P450 enzymes and Parkinson's disease: the story so far.
Identifieur interne : 004480 ( PubMed/Corpus ); précédent : 004479; suivant : 004481P450 enzymes and Parkinson's disease: the story so far.
Auteurs : A G Riedl ; P M Watts ; P. Jenner ; C D MarsdenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1998.
English descriptors
- KwdEn :
- Animals, Cell Death (genetics), Cytochrome P-450 CYP1A1 (genetics), Cytochrome P-450 CYP2D6 (genetics), Cytochrome P-450 Enzyme System (genetics), DNA Mutational Analysis, Gene Expression Regulation, Enzymologic (physiology), Genotype, Humans, Parkinson Disease (genetics), Parkinson Disease (pathology), Phenotype, Polymorphism, Genetic (genetics), Substantia Nigra (pathology).
- 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.
DOI: 10.1002/mds.870130204
PubMed: 9539332
Links to Exploration step
pubmed:9539332Le document en format XML
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Jenner</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9539332</idno><idno type="pmid">9539332</idno><idno type="doi">10.1002/mds.870130204</idno><idno type="wicri:Area/PubMed/Corpus">004480</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">P450 enzymes and Parkinson's disease: the story so far.</title><author><name sortKey="Riedl, A G" sort="Riedl, A G" uniqKey="Riedl A" first="A G" last="Riedl">A G Riedl</name><affiliation><nlm:affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, King's College, London, England.</nlm:affiliation></affiliation></author><author><name sortKey="Watts, P M" sort="Watts, P M" uniqKey="Watts P" first="P M" last="Watts">P M Watts</name></author><author><name sortKey="Jenner, P" sort="Jenner, P" uniqKey="Jenner P" first="P" last="Jenner">P. Jenner</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</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="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</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>DNA Mutational Analysis</term><term>Gene Expression Regulation, Enzymologic (physiology)</term><term>Genotype</term><term>Humans</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Phenotype</term><term>Polymorphism, Genetic (genetics)</term><term>Substantia Nigra (pathology)</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></textClass></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><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9539332</PMID><DateCreated><Year>1998</Year><Month>06</Month><Day>15</Day></DateCreated><DateCompleted><Year>1998</Year><Month>06</Month><Day>15</Day></DateCompleted><DateRevised><Year>2009</Year><Month>09</Month><Day>29</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>13</Volume><Issue>2</Issue><PubDate><Year>1998</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>P450 enzymes and Parkinson's disease: the story so far.</ArticleTitle><Pagination><MedlinePgn>212-20</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Riedl</LastName><ForeName>A G</ForeName><Initials>AG</Initials><AffiliationInfo><Affiliation>Neurodegenerative Diseases Research Centre, Pharmacology Group, King's College, London, England.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Watts</LastName><ForeName>P M</ForeName><Initials>PM</Initials></Author><Author ValidYN="Y"><LastName>Jenner</LastName><ForeName>P</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Marsden</LastName><ForeName>C D</ForeName><Initials>CD</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Wellcome Trust</Agency><Country>United Kingdom</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>9035-51-2</RegistryNumber><NameOfSubstance UI="D003577">Cytochrome P-450 Enzyme System</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="D019363">Cytochrome P-450 CYP1A1</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.14.14.1</RegistryNumber><NameOfSubstance UI="D019389">Cytochrome P-450 CYP2D6</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000818">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016923">Cell Death</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019363">Cytochrome P-450 CYP1A1</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019389">Cytochrome P-450 CYP2D6</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003577">Cytochrome P-450 Enzyme System</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004252">DNA Mutational Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015971">Gene Expression Regulation, Enzymologic</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005838">Genotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010641">Phenotype</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011110">Polymorphism, Genetic</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013378">Substantia Nigra</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading></MeshHeadingList><NumberOfReferences>91</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1998</Year><Month>4</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1998</Year><Month>4</Month><Day>16</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1998</Year><Month>4</Month><Day>16</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9539332</ArticleId><ArticleId IdType="doi">10.1002/mds.870130204</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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