Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study
Identifieur interne : 000777 ( PascalFrancis/Corpus ); précédent : 000776; suivant : 000778Herbicide 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. GolbeSource :
- Neurology [ 0028-3878 ] ; 2006.
Descripteurs français
- Pascal (Inist)
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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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NO : | PASCAL 07-0076731 INIST |
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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:07-0076731Le document en format XML
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<author><name sortKey="Sun, M" sort="Sun, M" uniqKey="Sun M" first="M." last="Sun">M. Sun</name>
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<author><name sortKey="Parsian, A" sort="Parsian, A" uniqKey="Parsian A" first="A." last="Parsian">A. Parsian</name>
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<author><name sortKey="Litvan, I" sort="Litvan, I" uniqKey="Litvan I" first="I." last="Litvan">I. Litvan</name>
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<affiliation><inist:fA14 i1="20"><s1>Department of Neurology, General Regional Hospital Bolzano</s1>
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<author><name sortKey="Nicholson, G" sort="Nicholson, G" uniqKey="Nicholson G" first="G." last="Nicholson">G. Nicholson</name>
<affiliation><inist:fA14 i1="21"><s1>Neurology Department, University of Sydney ANZAC Research Institute, Concord Hospital</s1>
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<author><name sortKey="Burn, D J" sort="Burn, D J" uniqKey="Burn D" first="D. J." last="Burn">D. J. Burn</name>
<affiliation><inist:fA14 i1="22"><s1>Regional Neurosciences Centre, Newcastle General Hospital</s1>
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<author><name sortKey="Chinnery, P F" sort="Chinnery, P F" uniqKey="Chinnery P" first="P. F." last="Chinnery">P. F. Chinnery</name>
<affiliation><inist:fA14 i1="22"><s1>Regional Neurosciences Centre, Newcastle General Hospital</s1>
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<author><name sortKey="Vieregge, P" sort="Vieregge, P" uniqKey="Vieregge P" first="P." last="Vieregge">P. Vieregge</name>
<affiliation><inist:fA14 i1="23"><s1>Klinik fur Neurologie, Klinikum Lippe-Lemgo</s1>
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<affiliation><inist:fA14 i1="24"><s1>Department of Neurology, University of Kentucky College of Medicine</s1>
<s3>USA</s3>
<sZ>33 aut.</sZ>
<sZ>34 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Macdonald, M E" sort="Macdonald, M E" uniqKey="Macdonald M" first="M. E." last="Macdonald">M. E. Macdonald</name>
<affiliation><inist:fA14 i1="14"><s1>Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>19 aut.</sZ>
<sZ>35 aut.</sZ>
<sZ>36 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Gusella, J F" sort="Gusella, J F" uniqKey="Gusella J" first="J. F." last="Gusella">J. F. Gusella</name>
<affiliation><inist:fA14 i1="14"><s1>Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>19 aut.</sZ>
<sZ>35 aut.</sZ>
<sZ>36 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Myers, R H" sort="Myers, R H" uniqKey="Myers R" first="R. H." last="Myers">R. H. Myers</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Golbe, L I" sort="Golbe, L I" uniqKey="Golbe L" first="L. I." last="Golbe">L. I. Golbe</name>
<affiliation><inist:fA14 i1="08"><s1>Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School</s1>
<s2>New Brunswick, NJ</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
<sZ>38 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">INIST</idno>
<idno type="inist">07-0076731</idno>
<date when="2006">2006</date>
<idno type="stanalyst">PASCAL 07-0076731 INIST</idno>
<idno type="RBID">Pascal:07-0076731</idno>
<idno type="wicri:Area/PascalFrancis/Corpus">000777</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Herbicide exposure modifies GSTP1 haplotype association to parkinson onset age : The GenePD study</title>
<author><name sortKey="Wilk, J B" sort="Wilk, J B" uniqKey="Wilk J" first="J. B." last="Wilk">J. B. Wilk</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tobin, J E" sort="Tobin, J E" uniqKey="Tobin J" first="J. E." last="Tobin">J. E. Tobin</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="02"><s1>Department of Anatomy and Neurobiology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>2 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Suchowersky, O" sort="Suchowersky, O" uniqKey="Suchowersky O" first="O." last="Suchowersky">O. Suchowersky</name>
<affiliation><inist:fA14 i1="03"><s1>Departments of Clinical Neurosciences and Medical Genetics, University of Calgary</s1>
<s2>Calgary, Alberta</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Shill, H A" sort="Shill, H A" uniqKey="Shill H" first="H. A." last="Shill">H. A. Shill</name>
<affiliation><inist:fA14 i1="04"><s1>Muhammad Ali Parkinson Center, Barrow Neurological Institute</s1>
<s2>Phoenix, AZ</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Klein, C" sort="Klein, C" uniqKey="Klein C" first="C." last="Klein">C. Klein</name>
<affiliation><inist:fA14 i1="05"><s1>Department of Neurology, University of Lübeck</s1>
<s2>Lübeck</s2>
<s3>DEU</s3>
<sZ>5 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Wooten, G F" sort="Wooten, G F" uniqKey="Wooten G" first="G. F." last="Wooten">G. F. Wooten</name>
<affiliation><inist:fA14 i1="06"><s1>Department of Neurology, University of Virginia Health System</s1>
<s2>Charlottesville, VA</s2>
<s3>USA</s3>
<sZ>6 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Lew, M F" sort="Lew, M F" uniqKey="Lew M" first="M. F." last="Lew">M. F. Lew</name>
<affiliation><inist:fA14 i1="07"><s1>Department of Neurology, University of Southern California</s1>
<s2>Los Angeles, CA</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Mark, M H" sort="Mark, M H" uniqKey="Mark M" first="M. H." last="Mark">M. H. Mark</name>
<affiliation><inist:fA14 i1="08"><s1>Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School</s1>
<s2>New Brunswick, NJ</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
<sZ>38 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Guttman, M" sort="Guttman, M" uniqKey="Guttman M" first="M." last="Guttman">M. Guttman</name>
<affiliation><inist:fA14 i1="09"><s1>Department of Medicine, University of Toronto</s1>
<s2>Toronto</s2>
<s3>CAN</s3>
<sZ>9 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Watts, R L" sort="Watts, R L" uniqKey="Watts R" first="R. L." last="Watts">R. L. Watts</name>
<affiliation><inist:fA14 i1="10"><s1>Department of Neurology, University of Alabama at Birmingham</s1>
<s2>Birmingham, AL</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Singer, C" sort="Singer, C" uniqKey="Singer C" first="C." last="Singer">C. Singer</name>
<affiliation><inist:fA14 i1="11"><s1>Department of Neurology, University of Miami</s1>
<s2>Miami, FL</s2>
<s3>USA</s3>
<sZ>11 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Growdon, J H" sort="Growdon, J H" uniqKey="Growdon J" first="J. H." last="Growdon">J. H. Growdon</name>
<affiliation><inist:fA14 i1="12"><s1>Department of Neurology, Massachusetts General Hospital, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Latourelle, J C" sort="Latourelle, J C" uniqKey="Latourelle J" first="J. C." last="Latourelle">J. C. Latourelle</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Saint Hilaire, M H" sort="Saint Hilaire, M H" uniqKey="Saint Hilaire M" first="M. H." last="Saint-Hilaire">M. H. Saint-Hilaire</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Destefano, A L" sort="Destefano, A L" uniqKey="Destefano A" first="A. L." last="Destefano">A. L. Destefano</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="13"><s1>Department of Biostatistics, Boston University School of Public Health</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>15 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Prakash, R" sort="Prakash, R" uniqKey="Prakash R" first="R." last="Prakash">R. Prakash</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
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<sZ>17 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Williamson, S" sort="Williamson, S" uniqKey="Williamson S" first="S." last="Williamson">S. Williamson</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
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<sZ>18 aut.</sZ>
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<author><name sortKey="Berg, C J" sort="Berg, C J" uniqKey="Berg C" first="C. J." last="Berg">C. J. Berg</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
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<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sun, M" sort="Sun, M" uniqKey="Sun M" first="M." last="Sun">M. Sun</name>
<affiliation><inist:fA14 i1="14"><s1>Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>19 aut.</sZ>
<sZ>35 aut.</sZ>
<sZ>36 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Goldwurm, S" sort="Goldwurm, S" uniqKey="Goldwurm S" first="S." last="Goldwurm">S. Goldwurm</name>
<affiliation><inist:fA14 i1="15"><s1>Parkinson Institute, Istituti Clinici di Perfezionamento</s1>
<s2>Milano</s2>
<s3>ITA</s3>
<sZ>20 aut.</sZ>
<sZ>21 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Pezzoli, G" sort="Pezzoli, G" uniqKey="Pezzoli G" first="G." last="Pezzoli">G. Pezzoli</name>
<affiliation><inist:fA14 i1="15"><s1>Parkinson Institute, Istituti Clinici di Perfezionamento</s1>
<s2>Milano</s2>
<s3>ITA</s3>
<sZ>20 aut.</sZ>
<sZ>21 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Racette, B A" sort="Racette, B A" uniqKey="Racette B" first="B. A." last="Racette">B. A. Racette</name>
<affiliation><inist:fA14 i1="16"><s1>Department of Neurology, Washington University School of Medicine</s1>
<s2>Saint Louis, MO</s2>
<s3>USA</s3>
<sZ>22 aut.</sZ>
<sZ>23 aut.</sZ>
</inist:fA14>
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<author><name sortKey="Perlmutter, J S" sort="Perlmutter, J S" uniqKey="Perlmutter J" first="J. S." last="Perlmutter">J. S. Perlmutter</name>
<affiliation><inist:fA14 i1="16"><s1>Department of Neurology, Washington University School of Medicine</s1>
<s2>Saint Louis, MO</s2>
<s3>USA</s3>
<sZ>22 aut.</sZ>
<sZ>23 aut.</sZ>
</inist:fA14>
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<author><name sortKey="Parsian, A" sort="Parsian, A" uniqKey="Parsian A" first="A." last="Parsian">A. Parsian</name>
<affiliation><inist:fA14 i1="17"><s1>Department of Pediatrics, Human Genomics Laboratories, University of Arkansas for Medical Sciences</s1>
<s2>AR</s2>
<s3>USA</s3>
<sZ>24 aut.</sZ>
</inist:fA14>
</affiliation>
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<author><name sortKey="Baker, K B" sort="Baker, K B" uniqKey="Baker K" first="K. B." last="Baker">K. B. Baker</name>
<affiliation><inist:fA14 i1="18"><s1>Departments of Neurology and Neuroscience, Cleveland Clinic Foundation</s1>
<s2>Cleveland, OH</s2>
<s3>USA</s3>
<sZ>25 aut.</sZ>
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</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Giroux, M L" sort="Giroux, M L" uniqKey="Giroux M" first="M. L." last="Giroux">M. L. Giroux</name>
<affiliation><inist:fA14 i1="18"><s1>Departments of Neurology and Neuroscience, Cleveland Clinic Foundation</s1>
<s2>Cleveland, OH</s2>
<s3>USA</s3>
<sZ>25 aut.</sZ>
<sZ>26 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Litvan, I" sort="Litvan, I" uniqKey="Litvan I" first="I." last="Litvan">I. Litvan</name>
<affiliation><inist:fA14 i1="19"><s1>Department of Neurology, University of Louisville School of Medicine</s1>
<s2>Louisville, KY</s2>
<s3>USA</s3>
<sZ>27 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Pramstaller, P P" sort="Pramstaller, P P" uniqKey="Pramstaller P" first="P. P." last="Pramstaller">P. P. Pramstaller</name>
<affiliation><inist:fA14 i1="20"><s1>Department of Neurology, General Regional Hospital Bolzano</s1>
<s2>Bolzano</s2>
<s3>ITA</s3>
<sZ>28 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Nicholson, G" sort="Nicholson, G" uniqKey="Nicholson G" first="G." last="Nicholson">G. Nicholson</name>
<affiliation><inist:fA14 i1="21"><s1>Neurology Department, University of Sydney ANZAC Research Institute, Concord Hospital</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>29 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Burn, D J" sort="Burn, D J" uniqKey="Burn D" first="D. J." last="Burn">D. J. Burn</name>
<affiliation><inist:fA14 i1="22"><s1>Regional Neurosciences Centre, Newcastle General Hospital</s1>
<s2>Newcastle upon Tyne</s2>
<s3>GBR</s3>
<sZ>30 aut.</sZ>
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</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Chinnery, P F" sort="Chinnery, P F" uniqKey="Chinnery P" first="P. F." last="Chinnery">P. F. Chinnery</name>
<affiliation><inist:fA14 i1="22"><s1>Regional Neurosciences Centre, Newcastle General Hospital</s1>
<s2>Newcastle upon Tyne</s2>
<s3>GBR</s3>
<sZ>30 aut.</sZ>
<sZ>31 aut.</sZ>
</inist:fA14>
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</author>
<author><name sortKey="Vieregge, P" sort="Vieregge, P" uniqKey="Vieregge P" first="P." last="Vieregge">P. Vieregge</name>
<affiliation><inist:fA14 i1="23"><s1>Klinik fur Neurologie, Klinikum Lippe-Lemgo</s1>
<s2>Lemgo</s2>
<s3>DEU</s3>
<sZ>32 aut.</sZ>
</inist:fA14>
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<author><name sortKey="Slevin, J T" sort="Slevin, J T" uniqKey="Slevin J" first="J. T." last="Slevin">J. T. Slevin</name>
<affiliation><inist:fA14 i1="24"><s1>Department of Neurology, University of Kentucky College of Medicine</s1>
<s3>USA</s3>
<sZ>33 aut.</sZ>
<sZ>34 aut.</sZ>
</inist:fA14>
</affiliation>
<affiliation><inist:fA14 i1="25"><s1>Veterans Affairs Medical Center</s1>
<s2>Lexington, KY</s2>
<s3>USA</s3>
<sZ>33 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Cambi, F" sort="Cambi, F" uniqKey="Cambi F" first="F." last="Cambi">F. Cambi</name>
<affiliation><inist:fA14 i1="24"><s1>Department of Neurology, University of Kentucky College of Medicine</s1>
<s3>USA</s3>
<sZ>33 aut.</sZ>
<sZ>34 aut.</sZ>
</inist:fA14>
</affiliation>
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<author><name sortKey="Macdonald, M E" sort="Macdonald, M E" uniqKey="Macdonald M" first="M. E." last="Macdonald">M. E. Macdonald</name>
<affiliation><inist:fA14 i1="14"><s1>Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>19 aut.</sZ>
<sZ>35 aut.</sZ>
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</inist:fA14>
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<author><name sortKey="Gusella, J F" sort="Gusella, J F" uniqKey="Gusella J" first="J. F." last="Gusella">J. F. Gusella</name>
<affiliation><inist:fA14 i1="14"><s1>Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School</s1>
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<s3>USA</s3>
<sZ>19 aut.</sZ>
<sZ>35 aut.</sZ>
<sZ>36 aut.</sZ>
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</affiliation>
</author>
<author><name sortKey="Myers, R H" sort="Myers, R H" uniqKey="Myers R" first="R. H." last="Myers">R. H. Myers</name>
<affiliation><inist:fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
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</author>
<author><name sortKey="Golbe, L I" sort="Golbe, L I" uniqKey="Golbe L" first="L. I." last="Golbe">L. I. Golbe</name>
<affiliation><inist:fA14 i1="08"><s1>Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School</s1>
<s2>New Brunswick, NJ</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
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<series><title level="j" type="main">Neurology</title>
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<idno type="ISSN">0028-3878</idno>
<imprint><date when="2006">2006</date>
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<term>Herbicide</term>
<term>Nervous system diseases</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term>
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<front><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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<fA11 i1="05" i2="1"><s1>KLEIN (C.)</s1>
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<fA11 i1="38" i2="1"><s1>GOLBE (L. I.)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Neurology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>37 aut.</sZ>
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<fA14 i1="02"><s1>Department of Anatomy and Neurobiology, Boston University School of Medicine</s1>
<s3>USA</s3>
<sZ>2 aut.</sZ>
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<fA14 i1="03"><s1>Departments of Clinical Neurosciences and Medical Genetics, University of Calgary</s1>
<s2>Calgary, Alberta</s2>
<s3>CAN</s3>
<sZ>3 aut.</sZ>
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<fA14 i1="04"><s1>Muhammad Ali Parkinson Center, Barrow Neurological Institute</s1>
<s2>Phoenix, AZ</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Neurology, University of Lübeck</s1>
<s2>Lübeck</s2>
<s3>DEU</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Neurology, University of Virginia Health System</s1>
<s2>Charlottesville, VA</s2>
<s3>USA</s3>
<sZ>6 aut.</sZ>
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<fA14 i1="07"><s1>Department of Neurology, University of Southern California</s1>
<s2>Los Angeles, CA</s2>
<s3>USA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Department of Neurology, University of Medicine and Dentistry of New Jersey-Robert Wood Johnson Medical School</s1>
<s2>New Brunswick, NJ</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
<sZ>38 aut.</sZ>
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<fA14 i1="09"><s1>Department of Medicine, University of Toronto</s1>
<s2>Toronto</s2>
<s3>CAN</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>Department of Neurology, University of Alabama at Birmingham</s1>
<s2>Birmingham, AL</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
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<fA14 i1="11"><s1>Department of Neurology, University of Miami</s1>
<s2>Miami, FL</s2>
<s3>USA</s3>
<sZ>11 aut.</sZ>
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<fA14 i1="12"><s1>Department of Neurology, Massachusetts General Hospital, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>12 aut.</sZ>
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<fA14 i1="13"><s1>Department of Biostatistics, Boston University School of Public Health</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>15 aut.</sZ>
</fA14>
<fA14 i1="14"><s1>Department of Molecular Neurogenetics Unit, Center for Human Genetic Research, Massachusetts General Hospital, Harvard Medical School</s1>
<s2>Boston, MA</s2>
<s3>USA</s3>
<sZ>19 aut.</sZ>
<sZ>35 aut.</sZ>
<sZ>36 aut.</sZ>
</fA14>
<fA14 i1="15"><s1>Parkinson Institute, Istituti Clinici di Perfezionamento</s1>
<s2>Milano</s2>
<s3>ITA</s3>
<sZ>20 aut.</sZ>
<sZ>21 aut.</sZ>
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<fA14 i1="16"><s1>Department of Neurology, Washington University School of Medicine</s1>
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<s3>USA</s3>
<sZ>22 aut.</sZ>
<sZ>23 aut.</sZ>
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<s2>AR</s2>
<s3>USA</s3>
<sZ>24 aut.</sZ>
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<fA14 i1="18"><s1>Departments of Neurology and Neuroscience, Cleveland Clinic Foundation</s1>
<s2>Cleveland, OH</s2>
<s3>USA</s3>
<sZ>25 aut.</sZ>
<sZ>26 aut.</sZ>
</fA14>
<fA14 i1="19"><s1>Department of Neurology, University of Louisville School of Medicine</s1>
<s2>Louisville, KY</s2>
<s3>USA</s3>
<sZ>27 aut.</sZ>
</fA14>
<fA14 i1="20"><s1>Department of Neurology, General Regional Hospital Bolzano</s1>
<s2>Bolzano</s2>
<s3>ITA</s3>
<sZ>28 aut.</sZ>
</fA14>
<fA14 i1="21"><s1>Neurology Department, University of Sydney ANZAC Research Institute, Concord Hospital</s1>
<s2>Sydney</s2>
<s3>AUS</s3>
<sZ>29 aut.</sZ>
</fA14>
<fA14 i1="22"><s1>Regional Neurosciences Centre, Newcastle General Hospital</s1>
<s2>Newcastle upon Tyne</s2>
<s3>GBR</s3>
<sZ>30 aut.</sZ>
<sZ>31 aut.</sZ>
</fA14>
<fA14 i1="23"><s1>Klinik fur Neurologie, Klinikum Lippe-Lemgo</s1>
<s2>Lemgo</s2>
<s3>DEU</s3>
<sZ>32 aut.</sZ>
</fA14>
<fA14 i1="24"><s1>Department of Neurology, University of Kentucky College of Medicine</s1>
<s3>USA</s3>
<sZ>33 aut.</sZ>
<sZ>34 aut.</sZ>
</fA14>
<fA14 i1="25"><s1>Veterans Affairs Medical Center</s1>
<s2>Lexington, KY</s2>
<s3>USA</s3>
<sZ>33 aut.</sZ>
</fA14>
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<fC01 i1="01" l="ENG"><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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<s5>01</s5>
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<fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
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<s5>09</s5>
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<s5>09</s5>
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<s5>09</s5>
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<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>
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