Head Injury, Alpha-Synuclein Rep1, and Parkinson's Disease
Identifieur interne : 000232 ( PascalFrancis/Corpus ); précédent : 000231; suivant : 000233Head Injury, Alpha-Synuclein Rep1, and Parkinson's Disease
Auteurs : Samuel M. Goldman ; Freya Kamel ; G. Webster Ross ; Sarah A. Jewell ; Grace S. Bhudhikanok ; David Umbach ; Connie Marras ; Robert A. Hauser ; Joseph Jankovic ; Stewart A. Factor ; Susan Bressman ; Kelly E. Lyons ; Cheryl Meng ; Monica Korell ; Diana F. Roucoux ; Jane A. Hoppin ; Dale P. Sandler ; J. William Langston ; Caroline M. TannerSource :
- Annals of neurology [ 0364-5134 ] ; 2012.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Objective: To test the hypothesis that variability in SNCA Rep1, a polymorphic dinucleotide microsatellite in the promoter region of the gene encoding α-synuclein, modifies the association between head injury and Parkinson's disease (PD) risk. Methods: Participants in the Farming and Movement Evaluation (FAME) and the Study of Environmental Association and Risk of Parkinsonism using Case-Control Historical Interviews (SEARCH), 2 independent case-control studies, were genotyped for Rep1 and interviewed regarding head injuries with loss of consciousness or concussion prior to Parkinson's disease (PD) diagnosis. Logistic regression modeling adjusted for potential confounding variables and tested interaction between Rep1 genotype and head injury. Results: Consistent with prior reports, relative to medium-length Rep1, short Rep1 genotype was associated with reduced PD risk (pooled odds ratio [OR], 0.7; 95% confidence interval [CI], 0.5-0.9), and long Rep1 with increased risk (pooled OR, 1.4; 95% CI, 0.95-2.2). Overall, head injury was not significantly associated with PD (pooled OR, 1.3; 95% CI, 0.9-1.8). However, head injury was strongly associated with PD in those with long Rep1 (FAME OR, 5.4; 95% CI, 1.5-19; SEARCH OR, 2.3; 95% CI, 0.6-9.2; pooled OR, 3.5; 95% CI 1.4-9.2, p-interaction = 0.02). Individuals with both head injury and long Rep1 were diagnosed 4.9 years earlier than those with neither risk factor (p = 0.03). Interpretation: While head injury alone was not associated with PD risk, our data suggest head injury may initiate and/or accelerate neurodegeneration when levels of synuclein are high, as in those with Rep1 expansion. Given the high population frequency of head injury, independent verification of these results is essential.
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Pour connaître la documentation sur le format Inist Standard.
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Format Inist (serveur)
NO : | PASCAL 12-0075975 INIST |
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ET : | Head Injury, Alpha-Synuclein Rep1, and Parkinson's Disease |
AU : | GOLDMAN (Samuel M.); KAMEL (Freya); WEBSTER ROSS (G.); JEWELL (Sarah A.); BHUDHIKANOK (Grace S.); UMBACH (David); MARRAS (Connie); HAUSER (Robert A.); JANKOVIC (Joseph); FACTOR (Stewart A.); BRESSMAN (Susan); LYONS (Kelly E.); MENG (Cheryl); KORELL (Monica); ROUCOUX (Diana F.); HOPPIN (Jane A.); SANDLER (Dale P.); WILLIAM LANGSTON (J.); TANNER (Caroline M.) |
AF : | The Parkinson's Institute/Sunnyvale, CA/Etats-Unis (1 aut., 4 aut., 5 aut., 13 aut., 14 aut., 15 aut., 18 aut., 19 aut.); Epidemiology Branch/Etats-Unis (2 aut., 16 aut., 17 aut.); Biostatistics Branch, National Institute of Environmental Health Sciences, NIH, DHHS/Research Triangle Park, NC;/Etats-Unis (6 aut.); Veterans Affairs Pacific Islands Health Care System/Honolulu, HI/Etats-Unis (3 aut.); DZNE, German Center for Neurodegenerative Diseases/Bonn/Allemagne (4 aut.); Neurology, Toronto Western Hospital, University of Toronto/Toronto, Ontario/Canada (7 aut.); Department of Neurology, University of South Florida/Tampa, FL/Etats-Unis (8 aut.); Department of Neurology, Baylor College of Medicine/Houston, TX/Etats-Unis (9 aut.); Department of Neurology, Emory University School of Medicine/Atlanta, GA;/Etats-Unis (10 aut.); Department of Neurology, Beth Israel Medical Center/New York, NY/Etats-Unis (11 aut.); Department of Neurology, University of Kansas Medical Center/Kansas City, KS/Etats-Unis (12 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2012; Vol. 71; No. 1; Pp. 40-48; Bibl. 68 ref. |
LA : | Anglais |
EA : | Objective: To test the hypothesis that variability in SNCA Rep1, a polymorphic dinucleotide microsatellite in the promoter region of the gene encoding α-synuclein, modifies the association between head injury and Parkinson's disease (PD) risk. Methods: Participants in the Farming and Movement Evaluation (FAME) and the Study of Environmental Association and Risk of Parkinsonism using Case-Control Historical Interviews (SEARCH), 2 independent case-control studies, were genotyped for Rep1 and interviewed regarding head injuries with loss of consciousness or concussion prior to Parkinson's disease (PD) diagnosis. Logistic regression modeling adjusted for potential confounding variables and tested interaction between Rep1 genotype and head injury. Results: Consistent with prior reports, relative to medium-length Rep1, short Rep1 genotype was associated with reduced PD risk (pooled odds ratio [OR], 0.7; 95% confidence interval [CI], 0.5-0.9), and long Rep1 with increased risk (pooled OR, 1.4; 95% CI, 0.95-2.2). Overall, head injury was not significantly associated with PD (pooled OR, 1.3; 95% CI, 0.9-1.8). However, head injury was strongly associated with PD in those with long Rep1 (FAME OR, 5.4; 95% CI, 1.5-19; SEARCH OR, 2.3; 95% CI, 0.6-9.2; pooled OR, 3.5; 95% CI 1.4-9.2, p-interaction = 0.02). Individuals with both head injury and long Rep1 were diagnosed 4.9 years earlier than those with neither risk factor (p = 0.03). Interpretation: While head injury alone was not associated with PD risk, our data suggest head injury may initiate and/or accelerate neurodegeneration when levels of synuclein are high, as in those with Rep1 expansion. Given the high population frequency of head injury, independent verification of these results is essential. |
CC : | 002B17; 002B17G |
FD : | Traumatisme crânien; Maladie de Parkinson; Pathologie du système nerveux; Crânioencéphalique |
FG : | Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
ED : | Head trauma; Parkinson disease; Nervous system diseases; Craniocerebral |
EG : | Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
SD : | Traumatismo craneoencefálico; Parkinson enfermedad; Sistema nervioso patología; Craneoencefálico |
LO : | INIST-16555.354000508658160070 |
ID : | 12-0075975 |
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Pascal:12-0075975Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Head Injury, Alpha-Synuclein Rep1, and Parkinson's Disease</title>
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<author><name sortKey="Kamel, Freya" sort="Kamel, Freya" uniqKey="Kamel F" first="Freya" last="Kamel">Freya Kamel</name>
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<author><name sortKey="Webster Ross, G" sort="Webster Ross, G" uniqKey="Webster Ross G" first="G." last="Webster Ross">G. Webster Ross</name>
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<author><name sortKey="Jewell, Sarah A" sort="Jewell, Sarah A" uniqKey="Jewell S" first="Sarah A." last="Jewell">Sarah A. Jewell</name>
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<author><name sortKey="Bhudhikanok, Grace S" sort="Bhudhikanok, Grace S" uniqKey="Bhudhikanok G" first="Grace S." last="Bhudhikanok">Grace S. Bhudhikanok</name>
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<author><name sortKey="Umbach, David" sort="Umbach, David" uniqKey="Umbach D" first="David" last="Umbach">David Umbach</name>
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<author><name sortKey="Marras, Connie" sort="Marras, Connie" uniqKey="Marras C" first="Connie" last="Marras">Connie Marras</name>
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<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
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<author><name sortKey="Hauser, Robert A" sort="Hauser, Robert A" uniqKey="Hauser R" first="Robert A." last="Hauser">Robert A. Hauser</name>
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<author><name sortKey="Jankovic, Joseph" sort="Jankovic, Joseph" uniqKey="Jankovic J" first="Joseph" last="Jankovic">Joseph Jankovic</name>
<affiliation><inist:fA14 i1="08"><s1>Department of Neurology, Baylor College of Medicine</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
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<author><name sortKey="Factor, Stewart A" sort="Factor, Stewart A" uniqKey="Factor S" first="Stewart A." last="Factor">Stewart A. Factor</name>
<affiliation><inist:fA14 i1="09"><s1>Department of Neurology, Emory University School of Medicine</s1>
<s2>Atlanta, GA;</s2>
<s3>USA</s3>
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<author><name sortKey="Bressman, Susan" sort="Bressman, Susan" uniqKey="Bressman S" first="Susan" last="Bressman">Susan Bressman</name>
<affiliation><inist:fA14 i1="10"><s1>Department of Neurology, Beth Israel Medical Center</s1>
<s2>New York, NY</s2>
<s3>USA</s3>
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<author><name sortKey="Lyons, Kelly E" sort="Lyons, Kelly E" uniqKey="Lyons K" first="Kelly E." last="Lyons">Kelly E. Lyons</name>
<affiliation><inist:fA14 i1="11"><s1>Department of Neurology, University of Kansas Medical Center</s1>
<s2>Kansas City, KS</s2>
<s3>USA</s3>
<sZ>12 aut.</sZ>
</inist:fA14>
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<author><name sortKey="Meng, Cheryl" sort="Meng, Cheryl" uniqKey="Meng C" first="Cheryl" last="Meng">Cheryl Meng</name>
<affiliation><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, CA</s2>
<s3>USA</s3>
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<author><name sortKey="Korell, Monica" sort="Korell, Monica" uniqKey="Korell M" first="Monica" last="Korell">Monica Korell</name>
<affiliation><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
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<author><name sortKey="Roucoux, Diana F" sort="Roucoux, Diana F" uniqKey="Roucoux D" first="Diana F." last="Roucoux">Diana F. Roucoux</name>
<affiliation><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, CA</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Hoppin, Jane A" sort="Hoppin, Jane A" uniqKey="Hoppin J" first="Jane A." last="Hoppin">Jane A. Hoppin</name>
<affiliation><inist:fA14 i1="02"><s1>Epidemiology Branch</s1>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Sandler, Dale P" sort="Sandler, Dale P" uniqKey="Sandler D" first="Dale P." last="Sandler">Dale P. Sandler</name>
<affiliation><inist:fA14 i1="02"><s1>Epidemiology Branch</s1>
<s3>USA</s3>
<sZ>2 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="William Langston, J" sort="William Langston, J" uniqKey="William Langston J" first="J." last="William Langston">J. William Langston</name>
<affiliation><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, CA</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
</author>
<author><name sortKey="Tanner, Caroline M" sort="Tanner, Caroline M" uniqKey="Tanner C" first="Caroline M." last="Tanner">Caroline M. Tanner</name>
<affiliation><inist:fA14 i1="01"><s1>The Parkinson's Institute</s1>
<s2>Sunnyvale, CA</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>13 aut.</sZ>
<sZ>14 aut.</sZ>
<sZ>15 aut.</sZ>
<sZ>18 aut.</sZ>
<sZ>19 aut.</sZ>
</inist:fA14>
</affiliation>
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</analytic>
<series><title level="j" type="main">Annals of neurology</title>
<title level="j" type="abbreviated">Ann. neurol.</title>
<idno type="ISSN">0364-5134</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
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<seriesStmt><title level="j" type="main">Annals of neurology</title>
<title level="j" type="abbreviated">Ann. neurol.</title>
<idno type="ISSN">0364-5134</idno>
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</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Craniocerebral</term>
<term>Head trauma</term>
<term>Nervous system diseases</term>
<term>Parkinson disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Traumatisme crânien</term>
<term>Maladie de Parkinson</term>
<term>Pathologie du système nerveux</term>
<term>Crânioencéphalique</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Objective: To test the hypothesis that variability in SNCA Rep1, a polymorphic dinucleotide microsatellite in the promoter region of the gene encoding α-synuclein, modifies the association between head injury and Parkinson's disease (PD) risk. Methods: Participants in the Farming and Movement Evaluation (FAME) and the Study of Environmental Association and Risk of Parkinsonism using Case-Control Historical Interviews (SEARCH), 2 independent case-control studies, were genotyped for Rep1 and interviewed regarding head injuries with loss of consciousness or concussion prior to Parkinson's disease (PD) diagnosis. Logistic regression modeling adjusted for potential confounding variables and tested interaction between Rep1 genotype and head injury. Results: Consistent with prior reports, relative to medium-length Rep1, short Rep1 genotype was associated with reduced PD risk (pooled odds ratio [OR], 0.7; 95% confidence interval [CI], 0.5-0.9), and long Rep1 with increased risk (pooled OR, 1.4; 95% CI, 0.95-2.2). Overall, head injury was not significantly associated with PD (pooled OR, 1.3; 95% CI, 0.9-1.8). However, head injury was strongly associated with PD in those with long Rep1 (FAME OR, 5.4; 95% CI, 1.5-19; SEARCH OR, 2.3; 95% CI, 0.6-9.2; pooled OR, 3.5; 95% CI 1.4-9.2, p-interaction = 0.02). Individuals with both head injury and long Rep1 were diagnosed 4.9 years earlier than those with neither risk factor (p = 0.03). Interpretation: While head injury alone was not associated with PD risk, our data suggest head injury may initiate and/or accelerate neurodegeneration when levels of synuclein are high, as in those with Rep1 expansion. Given the high population frequency of head injury, independent verification of these results is essential.</div>
</front>
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<fA08 i1="01" i2="1" l="ENG"><s1>Head Injury, Alpha-Synuclein Rep1, and Parkinson's Disease</s1>
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<fA11 i1="01" i2="1"><s1>GOLDMAN (Samuel M.)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>KAMEL (Freya)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>WEBSTER ROSS (G.)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>JEWELL (Sarah A.)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>BHUDHIKANOK (Grace S.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>UMBACH (David)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>MARRAS (Connie)</s1>
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<fA11 i1="08" i2="1"><s1>HAUSER (Robert A.)</s1>
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<fA11 i1="10" i2="1"><s1>FACTOR (Stewart A.)</s1>
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<fA11 i1="12" i2="1"><s1>LYONS (Kelly E.)</s1>
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<fA11 i1="13" i2="1"><s1>MENG (Cheryl)</s1>
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<fA11 i1="14" i2="1"><s1>KORELL (Monica)</s1>
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<fA11 i1="15" i2="1"><s1>ROUCOUX (Diana F.)</s1>
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<fA11 i1="18" i2="1"><s1>WILLIAM LANGSTON (J.)</s1>
</fA11>
<fA11 i1="19" i2="1"><s1>TANNER (Caroline M.)</s1>
</fA11>
<fA14 i1="01"><s1>The Parkinson's Institute</s1>
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<s3>USA</s3>
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<sZ>5 aut.</sZ>
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<sZ>19 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Epidemiology Branch</s1>
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<sZ>2 aut.</sZ>
<sZ>16 aut.</sZ>
<sZ>17 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Biostatistics Branch, National Institute of Environmental Health Sciences, NIH, DHHS</s1>
<s2>Research Triangle Park, NC;</s2>
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<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Veterans Affairs Pacific Islands Health Care System</s1>
<s2>Honolulu, HI</s2>
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<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>DZNE, German Center for Neurodegenerative Diseases</s1>
<s2>Bonn</s2>
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<fA14 i1="06"><s1>Neurology, Toronto Western Hospital, University of Toronto</s1>
<s2>Toronto, Ontario</s2>
<s3>CAN</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Department of Neurology, University of South Florida</s1>
<s2>Tampa, FL</s2>
<s3>USA</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Department of Neurology, Baylor College of Medicine</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>Department of Neurology, Emory University School of Medicine</s1>
<s2>Atlanta, GA;</s2>
<s3>USA</s3>
<sZ>10 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>Department of Neurology, Beth Israel Medical Center</s1>
<s2>New York, NY</s2>
<s3>USA</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="11"><s1>Department of Neurology, University of Kansas Medical Center</s1>
<s2>Kansas City, KS</s2>
<s3>USA</s3>
<sZ>12 aut.</sZ>
</fA14>
<fA20><s1>40-48</s1>
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<fC01 i1="01" l="ENG"><s0>Objective: To test the hypothesis that variability in SNCA Rep1, a polymorphic dinucleotide microsatellite in the promoter region of the gene encoding α-synuclein, modifies the association between head injury and Parkinson's disease (PD) risk. Methods: Participants in the Farming and Movement Evaluation (FAME) and the Study of Environmental Association and Risk of Parkinsonism using Case-Control Historical Interviews (SEARCH), 2 independent case-control studies, were genotyped for Rep1 and interviewed regarding head injuries with loss of consciousness or concussion prior to Parkinson's disease (PD) diagnosis. Logistic regression modeling adjusted for potential confounding variables and tested interaction between Rep1 genotype and head injury. Results: Consistent with prior reports, relative to medium-length Rep1, short Rep1 genotype was associated with reduced PD risk (pooled odds ratio [OR], 0.7; 95% confidence interval [CI], 0.5-0.9), and long Rep1 with increased risk (pooled OR, 1.4; 95% CI, 0.95-2.2). Overall, head injury was not significantly associated with PD (pooled OR, 1.3; 95% CI, 0.9-1.8). However, head injury was strongly associated with PD in those with long Rep1 (FAME OR, 5.4; 95% CI, 1.5-19; SEARCH OR, 2.3; 95% CI, 0.6-9.2; pooled OR, 3.5; 95% CI 1.4-9.2, p-interaction = 0.02). Individuals with both head injury and long Rep1 were diagnosed 4.9 years earlier than those with neither risk factor (p = 0.03). Interpretation: While head injury alone was not associated with PD risk, our data suggest head injury may initiate and/or accelerate neurodegeneration when levels of synuclein are high, as in those with Rep1 expansion. Given the high population frequency of head injury, independent verification of these results is essential.</s0>
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<server><NO>PASCAL 12-0075975 INIST</NO>
<ET>Head Injury, Alpha-Synuclein Rep1, and Parkinson's Disease</ET>
<AU>GOLDMAN (Samuel M.); KAMEL (Freya); WEBSTER ROSS (G.); JEWELL (Sarah A.); BHUDHIKANOK (Grace S.); UMBACH (David); MARRAS (Connie); HAUSER (Robert A.); JANKOVIC (Joseph); FACTOR (Stewart A.); BRESSMAN (Susan); LYONS (Kelly E.); MENG (Cheryl); KORELL (Monica); ROUCOUX (Diana F.); HOPPIN (Jane A.); SANDLER (Dale P.); WILLIAM LANGSTON (J.); TANNER (Caroline M.)</AU>
<AF>The Parkinson's Institute/Sunnyvale, CA/Etats-Unis (1 aut., 4 aut., 5 aut., 13 aut., 14 aut., 15 aut., 18 aut., 19 aut.); Epidemiology Branch/Etats-Unis (2 aut., 16 aut., 17 aut.); Biostatistics Branch, National Institute of Environmental Health Sciences, NIH, DHHS/Research Triangle Park, NC;/Etats-Unis (6 aut.); Veterans Affairs Pacific Islands Health Care System/Honolulu, HI/Etats-Unis (3 aut.); DZNE, German Center for Neurodegenerative Diseases/Bonn/Allemagne (4 aut.); Neurology, Toronto Western Hospital, University of Toronto/Toronto, Ontario/Canada (7 aut.); Department of Neurology, University of South Florida/Tampa, FL/Etats-Unis (8 aut.); Department of Neurology, Baylor College of Medicine/Houston, TX/Etats-Unis (9 aut.); Department of Neurology, Emory University School of Medicine/Atlanta, GA;/Etats-Unis (10 aut.); Department of Neurology, Beth Israel Medical Center/New York, NY/Etats-Unis (11 aut.); Department of Neurology, University of Kansas Medical Center/Kansas City, KS/Etats-Unis (12 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2012; Vol. 71; No. 1; Pp. 40-48; Bibl. 68 ref.</SO>
<LA>Anglais</LA>
<EA>Objective: To test the hypothesis that variability in SNCA Rep1, a polymorphic dinucleotide microsatellite in the promoter region of the gene encoding α-synuclein, modifies the association between head injury and Parkinson's disease (PD) risk. Methods: Participants in the Farming and Movement Evaluation (FAME) and the Study of Environmental Association and Risk of Parkinsonism using Case-Control Historical Interviews (SEARCH), 2 independent case-control studies, were genotyped for Rep1 and interviewed regarding head injuries with loss of consciousness or concussion prior to Parkinson's disease (PD) diagnosis. Logistic regression modeling adjusted for potential confounding variables and tested interaction between Rep1 genotype and head injury. Results: Consistent with prior reports, relative to medium-length Rep1, short Rep1 genotype was associated with reduced PD risk (pooled odds ratio [OR], 0.7; 95% confidence interval [CI], 0.5-0.9), and long Rep1 with increased risk (pooled OR, 1.4; 95% CI, 0.95-2.2). Overall, head injury was not significantly associated with PD (pooled OR, 1.3; 95% CI, 0.9-1.8). However, head injury was strongly associated with PD in those with long Rep1 (FAME OR, 5.4; 95% CI, 1.5-19; SEARCH OR, 2.3; 95% CI, 0.6-9.2; pooled OR, 3.5; 95% CI 1.4-9.2, p-interaction = 0.02). Individuals with both head injury and long Rep1 were diagnosed 4.9 years earlier than those with neither risk factor (p = 0.03). Interpretation: While head injury alone was not associated with PD risk, our data suggest head injury may initiate and/or accelerate neurodegeneration when levels of synuclein are high, as in those with Rep1 expansion. Given the high population frequency of head injury, independent verification of these results is essential.</EA>
<CC>002B17; 002B17G</CC>
<FD>Traumatisme crânien; Maladie de Parkinson; Pathologie du système nerveux; Crânioencéphalique</FD>
<FG>Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central</FG>
<ED>Head trauma; Parkinson disease; Nervous system diseases; Craniocerebral</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Traumatismo craneoencefálico; Parkinson enfermedad; Sistema nervioso patología; Craneoencefálico</SD>
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