A case-control study of Parkinson's disease and tobacco use: Gene-tobacco interactions
A case‐control study of genetic, environmental, and occupational risk factors for Parkinson's disease (PD) was carried out in five European countries (Italy, Malta, Romania, Scotland, and Sweden) to explore the possible contribution of interactions among host and environmental factors in sporad...
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| Veröffentlicht in: | Movement disorders 2010-05, Vol.25 (7), p.912-919 |
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| creator | De Palma, Giuseppe Dick, Finlay D. Calzetti, Stefano Scott, Neil W. Prescott, Gordon J. Osborne, Aileen Haites, Neva Mozzoni, Paola Negrotti, Anna Scaglioni, Augusto Mutti, Antonio |
| description | A case‐control study of genetic, environmental, and occupational risk factors for Parkinson's disease (PD) was carried out in five European countries (Italy, Malta, Romania, Scotland, and Sweden) to explore the possible contribution of interactions among host and environmental factors in sporadic PD. Whereas smoking habits confirmed its negative association with PD, a possible modulatory role of genetic polymorphisms was investigated to obtain further mechanistic insights. We recruited 767 cases of PD and 1989 age‐matched and gender‐matched controls. Participants completed an interviewer‐administered questionnaire including the history of smoking habits. The polymorphisms of genes involved either in metabolism of compounds contained in tobacco smoke (CYP2D6, CYP1B1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, SOD2, EPHX and NAT2) or in dopaminergic neurotransmission (MAOA, MAOB, DAT1 and DRD2) were characterized by PCR based methods on genomic DNA. We found evidence of statistically significant gene‐tobacco interaction for GSTM1, NAT2, and GSTP1, the negative association between tobacco smoking and PD being significantly enhanced in subjects expressing GSTM1‐1 activity, in NAT2 fast acetylators, and in those with the GSTP1*B*C haplotype. Owing to the retrospective design of the study, these results require confirmation. © 2010 Movement Disorder Society |
| doi_str_mv | 10.1002/mds.22980 |
| format | Article |
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Whereas smoking habits confirmed its negative association with PD, a possible modulatory role of genetic polymorphisms was investigated to obtain further mechanistic insights. We recruited 767 cases of PD and 1989 age‐matched and gender‐matched controls. Participants completed an interviewer‐administered questionnaire including the history of smoking habits. The polymorphisms of genes involved either in metabolism of compounds contained in tobacco smoke (CYP2D6, CYP1B1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, SOD2, EPHX and NAT2) or in dopaminergic neurotransmission (MAOA, MAOB, DAT1 and DRD2) were characterized by PCR based methods on genomic DNA. We found evidence of statistically significant gene‐tobacco interaction for GSTM1, NAT2, and GSTP1, the negative association between tobacco smoking and PD being significantly enhanced in subjects expressing GSTM1‐1 activity, in NAT2 fast acetylators, and in those with the GSTP1*B*C haplotype. Owing to the retrospective design of the study, these results require confirmation. © 2010 Movement Disorder Society</description><identifier>ISSN: 0885-3185</identifier><identifier>EISSN: 1531-8257</identifier><identifier>DOI: 10.1002/mds.22980</identifier><identifier>PMID: 20461808</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Aged ; Biological and medical sciences ; Case-Control Studies ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. 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Disord</addtitle><description>A case‐control study of genetic, environmental, and occupational risk factors for Parkinson's disease (PD) was carried out in five European countries (Italy, Malta, Romania, Scotland, and Sweden) to explore the possible contribution of interactions among host and environmental factors in sporadic PD. Whereas smoking habits confirmed its negative association with PD, a possible modulatory role of genetic polymorphisms was investigated to obtain further mechanistic insights. We recruited 767 cases of PD and 1989 age‐matched and gender‐matched controls. Participants completed an interviewer‐administered questionnaire including the history of smoking habits. The polymorphisms of genes involved either in metabolism of compounds contained in tobacco smoke (CYP2D6, CYP1B1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, SOD2, EPHX and NAT2) or in dopaminergic neurotransmission (MAOA, MAOB, DAT1 and DRD2) were characterized by PCR based methods on genomic DNA. We found evidence of statistically significant gene‐tobacco interaction for GSTM1, NAT2, and GSTP1, the negative association between tobacco smoking and PD being significantly enhanced in subjects expressing GSTM1‐1 activity, in NAT2 fast acetylators, and in those with the GSTP1*B*C haplotype. Owing to the retrospective design of the study, these results require confirmation. © 2010 Movement Disorder Society</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Case-Control Studies</subject><subject>Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases</subject><subject>Female</subject><subject>Gene Expression - genetics</subject><subject>gene-environment interactions</subject><subject>genetic polymorphism</subject><subject>Genotype</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Occupational Exposure - adverse effects</subject><subject>Parkinson Disease - epidemiology</subject><subject>Parkinson's disease</subject><subject>Polymerase Chain Reaction</subject><subject>Polymorphism, Genetic - genetics</subject><subject>tobacco smoking</subject><subject>Tobacco Use Disorder - epidemiology</subject><subject>Tobacco Use Disorder - genetics</subject><issn>0885-3185</issn><issn>1531-8257</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0U1v1DAQBmALgehSOPAHkC-o4pDWH3Fic6sKXRBtqfi-WbYzkQJZu_Ukavff47K75YQ4WbaemdG8JuQ5Z4ecMXG06vBQCKPZA7LgSvJKC9U-JAumtaok12qPPEH8yRjnijePyZ5gdcM10wvy7ZgGh1CFFKecRorT3K1p6umly7-GiCkeIO0GhIKoix2dknchJDojvKZLiFDtXoY4QXZhGlLEp-RR70aEZ9tzn3w9ffvl5F119nH5_uT4rAq1Yazyxiile-YbB7oTnjvV9Yob40Mwum5BqA58o3hv7u5GGGkU09zXAFw5L_fJwabvVU7XM-BkVwMGGEcXIc1oW1UrVSIx_5dSqhJP2xb5aiNDTogZenuVh5XLa8uZvcvblrztn7yLfbHtOvsVdPdyF3ABL7fAYXBjn10MA_51omxZS17c0cbdDCOs_z3Rnr_5vBtdbSoGnOD2vqJ8m21a2Sr7_WJplz8uP9SfTs_thfwN4xKlIg</recordid><startdate>20100515</startdate><enddate>20100515</enddate><creator>De Palma, Giuseppe</creator><creator>Dick, Finlay D.</creator><creator>Calzetti, Stefano</creator><creator>Scott, Neil W.</creator><creator>Prescott, Gordon J.</creator><creator>Osborne, Aileen</creator><creator>Haites, Neva</creator><creator>Mozzoni, Paola</creator><creator>Negrotti, Anna</creator><creator>Scaglioni, Augusto</creator><creator>Mutti, Antonio</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20100515</creationdate><title>A case-control study of Parkinson's disease and tobacco use: Gene-tobacco interactions</title><author>De Palma, Giuseppe ; Dick, Finlay D. ; Calzetti, Stefano ; Scott, Neil W. ; Prescott, Gordon J. ; Osborne, Aileen ; Haites, Neva ; Mozzoni, Paola ; Negrotti, Anna ; Scaglioni, Augusto ; Mutti, Antonio</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4900-b99558f0b6ae8d2b1a5df5199bcc9847e25deb651f9c984929395081b4ee15ab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Case-Control Studies</topic><topic>Degenerative and inherited degenerative diseases of the nervous system. 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Prion diseases</topic><topic>Female</topic><topic>Gene Expression - genetics</topic><topic>gene-environment interactions</topic><topic>genetic polymorphism</topic><topic>Genotype</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Occupational Exposure - adverse effects</topic><topic>Parkinson Disease - epidemiology</topic><topic>Parkinson's disease</topic><topic>Polymerase Chain Reaction</topic><topic>Polymorphism, Genetic - genetics</topic><topic>tobacco smoking</topic><topic>Tobacco Use Disorder - epidemiology</topic><topic>Tobacco Use Disorder - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>De Palma, Giuseppe</creatorcontrib><creatorcontrib>Dick, Finlay D.</creatorcontrib><creatorcontrib>Calzetti, Stefano</creatorcontrib><creatorcontrib>Scott, Neil W.</creatorcontrib><creatorcontrib>Prescott, Gordon J.</creatorcontrib><creatorcontrib>Osborne, Aileen</creatorcontrib><creatorcontrib>Haites, Neva</creatorcontrib><creatorcontrib>Mozzoni, Paola</creatorcontrib><creatorcontrib>Negrotti, Anna</creatorcontrib><creatorcontrib>Scaglioni, Augusto</creatorcontrib><creatorcontrib>Mutti, Antonio</creatorcontrib><creatorcontrib>Geoparkinson Study Group</creatorcontrib><creatorcontrib>On Behalf of the Geoparkinson Study Group</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Movement disorders</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>De Palma, Giuseppe</au><au>Dick, Finlay D.</au><au>Calzetti, Stefano</au><au>Scott, Neil W.</au><au>Prescott, Gordon J.</au><au>Osborne, Aileen</au><au>Haites, Neva</au><au>Mozzoni, Paola</au><au>Negrotti, Anna</au><au>Scaglioni, Augusto</au><au>Mutti, Antonio</au><aucorp>Geoparkinson Study Group</aucorp><aucorp>On Behalf of the Geoparkinson Study Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A case-control study of Parkinson's disease and tobacco use: Gene-tobacco interactions</atitle><jtitle>Movement disorders</jtitle><addtitle>Mov. Disord</addtitle><date>2010-05-15</date><risdate>2010</risdate><volume>25</volume><issue>7</issue><spage>912</spage><epage>919</epage><pages>912-919</pages><issn>0885-3185</issn><eissn>1531-8257</eissn><abstract>A case‐control study of genetic, environmental, and occupational risk factors for Parkinson's disease (PD) was carried out in five European countries (Italy, Malta, Romania, Scotland, and Sweden) to explore the possible contribution of interactions among host and environmental factors in sporadic PD. Whereas smoking habits confirmed its negative association with PD, a possible modulatory role of genetic polymorphisms was investigated to obtain further mechanistic insights. We recruited 767 cases of PD and 1989 age‐matched and gender‐matched controls. Participants completed an interviewer‐administered questionnaire including the history of smoking habits. The polymorphisms of genes involved either in metabolism of compounds contained in tobacco smoke (CYP2D6, CYP1B1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, SOD2, EPHX and NAT2) or in dopaminergic neurotransmission (MAOA, MAOB, DAT1 and DRD2) were characterized by PCR based methods on genomic DNA. We found evidence of statistically significant gene‐tobacco interaction for GSTM1, NAT2, and GSTP1, the negative association between tobacco smoking and PD being significantly enhanced in subjects expressing GSTM1‐1 activity, in NAT2 fast acetylators, and in those with the GSTP1*B*C haplotype. Owing to the retrospective design of the study, these results require confirmation. © 2010 Movement Disorder Society</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20461808</pmid><doi>10.1002/mds.22980</doi><tpages>8</tpages></addata></record> |
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| subjects | Aged Biological and medical sciences Case-Control Studies Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Female Gene Expression - genetics gene-environment interactions genetic polymorphism Genotype Humans Male Medical sciences Neurology Occupational Exposure - adverse effects Parkinson Disease - epidemiology Parkinson's disease Polymerase Chain Reaction Polymorphism, Genetic - genetics tobacco smoking Tobacco Use Disorder - epidemiology Tobacco Use Disorder - genetics |
| title | A case-control study of Parkinson's disease and tobacco use: Gene-tobacco interactions |
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