Genetic Association Study of the P-Type ATPase ATP13A2 in Late-Onset Parkinson's Disease
Identifieur interne : 000F67 ( PascalFrancis/Corpus ); précédent : 000F66; suivant : 000F68Genetic Association Study of the P-Type ATPase ATP13A2 in Late-Onset Parkinson's Disease
Auteurs : Aleksandar Rakovic ; Barbara Stiller ; Ana Djarmati ; Antonia Flaquer ; Jan Freudenberg ; Mohammad-Reza Toliat ; Michael Linnebank ; Vladimir Kostic ; Katja Lohmann ; Sebastian Paus ; Peter Nürnberg ; Christian Kubisch ; Christine Klein ; Ullrich Wüllner ; Alfredo RamirezSource :
- Movement disorders [ 0885-3185 ] ; 2009.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
A role of ATP13A2 in early-onset Parkinsonism (EOP) has been proposed. Conversely, the contribution of this ATPase to late-onset Parkinson's disease (PD) remains unexplored. We therefore conducted a case-control association study in this age-of-onset group with PD. The initial sample was of German origin and consisted of 220 patients with late-onset PD (mean age of onset 60.1 years) and 232 age-matched unrelated controls. Five single nucleotide polymorphisms (SNPs) covering ATP13A2 and its common haplotypes were genotyped. The overall association results in this sample were negative. Interestingly, gender stratification gave a positive result for SNP rs11203280 (PUNC = 0.016) in men. This result could not be reproduced in a replication sample of German and Serbian origin composed of 161 patients with late-onset PD (mean age of onset 51.7 years) and 150 age- and ethnic-matched controls. In conclusion, we found no consistent evidence for an association between ATP13A2 and late-onset PD.
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Format Inist (serveur)
| NO : | PASCAL 09-0136789 INIST |
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| ET : | Genetic Association Study of the P-Type ATPase ATP13A2 in Late-Onset Parkinson's Disease |
| AU : | RAKOVIC (Aleksandar); STILLER (Barbara); DJARMATI (Ana); FLAQUER (Antonia); FREUDENBERG (Jan); TOLIAT (Mohammad-Reza); LINNEBANK (Michael); KOSTIC (Vladimir); LOHMANN (Katja); PAUS (Sebastian); NÜRNBERG (Peter); KUBISCH (Christian); KLEIN (Christine); WÜLLNER (Ullrich); RAMIREZ (Alfredo) |
| AF : | Department of Neurology, University of Lübeck/Lübeck/Allemagne (1 aut., 3 aut., 9 aut., 13 aut.); Department of Human Genetics, University of Lubeck/Lubeck/Allemagne (1 aut., 3 aut., 9 aut., 13 aut.); Institute of Human Genetics, University of Cologne/Cologne/Allemagne (2 aut., 12 aut., 15 aut.); Institute for Genetics, University of Cologne/Cologne/Allemagne (2 aut., 6 aut., 11 aut., 12 aut., 15 aut.); Center for Molecular Medicine Cologne, University of Cologne/Cologne/Allemagne (2 aut., 12 aut., 15 aut.); Institute for Medical Biometry, Informatics and Epidemiology, University of Bonn/Bonn/Allemagne (4 aut.); Laboratories of Neurogenetics, Department of Neurology, University of California at San Franscisco/San Francisco, California/Etats-Unis (5 aut.); Cologne Center for Genomics, University of Cologne/Cologne/Allemagne (6 aut., 11 aut., 12 aut.); Department of Neurology, University of Bonn/Bonn/Allemagne (7 aut., 10 aut., 14 aut.); Department of Neurology, University of Belgrade/Belgrade/Serbie (8 aut.); Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECEAD), University of Cologne/Cologne/Allemagne (11 aut., 12 aut.) |
| DT : | Publication en série; Courte communication, note brève; Niveau analytique |
| SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2009; Vol. 24; No. 3; Pp. 429-433; Bibl. 21 ref. |
| LA : | Anglais |
| EA : | A role of ATP13A2 in early-onset Parkinsonism (EOP) has been proposed. Conversely, the contribution of this ATPase to late-onset Parkinson's disease (PD) remains unexplored. We therefore conducted a case-control association study in this age-of-onset group with PD. The initial sample was of German origin and consisted of 220 patients with late-onset PD (mean age of onset 60.1 years) and 232 age-matched unrelated controls. Five single nucleotide polymorphisms (SNPs) covering ATP13A2 and its common haplotypes were genotyped. The overall association results in this sample were negative. Interestingly, gender stratification gave a positive result for SNP rs11203280 (PUNC = 0.016) in men. This result could not be reproduced in a replication sample of German and Serbian origin composed of 161 patients with late-onset PD (mean age of onset 51.7 years) and 150 age- and ethnic-matched controls. In conclusion, we found no consistent evidence for an association between ATP13A2 and late-onset PD. |
| CC : | 002B17; 002B17G |
| FD : | Maladie de Parkinson; Parkinsonisme; Pathologie du système nerveux; Adenosinetriphosphatase |
| FG : | Hydrolases; Enzyme; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
| ED : | Parkinson disease; Parkinsonism; Nervous system diseases; Adenosinetriphosphatase |
| EG : | Hydrolases; Enzyme; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
| SD : | Parkinson enfermedad; Parkinson síndrome; Sistema nervioso patología; Adenosinetriphosphatase |
| LO : | INIST-20953.354000186999840170 |
| ID : | 09-0136789 |
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aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Center for Molecular Medicine Cologne, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="08"><s1>Cologne Center for Genomics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="11"><s1>Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECEAD), University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>11 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, University of Lübeck</s1><s2>Lübeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Human Genetics, University of Lubeck</s1><s2>Lubeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Wullner, Ullrich" sort="Wullner, Ullrich" uniqKey="Wullner U" first="Ullrich" last="Wüllner">Ullrich Wüllner</name><affiliation><inist:fA14 i1="09"><s1>Department of Neurology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>7 aut.</sZ><sZ>10 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ramirez, Alfredo" sort="Ramirez, Alfredo" uniqKey="Ramirez A" first="Alfredo" last="Ramirez">Alfredo Ramirez</name><affiliation><inist:fA14 i1="03"><s1>Institute of Human Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Center for Molecular Medicine Cologne, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">09-0136789</idno><date when="2009">2009</date><idno type="stanalyst">PASCAL 09-0136789 INIST</idno><idno type="RBID">Pascal:09-0136789</idno><idno type="wicri:Area/PascalFrancis/Corpus">000F67</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Genetic Association Study of the P-Type ATPase ATP13A2 in Late-Onset Parkinson's Disease</title><author><name sortKey="Rakovic, Aleksandar" sort="Rakovic, Aleksandar" uniqKey="Rakovic A" first="Aleksandar" last="Rakovic">Aleksandar Rakovic</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, University of Lübeck</s1><s2>Lübeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Human Genetics, University of Lubeck</s1><s2>Lubeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Stiller, Barbara" sort="Stiller, Barbara" uniqKey="Stiller B" first="Barbara" last="Stiller">Barbara Stiller</name><affiliation><inist:fA14 i1="03"><s1>Institute of Human Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Center for Molecular Medicine Cologne, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Djarmati, Ana" sort="Djarmati, Ana" uniqKey="Djarmati A" first="Ana" last="Djarmati">Ana Djarmati</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, University of Lübeck</s1><s2>Lübeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Human Genetics, University of Lubeck</s1><s2>Lubeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Flaquer, Antonia" sort="Flaquer, Antonia" uniqKey="Flaquer A" first="Antonia" last="Flaquer">Antonia Flaquer</name><affiliation><inist:fA14 i1="06"><s1>Institute for Medical Biometry, Informatics and Epidemiology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Freudenberg, Jan" sort="Freudenberg, Jan" uniqKey="Freudenberg J" first="Jan" last="Freudenberg">Jan Freudenberg</name><affiliation><inist:fA14 i1="07"><s1>Laboratories of Neurogenetics, Department of Neurology, University of California at San Franscisco</s1><s2>San Francisco, California</s2><s3>USA</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Toliat, Mohammad Reza" sort="Toliat, Mohammad Reza" uniqKey="Toliat M" first="Mohammad-Reza" last="Toliat">Mohammad-Reza Toliat</name><affiliation><inist:fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="08"><s1>Cologne Center for Genomics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Linnebank, Michael" sort="Linnebank, Michael" uniqKey="Linnebank M" first="Michael" last="Linnebank">Michael Linnebank</name><affiliation><inist:fA14 i1="09"><s1>Department of Neurology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>7 aut.</sZ><sZ>10 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Kostic, Vladimir" sort="Kostic, Vladimir" uniqKey="Kostic V" first="Vladimir" last="Kostic">Vladimir Kostic</name><affiliation><inist:fA14 i1="10"><s1>Department of Neurology, University of Belgrade</s1><s2>Belgrade</s2><s3>SRB</s3><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lohmann, Katja" sort="Lohmann, Katja" uniqKey="Lohmann K" first="Katja" last="Lohmann">Katja Lohmann</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, University of Lübeck</s1><s2>Lübeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Human Genetics, University of Lubeck</s1><s2>Lubeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Paus, Sebastian" sort="Paus, Sebastian" uniqKey="Paus S" first="Sebastian" last="Paus">Sebastian Paus</name><affiliation><inist:fA14 i1="09"><s1>Department of Neurology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>7 aut.</sZ><sZ>10 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Nurnberg, Peter" sort="Nurnberg, Peter" uniqKey="Nurnberg P" first="Peter" last="Nürnberg">Peter Nürnberg</name><affiliation><inist:fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="08"><s1>Cologne Center for Genomics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="11"><s1>Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECEAD), University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>11 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Kubisch, Christian" sort="Kubisch, Christian" uniqKey="Kubisch C" first="Christian" last="Kubisch">Christian Kubisch</name><affiliation><inist:fA14 i1="03"><s1>Institute of Human Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Center for Molecular Medicine Cologne, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="08"><s1>Cologne Center for Genomics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="11"><s1>Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECEAD), University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>11 aut.</sZ><sZ>12 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name><affiliation><inist:fA14 i1="01"><s1>Department of Neurology, University of Lübeck</s1><s2>Lübeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="02"><s1>Department of Human Genetics, University of Lubeck</s1><s2>Lubeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Wullner, Ullrich" sort="Wullner, Ullrich" uniqKey="Wullner U" first="Ullrich" last="Wüllner">Ullrich Wüllner</name><affiliation><inist:fA14 i1="09"><s1>Department of Neurology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>7 aut.</sZ><sZ>10 aut.</sZ><sZ>14 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Ramirez, Alfredo" sort="Ramirez, Alfredo" uniqKey="Ramirez A" first="Alfredo" last="Ramirez">Alfredo Ramirez</name><affiliation><inist:fA14 i1="03"><s1>Institute of Human Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation><affiliation><inist:fA14 i1="05"><s1>Center for Molecular Medicine Cologne, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2009">2009</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenosinetriphosphatase</term><term>Nervous system diseases</term><term>Parkinson disease</term><term>Parkinsonism</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Parkinsonisme</term><term>Pathologie du système nerveux</term><term>Adenosinetriphosphatase</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A role of ATP13A2 in early-onset Parkinsonism (EOP) has been proposed. Conversely, the contribution of this ATPase to late-onset Parkinson's disease (PD) remains unexplored. We therefore conducted a case-control association study in this age-of-onset group with PD. The initial sample was of German origin and consisted of 220 patients with late-onset PD (mean age of onset 60.1 years) and 232 age-matched unrelated controls. Five single nucleotide polymorphisms (SNPs) covering ATP13A2 and its common haplotypes were genotyped. The overall association results in this sample were negative. Interestingly, gender stratification gave a positive result for SNP rs11203280 (P<sub>UNC</sub> = 0.016) in men. This result could not be reproduced in a replication sample of German and Serbian origin composed of 161 patients with late-onset PD (mean age of onset 51.7 years) and 150 age- and ethnic-matched controls. In conclusion, we found no consistent evidence for an association between ATP13A2 and late-onset PD.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>24</s2></fA05><fA06><s2>3</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Genetic Association Study of the P-Type ATPase ATP13A2 in Late-Onset Parkinson's Disease</s1></fA08><fA11 i1="01" i2="1"><s1>RAKOVIC (Aleksandar)</s1></fA11><fA11 i1="02" i2="1"><s1>STILLER (Barbara)</s1></fA11><fA11 i1="03" i2="1"><s1>DJARMATI (Ana)</s1></fA11><fA11 i1="04" i2="1"><s1>FLAQUER (Antonia)</s1></fA11><fA11 i1="05" i2="1"><s1>FREUDENBERG (Jan)</s1></fA11><fA11 i1="06" i2="1"><s1>TOLIAT (Mohammad-Reza)</s1></fA11><fA11 i1="07" i2="1"><s1>LINNEBANK (Michael)</s1></fA11><fA11 i1="08" i2="1"><s1>KOSTIC (Vladimir)</s1></fA11><fA11 i1="09" i2="1"><s1>LOHMANN (Katja)</s1></fA11><fA11 i1="10" i2="1"><s1>PAUS (Sebastian)</s1></fA11><fA11 i1="11" i2="1"><s1>NÜRNBERG (Peter)</s1></fA11><fA11 i1="12" i2="1"><s1>KUBISCH (Christian)</s1></fA11><fA11 i1="13" i2="1"><s1>KLEIN (Christine)</s1></fA11><fA11 i1="14" i2="1"><s1>WÜLLNER (Ullrich)</s1></fA11><fA11 i1="15" i2="1"><s1>RAMIREZ (Alfredo)</s1></fA11><fA14 i1="01"><s1>Department of Neurology, University of Lübeck</s1><s2>Lübeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></fA14><fA14 i1="02"><s1>Department of Human Genetics, University of Lubeck</s1><s2>Lubeck</s2><s3>DEU</s3><sZ>1 aut.</sZ><sZ>3 aut.</sZ><sZ>9 aut.</sZ><sZ>13 aut.</sZ></fA14><fA14 i1="03"><s1>Institute of Human Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></fA14><fA14 i1="04"><s1>Institute for Genetics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></fA14><fA14 i1="05"><s1>Center for Molecular Medicine Cologne, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>2 aut.</sZ><sZ>12 aut.</sZ><sZ>15 aut.</sZ></fA14><fA14 i1="06"><s1>Institute for Medical Biometry, Informatics and Epidemiology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>4 aut.</sZ></fA14><fA14 i1="07"><s1>Laboratories of Neurogenetics, Department of Neurology, University of California at San Franscisco</s1><s2>San Francisco, California</s2><s3>USA</s3><sZ>5 aut.</sZ></fA14><fA14 i1="08"><s1>Cologne Center for Genomics, University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>6 aut.</sZ><sZ>11 aut.</sZ><sZ>12 aut.</sZ></fA14><fA14 i1="09"><s1>Department of Neurology, University of Bonn</s1><s2>Bonn</s2><s3>DEU</s3><sZ>7 aut.</sZ><sZ>10 aut.</sZ><sZ>14 aut.</sZ></fA14><fA14 i1="10"><s1>Department of Neurology, University of Belgrade</s1><s2>Belgrade</s2><s3>SRB</s3><sZ>8 aut.</sZ></fA14><fA14 i1="11"><s1>Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECEAD), University of Cologne</s1><s2>Cologne</s2><s3>DEU</s3><sZ>11 aut.</sZ><sZ>12 aut.</sZ></fA14><fA20><s1>429-433</s1></fA20><fA21><s1>2009</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000186999840170</s5></fA43><fA44><s0>0000</s0><s1>© 2009 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>21 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>09-0136789</s0></fA47><fA60><s1>P</s1><s3>CC</s3></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>A role of ATP13A2 in early-onset Parkinsonism (EOP) has been proposed. Conversely, the contribution of this ATPase to late-onset Parkinson's disease (PD) remains unexplored. We therefore conducted a case-control association study in this age-of-onset group with PD. The initial sample was of German origin and consisted of 220 patients with late-onset PD (mean age of onset 60.1 years) and 232 age-matched unrelated controls. Five single nucleotide polymorphisms (SNPs) covering ATP13A2 and its common haplotypes were genotyped. The overall association results in this sample were negative. Interestingly, gender stratification gave a positive result for SNP rs11203280 (P<sub>UNC</sub> = 0.016) in men. This result could not be reproduced in a replication sample of German and Serbian origin composed of 161 patients with late-onset PD (mean age of onset 51.7 years) and 150 age- and ethnic-matched controls. In conclusion, we found no consistent evidence for an association between ATP13A2 and late-onset PD.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17</s0></fC02><fC02 i1="02" i2="X"><s0>002B17G</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Parkinsonisme</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Parkinsonism</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Parkinson síndrome</s0><s2>NM</s2><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Adenosinetriphosphatase</s0><s2>FE</s2><s5>09</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Adenosinetriphosphatase</s0><s2>FE</s2><s5>09</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Adenosinetriphosphatase</s0><s2>FE</s2><s5>09</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Hydrolases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Hydrolases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Hydrolases</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0><s2>FE</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>37</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>38</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>39</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>40</s5></fC07><fN21><s1>096</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 09-0136789 INIST</NO><ET>Genetic Association Study of the P-Type ATPase ATP13A2 in Late-Onset Parkinson's Disease</ET><AU>RAKOVIC (Aleksandar); STILLER (Barbara); DJARMATI (Ana); FLAQUER (Antonia); FREUDENBERG (Jan); TOLIAT (Mohammad-Reza); LINNEBANK (Michael); KOSTIC (Vladimir); LOHMANN (Katja); PAUS (Sebastian); NÜRNBERG (Peter); KUBISCH (Christian); KLEIN (Christine); WÜLLNER (Ullrich); RAMIREZ (Alfredo)</AU><AF>Department of Neurology, University of Lübeck/Lübeck/Allemagne (1 aut., 3 aut., 9 aut., 13 aut.); Department of Human Genetics, University of Lubeck/Lubeck/Allemagne (1 aut., 3 aut., 9 aut., 13 aut.); Institute of Human Genetics, University of Cologne/Cologne/Allemagne (2 aut., 12 aut., 15 aut.); Institute for Genetics, University of Cologne/Cologne/Allemagne (2 aut., 6 aut., 11 aut., 12 aut., 15 aut.); Center for Molecular Medicine Cologne, University of Cologne/Cologne/Allemagne (2 aut., 12 aut., 15 aut.); Institute for Medical Biometry, Informatics and Epidemiology, University of Bonn/Bonn/Allemagne (4 aut.); Laboratories of Neurogenetics, Department of Neurology, University of California at San Franscisco/San Francisco, California/Etats-Unis (5 aut.); Cologne Center for Genomics, University of Cologne/Cologne/Allemagne (6 aut., 11 aut., 12 aut.); Department of Neurology, University of Bonn/Bonn/Allemagne (7 aut., 10 aut., 14 aut.); Department of Neurology, University of Belgrade/Belgrade/Serbie (8 aut.); Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECEAD), University of Cologne/Cologne/Allemagne (11 aut., 12 aut.)</AF><DT>Publication en série; Courte communication, note brève; Niveau analytique</DT><SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2009; Vol. 24; No. 3; Pp. 429-433; Bibl. 21 ref.</SO><LA>Anglais</LA><EA>A role of ATP13A2 in early-onset Parkinsonism (EOP) has been proposed. Conversely, the contribution of this ATPase to late-onset Parkinson's disease (PD) remains unexplored. We therefore conducted a case-control association study in this age-of-onset group with PD. The initial sample was of German origin and consisted of 220 patients with late-onset PD (mean age of onset 60.1 years) and 232 age-matched unrelated controls. Five single nucleotide polymorphisms (SNPs) covering ATP13A2 and its common haplotypes were genotyped. The overall association results in this sample were negative. Interestingly, gender stratification gave a positive result for SNP rs11203280 (P<sub>UNC</sub> = 0.016) in men. This result could not be reproduced in a replication sample of German and Serbian origin composed of 161 patients with late-onset PD (mean age of onset 51.7 years) and 150 age- and ethnic-matched controls. In conclusion, we found no consistent evidence for an association between ATP13A2 and late-onset PD.</EA><CC>002B17; 002B17G</CC><FD>Maladie de Parkinson; Parkinsonisme; Pathologie du système nerveux; Adenosinetriphosphatase</FD><FG>Hydrolases; Enzyme; Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central</FG><ED>Parkinson disease; Parkinsonism; Nervous system diseases; Adenosinetriphosphatase</ED><EG>Hydrolases; Enzyme; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG><SD>Parkinson enfermedad; Parkinson síndrome; Sistema nervioso patología; Adenosinetriphosphatase</SD><LO>INIST-20953.354000186999840170</LO><ID>09-0136789</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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