYP2D6, Cytochrome P-450 Enzyme System.
- genetics : Cell Death, Parkinson Disease, Polymorphism, Genetic.
- pathology : Parkinson Disease, Substantia Nigra.
- physiology : Gene Expression Regulation, Enzymologic.
- Animals, DNA Mutational Analysis, Genotype, Humans, Phenotype.
Abstract
Environmental or endogenous toxins may cause nigral cell death in Parkinson's disease (PD) as a result of genetic susceptibility conferred by altered expression of P450 enzymes. Attention over the last 10 years has focused on CYP2D6 polymorphisms and susceptibility to PD. This review summarizes reports arising from both phenotypic and genotypic studies involving CYP2D6 and PD. Phenotypic studies have failed to support a link between CYP2D6 and PD. The more powerful genetic studies initially indicated a link between CYP2D6B mutations and PD, but critical analysis of the literature and recent studies emerging from independent laboratories fail to confirm this. Mutations in CYP2D6B are also not implicated in familial PD. As yet, there is no conclusive evidence to suggest that CYP2D6 polymorphisms confer susceptibility to PD. Whether polymorphisms in other P450s (for example, CYP1A1 and CYP2E1) are implicated in PD remains to be established.
Url:
DOI: 10.1002/mds.870130204
Affiliations:
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Le document en format XML
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Riedl</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Disease Research Centre, Pharmacology Group, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="Watts, Paul M" sort="Watts, Paul M" uniqKey="Watts P" first="Paul M." last="Watts">Paul M. Watts</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Disease Research Centre, Pharmacology Group, King's College, London</wicri:cityArea></affiliation><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology, Institute of Neurology, National Hospital for Neurology and Neurosurgery, London</wicri:cityArea></affiliation></author><author><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Neurodegenerative Disease Research Centre, Pharmacology Group, King's College, London</wicri:cityArea></affiliation></author><author><name sortKey="David Marsden, C" sort="David Marsden, C" uniqKey="David Marsden C" first="C." last="David Marsden">C. David Marsden</name><affiliation wicri:level="2"><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>University Department of Clinical Neurology, Institute of Neurology, National Hospital for Neurology and Neurosurgery, 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="1998-03">1998-03</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="212">212</biblScope><biblScope unit="page" to="220">220</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">345F9285D2146769294488D56F23E8836392B787</idno><idno type="DOI">10.1002/mds.870130204</idno><idno type="ArticleID">MDS870130204</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>CYP2D6</term><term>Cell Death (genetics)</term><term>Cytochrome P-450 CYP1A1 (genetics)</term><term>Cytochrome P-450 CYP2D6 (genetics)</term><term>Cytochrome P-450 Enzyme System (genetics)</term><term>Cytochrome P450</term><term>DNA Mutational Analysis</term><term>Debrisoquine</term><term>Gene Expression Regulation, Enzymologic (physiology)</term><term>Gene expression</term><term>Genetic determinism</term><term>Genotype</term><term>Human</term><term>Humans</term><term>Mutation</term><term>P450</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Phenotype</term><term>Polymorphism</term><term>Polymorphism, Genetic (genetics)</term><term>Polymorphisms</term><term>Review</term><term>Risk factor</term><term>Substantia Nigra (pathology)</term><term>Young‐onset Parkinson's disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytochrome P-450 CYP1A1</term><term>Cytochrome P-450 CYP2D6</term><term>Cytochrome P-450 Enzyme System</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Death</term><term>Parkinson Disease</term><term>Polymorphism, Genetic</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Gene Expression Regulation, Enzymologic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>DNA Mutational Analysis</term><term>Genotype</term><term>Humans</term><term>Phenotype</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Article synthèse</term><term>CYP2D6</term><term>Cytochrome P450</term><term>Déterminisme génétique</term><term>Expression génique</term><term>Facteur risque</term><term>Génotype</term><term>Homme</term><term>Mutation</term><term>Parkinson maladie</term><term>Phénotype</term><term>Polymorphisme</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Environmental or endogenous toxins may cause nigral cell death in Parkinson's disease (PD) as a result of genetic susceptibility conferred by altered expression of P450 enzymes. Attention over the last 10 years has focused on CYP2D6 polymorphisms and susceptibility to PD. This review summarizes reports arising from both phenotypic and genotypic studies involving CYP2D6 and PD. Phenotypic studies have failed to support a link between CYP2D6 and PD. The more powerful genetic studies initially indicated a link between CYP2D6B mutations and PD, but critical analysis of the literature and recent studies emerging from independent laboratories fail to confirm this. Mutations in CYP2D6B are also not implicated in familial PD. As yet, there is no conclusive evidence to suggest that CYP2D6 polymorphisms confer susceptibility to PD. Whether polymorphisms in other P450s (for example, CYP1A1 and CYP2E1) are implicated in PD remains to be established.</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="Riedl, Andrew G" sort="Riedl, Andrew G" uniqKey="Riedl A" first="Andrew G." last="Riedl">Andrew G. Riedl</name></region><name sortKey="David Marsden, C" sort="David Marsden, C" uniqKey="David Marsden C" first="C." last="David Marsden">C. David Marsden</name><name sortKey="Jenner" sort="Jenner" uniqKey="Jenner" last="Jenner">Jenner</name><name sortKey="Watts, Paul M" sort="Watts, Paul M" uniqKey="Watts P" first="Paul M." last="Watts">Paul M. Watts</name><name sortKey="Watts, Paul M" sort="Watts, Paul M" uniqKey="Watts P" first="Paul M." last="Watts">Paul M. Watts</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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