La maladie de Parkinson au Canada (serveur d'exploration)

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Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study

Identifieur interne : 000777 ( PascalFrancis/Corpus ); précédent : 000776; suivant : 000778

Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study

Auteurs : J. B. Wilk ; J. E. Tobin ; O. Suchowersky ; H. A. Shill ; C. Klein ; G. F. Wooten ; M. F. Lew ; M. H. Mark ; M. Guttman ; R. L. Watts ; C. Singer ; J. H. Growdon ; J. C. Latourelle ; M. H. Saint-Hilaire ; A. L. Destefano ; R. Prakash ; S. Williamson ; C. J. Berg ; M. Sun ; S. Goldwurm ; G. Pezzoli ; B. A. Racette ; J. S. Perlmutter ; A. Parsian ; K. B. Baker ; M. L. Giroux ; I. Litvan ; P. P. Pramstaller ; G. Nicholson ; D. J. Burn ; P. F. Chinnery ; P. Vieregge ; J. T. Slevin ; F. Cambi ; M. E. Macdonald ; J. F. Gusella ; R. H. Myers ; L. I. Golbe

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RBID : Pascal:07-0076731

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English descriptors

Abstract

Background: Polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson disease (PD) with exposure to pesticides. Using the GenePD Study sample of familial PD cases, we explored whether GSTP1 polymorphisms were associated with the age at onset of PD symptoms and whether that relation was modified by exposure to herbicides. Methods: Seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with PD onset age in men in three strata: no exposure to herbicides, residential exposure to herbicides, and occupational exposure to herbicides. Haplotypes were similarly evaluated in stratified analyses. Results: Three SNPs were associated with PD onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of PD onset age across the herbicide exposure groups. Haplotype results also provided evidence that the relation between GSTP1 and onset age is modified by herbicide exposure. One haplotype was associated with an approximately 8-years-earlier onset in the occupationally exposed group and a 2.8-years-later onset in the nonexposed group. Conclusions: Herbicide exposure may be an effect modifier of the relation between glutathione S-transferase pi gene polymorphisms and onset age in familial PD.

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Pour connaître la documentation sur le format Inist Standard.

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A08 01  1  ENG  @1 Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study
A11 01  1    @1 WILK (J. B.)
A11 02  1    @1 TOBIN (J. E.)
A11 03  1    @1 SUCHOWERSKY (O.)
A11 04  1    @1 SHILL (H. A.)
A11 05  1    @1 KLEIN (C.)
A11 06  1    @1 WOOTEN (G. F.)
A11 07  1    @1 LEW (M. F.)
A11 08  1    @1 MARK (M. H.)
A11 09  1    @1 GUTTMAN (M.)
A11 10  1    @1 WATTS (R. L.)
A11 11  1    @1 SINGER (C.)
A11 12  1    @1 GROWDON (J. H.)
A11 13  1    @1 LATOURELLE (J. C.)
A11 14  1    @1 SAINT-HILAIRE (M. H.)
A11 15  1    @1 DESTEFANO (A. L.)
A11 16  1    @1 PRAKASH (R.)
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A11 21  1    @1 PEZZOLI (G.)
A11 22  1    @1 RACETTE (B. A.)
A11 23  1    @1 PERLMUTTER (J. S.)
A11 24  1    @1 PARSIAN (A.)
A11 25  1    @1 BAKER (K. B.)
A11 26  1    @1 GIROUX (M. L.)
A11 27  1    @1 LITVAN (I.)
A11 28  1    @1 PRAMSTALLER (P. P.)
A11 29  1    @1 NICHOLSON (G.)
A11 30  1    @1 BURN (D. J.)
A11 31  1    @1 CHINNERY (P. F.)
A11 32  1    @1 VIEREGGE (P.)
A11 33  1    @1 SLEVIN (J. T.)
A11 34  1    @1 CAMBI (F.)
A11 35  1    @1 MACDONALD (M. E.)
A11 36  1    @1 GUSELLA (J. F.)
A11 37  1    @1 MYERS (R. H.)
A11 38  1    @1 GOLBE (L. I.)
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A14 02      @1 Department of Anatomy and Neurobiology, Boston University School of Medicine @3 USA @Z 2 aut.
A14 03      @1 Departments of Clinical Neurosciences and Medical Genetics, University of Calgary @2 Calgary, Alberta @3 CAN @Z 3 aut.
A14 04      @1 Muhammad Ali Parkinson Center, Barrow Neurological Institute @2 Phoenix, AZ @3 USA @Z 4 aut.
A14 05      @1 Department of Neurology, University of Lübeck @2 Lübeck @3 DEU @Z 5 aut.
A14 06      @1 Department of Neurology, University of Virginia Health System @2 Charlottesville, VA @3 USA @Z 6 aut.
A14 07      @1 Department of Neurology, University of Southern California @2 Los Angeles, CA @3 USA @Z 7 aut.
A14 08      @1 Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School @2 New Brunswick, NJ @3 USA @Z 8 aut. @Z 38 aut.
A14 09      @1 Department of Medicine, University of Toronto @2 Toronto @3 CAN @Z 9 aut.
A14 10      @1 Department of Neurology, University of Alabama at Birmingham @2 Birmingham, AL @3 USA @Z 10 aut.
A14 11      @1 Department of Neurology, University of Miami @2 Miami, FL @3 USA @Z 11 aut.
A14 12      @1 Department of Neurology, Massachusetts General Hospital, Harvard Medical School @2 Boston, MA @3 USA @Z 12 aut.
A14 13      @1 Department of Biostatistics, Boston University School of Public Health @2 Boston, MA @3 USA @Z 15 aut.
A14 14      @1 Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School @2 Boston, MA @3 USA @Z 19 aut. @Z 35 aut. @Z 36 aut.
A14 15      @1 Parkinson Institute, Istituti Clinici di Perfezionamento @2 Milano @3 ITA @Z 20 aut. @Z 21 aut.
A14 16      @1 Department of Neurology, Washington University School of Medicine @2 Saint Louis, MO @3 USA @Z 22 aut. @Z 23 aut.
A14 17      @1 Department of Pediatrics, Human Genomics Laboratories, University of Arkansas for Medical Sciences @2 AR @3 USA @Z 24 aut.
A14 18      @1 Departments of Neurology and Neuroscience, Cleveland Clinic Foundation @2 Cleveland, OH @3 USA @Z 25 aut. @Z 26 aut.
A14 19      @1 Department of Neurology, University of Louisville School of Medicine @2 Louisville, KY @3 USA @Z 27 aut.
A14 20      @1 Department of Neurology, General Regional Hospital Bolzano @2 Bolzano @3 ITA @Z 28 aut.
A14 21      @1 Neurology Department, University of Sydney ANZAC Research Institute, Concord Hospital @2 Sydney @3 AUS @Z 29 aut.
A14 22      @1 Regional Neurosciences Centre, Newcastle General Hospital @2 Newcastle upon Tyne @3 GBR @Z 30 aut. @Z 31 aut.
A14 23      @1 Klinik fur Neurologie, Klinikum Lippe-Lemgo @2 Lemgo @3 DEU @Z 32 aut.
A14 24      @1 Department of Neurology, University of Kentucky College of Medicine @3 USA @Z 33 aut. @Z 34 aut.
A14 25      @1 Veterans Affairs Medical Center @2 Lexington, KY @3 USA @Z 33 aut.
A20       @1 2206-2210
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A23 01      @0 ENG
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A44       @0 0000 @1 © 2007 INIST-CNRS. All rights reserved.
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A47 01  1    @0 07-0076731
A60       @1 P
A61       @0 A
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C01 01    ENG  @0 Background: Polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson disease (PD) with exposure to pesticides. Using the GenePD Study sample of familial PD cases, we explored whether GSTP1 polymorphisms were associated with the age at onset of PD symptoms and whether that relation was modified by exposure to herbicides. Methods: Seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with PD onset age in men in three strata: no exposure to herbicides, residential exposure to herbicides, and occupational exposure to herbicides. Haplotypes were similarly evaluated in stratified analyses. Results: Three SNPs were associated with PD onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of PD onset age across the herbicide exposure groups. Haplotype results also provided evidence that the relation between GSTP1 and onset age is modified by herbicide exposure. One haplotype was associated with an approximately 8-years-earlier onset in the occupationally exposed group and a 2.8-years-later onset in the nonexposed group. Conclusions: Herbicide exposure may be an effect modifier of the relation between glutathione S-transferase pi gene polymorphisms and onset age in familial PD.
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C02 03  X    @0 002B17F
C03 01  X  FRE  @0 Système nerveux pathologie @5 01
C03 01  X  ENG  @0 Nervous system diseases @5 01
C03 01  X  SPA  @0 Sistema nervioso patología @5 01
C03 02  X  FRE  @0 Herbicide @5 09
C03 02  X  ENG  @0 Herbicide @5 09
C03 02  X  SPA  @0 Herbicida @5 09
C03 03  X  FRE  @0 Haplotype @5 10
C03 03  X  ENG  @0 Haplotype @5 10
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C07 01  X  SPA  @0 Plaguicida
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N44 01      @1 OTO
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Format Inist (serveur)

NO : PASCAL 07-0076731 INIST
ET : Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study
AU : WILK (J. B.); TOBIN (J. E.); SUCHOWERSKY (O.); SHILL (H. A.); KLEIN (C.); WOOTEN (G. F.); LEW (M. F.); MARK (M. H.); GUTTMAN (M.); WATTS (R. L.); SINGER (C.); GROWDON (J. H.); LATOURELLE (J. C.); SAINT-HILAIRE (M. H.); DESTEFANO (A. L.); PRAKASH (R.); WILLIAMSON (S.); BERG (C. J.); SUN (M.); GOLDWURM (S.); PEZZOLI (G.); RACETTE (B. A.); PERLMUTTER (J. S.); PARSIAN (A.); BAKER (K. B.); GIROUX (M. L.); LITVAN (I.); PRAMSTALLER (P. P.); NICHOLSON (G.); BURN (D. J.); CHINNERY (P. F.); VIEREGGE (P.); SLEVIN (J. T.); CAMBI (F.); MACDONALD (M. E.); GUSELLA (J. F.); MYERS (R. H.); GOLBE (L. I.)
AF : Department of Neurology, Boston University School of Medicine/Etats-Unis (1 aut., 2 aut., 13 aut., 14 aut., 15 aut., 16 aut., 17 aut., 18 aut., 37 aut.); Department of Anatomy and Neurobiology, Boston University School of Medicine/Etats-Unis (2 aut.); Departments of Clinical Neurosciences and Medical Genetics, University of Calgary/Calgary, Alberta/Canada (3 aut.); Muhammad Ali Parkinson Center, Barrow Neurological Institute/Phoenix, AZ/Etats-Unis (4 aut.); Department of Neurology, University of Lübeck/Lübeck/Allemagne (5 aut.); Department of Neurology, University of Virginia Health System/Charlottesville, VA/Etats-Unis (6 aut.); Department of Neurology, University of Southern California/Los Angeles, CA/Etats-Unis (7 aut.); Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School/New Brunswick, NJ/Etats-Unis (8 aut., 38 aut.); Department of Medicine, University of Toronto/Toronto/Canada (9 aut.); Department of Neurology, University of Alabama at Birmingham/Birmingham, AL/Etats-Unis (10 aut.); Department of Neurology, University of Miami/Miami, FL/Etats-Unis (11 aut.); Department of Neurology, Massachusetts General Hospital, Harvard Medical School/Boston, MA/Etats-Unis (12 aut.); Department of Biostatistics, Boston University School of Public Health/Boston, MA/Etats-Unis (15 aut.); Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School/Boston, MA/Etats-Unis (19 aut., 35 aut., 36 aut.); Parkinson Institute, Istituti Clinici di Perfezionamento/Milano/Italie (20 aut., 21 aut.); Department of Neurology, Washington University School of Medicine/Saint Louis, MO/Etats-Unis (22 aut., 23 aut.); Department of Pediatrics, Human Genomics Laboratories, University of Arkansas for Medical Sciences/AR/Etats-Unis (24 aut.); Departments of Neurology and Neuroscience, Cleveland Clinic Foundation/Cleveland, OH/Etats-Unis (25 aut., 26 aut.); Department of Neurology, University of Louisville School of Medicine/Louisville, KY/Etats-Unis (27 aut.); Department of Neurology, General Regional Hospital Bolzano/Bolzano/Italie (28 aut.); Neurology Department, University of Sydney ANZAC Research Institute, Concord Hospital/Sydney/Australie (29 aut.); Regional Neurosciences Centre, Newcastle General Hospital/Newcastle upon Tyne/Royaume-Uni (30 aut., 31 aut.); Klinik fur Neurologie, Klinikum Lippe-Lemgo/Lemgo/Allemagne (32 aut.); Department of Neurology, University of Kentucky College of Medicine/Etats-Unis (33 aut., 34 aut.); Veterans Affairs Medical Center/Lexington, KY/Etats-Unis (33 aut.)
DT : Publication en série; Niveau analytique
SO : Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 2006; Vol. 67; No. 12; Pp. 2206-2210; Bibl. 25 ref.
LA : Anglais
EA : Background: Polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson disease (PD) with exposure to pesticides. Using the GenePD Study sample of familial PD cases, we explored whether GSTP1 polymorphisms were associated with the age at onset of PD symptoms and whether that relation was modified by exposure to herbicides. Methods: Seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with PD onset age in men in three strata: no exposure to herbicides, residential exposure to herbicides, and occupational exposure to herbicides. Haplotypes were similarly evaluated in stratified analyses. Results: Three SNPs were associated with PD onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of PD onset age across the herbicide exposure groups. Haplotype results also provided evidence that the relation between GSTP1 and onset age is modified by herbicide exposure. One haplotype was associated with an approximately 8-years-earlier onset in the occupationally exposed group and a 2.8-years-later onset in the nonexposed group. Conclusions: Herbicide exposure may be an effect modifier of the relation between glutathione S-transferase pi gene polymorphisms and onset age in familial PD.
CC : 002B17; 002B17G; 002B17F
FD : Système nerveux pathologie; Herbicide; Haplotype
FG : Pesticide
ED : Nervous system diseases; Herbicide; Haplotype
EG : Pesticides
SD : Sistema nervioso patología; Herbicida; Haplotipo
LO : INIST-6345.354000145253990210
ID : 07-0076731

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Pascal:07-0076731

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<s1>Department of Neurology, University of Louisville School of Medicine</s1>
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<s1>Department of Neurology, General Regional Hospital Bolzano</s1>
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<s1>Klinik fur Neurologie, Klinikum Lippe-Lemgo</s1>
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<s1>Veterans Affairs Medical Center</s1>
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<s1>Department of Neurology, University of Kentucky College of Medicine</s1>
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<s1>Department of Neurology, Boston University School of Medicine</s1>
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<name sortKey="Golbe, L I" sort="Golbe, L I" uniqKey="Golbe L" first="L. I." last="Golbe">L. I. Golbe</name>
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<inist:fA14 i1="08">
<s1>Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School</s1>
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<title xml:lang="en" level="a">Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study</title>
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<name sortKey="Wilk, J B" sort="Wilk, J B" uniqKey="Wilk J" first="J. B." last="Wilk">J. B. Wilk</name>
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<inist:fA14 i1="01">
<s1>Department of Neurology, Boston University School of Medicine</s1>
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<name sortKey="Tobin, J E" sort="Tobin, J E" uniqKey="Tobin J" first="J. E." last="Tobin">J. E. Tobin</name>
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<inist:fA14 i1="01">
<s1>Department of Neurology, Boston University School of Medicine</s1>
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<inist:fA14 i1="02">
<s1>Department of Anatomy and Neurobiology, Boston University School of Medicine</s1>
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</affiliation>
</author>
<author>
<name sortKey="Suchowersky, O" sort="Suchowersky, O" uniqKey="Suchowersky O" first="O." last="Suchowersky">O. Suchowersky</name>
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<inist:fA14 i1="03">
<s1>Departments of Clinical Neurosciences and Medical Genetics, University of Calgary</s1>
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<name sortKey="Shill, H A" sort="Shill, H A" uniqKey="Shill H" first="H. A." last="Shill">H. A. Shill</name>
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<inist:fA14 i1="04">
<s1>Muhammad Ali Parkinson Center, Barrow Neurological Institute</s1>
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<inist:fA14 i1="05">
<s1>Department of Neurology, University of Lübeck</s1>
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<inist:fA14 i1="06">
<s1>Department of Neurology, University of Virginia Health System</s1>
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<s1>Department of Neurology, University of Southern California</s1>
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<s1>Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School</s1>
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<inist:fA14 i1="09">
<s1>Department of Medicine, University of Toronto</s1>
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<s1>Department of Neurology, University of Alabama at Birmingham</s1>
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<name sortKey="Williamson, S" sort="Williamson, S" uniqKey="Williamson S" first="S." last="Williamson">S. Williamson</name>
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<name sortKey="Berg, C J" sort="Berg, C J" uniqKey="Berg C" first="C. J." last="Berg">C. J. Berg</name>
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<name sortKey="Sun, M" sort="Sun, M" uniqKey="Sun M" first="M." last="Sun">M. Sun</name>
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<s1>Parkinson Institute, Istituti Clinici di Perfezionamento</s1>
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<s1>Parkinson Institute, Istituti Clinici di Perfezionamento</s1>
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<series>
<title level="j" type="main">Neurology</title>
<title level="j" type="abbreviated">Neurology</title>
<idno type="ISSN">0028-3878</idno>
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<date when="2006">2006</date>
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<term>Haplotype</term>
<term>Herbicide</term>
<term>Nervous system diseases</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Système nerveux pathologie</term>
<term>Herbicide</term>
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<div type="abstract" xml:lang="en">Background: Polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson disease (PD) with exposure to pesticides. Using the GenePD Study sample of familial PD cases, we explored whether GSTP1 polymorphisms were associated with the age at onset of PD symptoms and whether that relation was modified by exposure to herbicides. Methods: Seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with PD onset age in men in three strata: no exposure to herbicides, residential exposure to herbicides, and occupational exposure to herbicides. Haplotypes were similarly evaluated in stratified analyses. Results: Three SNPs were associated with PD onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of PD onset age across the herbicide exposure groups. Haplotype results also provided evidence that the relation between GSTP1 and onset age is modified by herbicide exposure. One haplotype was associated with an approximately 8-years-earlier onset in the occupationally exposed group and a 2.8-years-later onset in the nonexposed group. Conclusions: Herbicide exposure may be an effect modifier of the relation between glutathione S-transferase pi gene polymorphisms and onset age in familial PD.</div>
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<sZ>25 aut.</sZ>
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<s0>Background: Polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson disease (PD) with exposure to pesticides. Using the GenePD Study sample of familial PD cases, we explored whether GSTP1 polymorphisms were associated with the age at onset of PD symptoms and whether that relation was modified by exposure to herbicides. Methods: Seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with PD onset age in men in three strata: no exposure to herbicides, residential exposure to herbicides, and occupational exposure to herbicides. Haplotypes were similarly evaluated in stratified analyses. Results: Three SNPs were associated with PD onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of PD onset age across the herbicide exposure groups. Haplotype results also provided evidence that the relation between GSTP1 and onset age is modified by herbicide exposure. One haplotype was associated with an approximately 8-years-earlier onset in the occupationally exposed group and a 2.8-years-later onset in the nonexposed group. Conclusions: Herbicide exposure may be an effect modifier of the relation between glutathione S-transferase pi gene polymorphisms and onset age in familial PD.</s0>
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<s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B17G</s0>
</fC02>
<fC02 i1="03" i2="X">
<s0>002B17F</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Herbicide</s0>
<s5>09</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Herbicide</s0>
<s5>09</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Herbicida</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Haplotype</s0>
<s5>10</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Haplotype</s0>
<s5>10</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Haplotipo</s0>
<s5>10</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Pesticide</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Pesticides</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Plaguicida</s0>
</fC07>
<fN21>
<s1>050</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
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<NO>PASCAL 07-0076731 INIST</NO>
<ET>Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study</ET>
<AU>WILK (J. B.); TOBIN (J. E.); SUCHOWERSKY (O.); SHILL (H. A.); KLEIN (C.); WOOTEN (G. F.); LEW (M. F.); MARK (M. H.); GUTTMAN (M.); WATTS (R. L.); SINGER (C.); GROWDON (J. H.); LATOURELLE (J. C.); SAINT-HILAIRE (M. H.); DESTEFANO (A. L.); PRAKASH (R.); WILLIAMSON (S.); BERG (C. J.); SUN (M.); GOLDWURM (S.); PEZZOLI (G.); RACETTE (B. A.); PERLMUTTER (J. S.); PARSIAN (A.); BAKER (K. B.); GIROUX (M. L.); LITVAN (I.); PRAMSTALLER (P. P.); NICHOLSON (G.); BURN (D. J.); CHINNERY (P. F.); VIEREGGE (P.); SLEVIN (J. T.); CAMBI (F.); MACDONALD (M. E.); GUSELLA (J. F.); MYERS (R. H.); GOLBE (L. I.)</AU>
<AF>Department of Neurology, Boston University School of Medicine/Etats-Unis (1 aut., 2 aut., 13 aut., 14 aut., 15 aut., 16 aut., 17 aut., 18 aut., 37 aut.); Department of Anatomy and Neurobiology, Boston University School of Medicine/Etats-Unis (2 aut.); Departments of Clinical Neurosciences and Medical Genetics, University of Calgary/Calgary, Alberta/Canada (3 aut.); Muhammad Ali Parkinson Center, Barrow Neurological Institute/Phoenix, AZ/Etats-Unis (4 aut.); Department of Neurology, University of Lübeck/Lübeck/Allemagne (5 aut.); Department of Neurology, University of Virginia Health System/Charlottesville, VA/Etats-Unis (6 aut.); Department of Neurology, University of Southern California/Los Angeles, CA/Etats-Unis (7 aut.); Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School/New Brunswick, NJ/Etats-Unis (8 aut., 38 aut.); Department of Medicine, University of Toronto/Toronto/Canada (9 aut.); Department of Neurology, University of Alabama at Birmingham/Birmingham, AL/Etats-Unis (10 aut.); Department of Neurology, University of Miami/Miami, FL/Etats-Unis (11 aut.); Department of Neurology, Massachusetts General Hospital, Harvard Medical School/Boston, MA/Etats-Unis (12 aut.); Department of Biostatistics, Boston University School of Public Health/Boston, MA/Etats-Unis (15 aut.); Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School/Boston, MA/Etats-Unis (19 aut., 35 aut., 36 aut.); Parkinson Institute, Istituti Clinici di Perfezionamento/Milano/Italie (20 aut., 21 aut.); Department of Neurology, Washington University School of Medicine/Saint Louis, MO/Etats-Unis (22 aut., 23 aut.); Department of Pediatrics, Human Genomics Laboratories, University of Arkansas for Medical Sciences/AR/Etats-Unis (24 aut.); Departments of Neurology and Neuroscience, Cleveland Clinic Foundation/Cleveland, OH/Etats-Unis (25 aut., 26 aut.); Department of Neurology, University of Louisville School of Medicine/Louisville, KY/Etats-Unis (27 aut.); Department of Neurology, General Regional Hospital Bolzano/Bolzano/Italie (28 aut.); Neurology Department, University of Sydney ANZAC Research Institute, Concord Hospital/Sydney/Australie (29 aut.); Regional Neurosciences Centre, Newcastle General Hospital/Newcastle upon Tyne/Royaume-Uni (30 aut., 31 aut.); Klinik fur Neurologie, Klinikum Lippe-Lemgo/Lemgo/Allemagne (32 aut.); Department of Neurology, University of Kentucky College of Medicine/Etats-Unis (33 aut., 34 aut.); Veterans Affairs Medical Center/Lexington, KY/Etats-Unis (33 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Neurology; ISSN 0028-3878; Coden NEURAI; Etats-Unis; Da. 2006; Vol. 67; No. 12; Pp. 2206-2210; Bibl. 25 ref.</SO>
<LA>Anglais</LA>
<EA>Background: Polymorphisms in the glutathione S-transferase pi gene (GSTP1), encoding GSTP1-1, a detoxification enzyme, may increase the risk of Parkinson disease (PD) with exposure to pesticides. Using the GenePD Study sample of familial PD cases, we explored whether GSTP1 polymorphisms were associated with the age at onset of PD symptoms and whether that relation was modified by exposure to herbicides. Methods: Seven single-nucleotide polymorphisms (SNPs) were genotyped and tested for association with PD onset age in men in three strata: no exposure to herbicides, residential exposure to herbicides, and occupational exposure to herbicides. Haplotypes were similarly evaluated in stratified analyses. Results: Three SNPs were associated with PD onset age in the group of men occupationally exposed to herbicides. Three additional SNPs had significant trends for the association of PD onset age across the herbicide exposure groups. Haplotype results also provided evidence that the relation between GSTP1 and onset age is modified by herbicide exposure. One haplotype was associated with an approximately 8-years-earlier onset in the occupationally exposed group and a 2.8-years-later onset in the nonexposed group. Conclusions: Herbicide exposure may be an effect modifier of the relation between glutathione S-transferase pi gene polymorphisms and onset age in familial PD.</EA>
<CC>002B17; 002B17G; 002B17F</CC>
<FD>Système nerveux pathologie; Herbicide; Haplotype</FD>
<FG>Pesticide</FG>
<ED>Nervous system diseases; Herbicide; Haplotype</ED>
<EG>Pesticides</EG>
<SD>Sistema nervioso patología; Herbicida; Haplotipo</SD>
<LO>INIST-6345.354000145253990210</LO>
<ID>07-0076731</ID>
</server>
</inist>
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