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dc.creatorEvangelou, E.en
dc.creatorMaraganore, D. M.en
dc.creatorAnnesi, G.en
dc.creatorBrighina, L.en
dc.creatorBrice, A.en
dc.creatorElbaz, A.en
dc.creatorFerrarese, C.en
dc.creatorHadjigeorgiou, G. M.en
dc.creatorKrueger, R.en
dc.creatorLambert, J. C.en
dc.creatorLesage, S.en
dc.creatorMarkopoulou, K.en
dc.creatorMellick, G. D.en
dc.creatorMeeus, B.en
dc.creatorPedersen, N. L.en
dc.creatorQuattrone, A.en
dc.creatorVan Broeckhoven, C.en
dc.creatorSharma, M.en
dc.creatorSilburn, P. A.en
dc.creatorTan, E. K.en
dc.creatorWirdefeldt, K.en
dc.creatorIoannidis, J. P. A.en
dc.date.accessioned2015-11-23T10:26:24Z
dc.date.available2015-11-23T10:26:24Z
dc.date.issued2010
dc.identifier10.1002/ajmg.b.30980
dc.identifier.issn15524841
dc.identifier.urihttp://hdl.handle.net/11615/27391
dc.description.abstractEarly genome-wide association (GWA) studies on Parkinson's disease (PD) have not been able to yield conclusive, replicable signals of association, perhaps due to limited sample size. We aimed to investigate whether association signals derived from the meta-analysis of the first two GWA investigations might be replicable in different populations. We examined six single-nucleotide polymorphisms (SNPs) (rs1000291, rs1865997, rs2241743, rs2282048, rs2313982, and rs3018626) that had reached nominal significance with at least two of three different strategies proposed in a previous analysis of the original GWA studies. Investigators from the "Genetic Epidemiology of Parkinson's Disease" (GEOPD) consortium were invited to join in this study. Ten teams contributed replication data from 3,458 PD cases and 3,719 controls. The data from the two previously published GWAs (599 PD cases, 592 controls and 443 sibling pairs) were considered as well. All data were synthesized using both fixed and random effects models. The summary allelic odds ratios were ranging from 0.97 to 1.09 by random effects, when all data were included. The summary estimates of the replication data sets (excluding the original GWA data) were very close to 1.00 (range 0.98-1.09) and none of the effects were nominally statistically significant. The replication data sets had significantly different results than the GWA data. Our data do not support evidence that any of these six SNPs reflect susceptibility markers for PD. Much stronger signals of statistical significance in GWA platforms are needed to have substantial chances of replication. Specifically in PD genetics, this would require much largerGWA studies and perhaps novel analytical techniques. © 2009 Wiley-Liss, Inc.en
dc.sourceAmerican Journal of Medical Genetics, Part B: Neuropsychiatric Geneticsen
dc.source.urihttp://www.scopus.com/inward/record.url?eid=2-s2.0-73949093664&partnerID=40&md5=55e49a35a3ebeb5617c6659caa344c20
dc.subjectGenome-wide associationen
dc.subjectMeta-analysisen
dc.subjectParkinson's diseaseen
dc.subjectmarkeren
dc.subjectadulten
dc.subjectageden
dc.subjectalleleen
dc.subjectarticleen
dc.subjectcontrolled studyen
dc.subjectfemaleen
dc.subjectgene replicationen
dc.subjectgenetic polymorphismen
dc.subjectgenetic susceptibilityen
dc.subjecthumanen
dc.subjectmajor clinical studyen
dc.subjectmaleen
dc.subjectmarker geneen
dc.subjectParkinson diseaseen
dc.subjectpriority journalen
dc.subjectrisken
dc.subjectsignal transductionen
dc.subjectsingle nucleotide polymorphismen
dc.subjectGenome-Wide Association Studyen
dc.subjectHumansen
dc.subjectPolymorphism, Geneticen
dc.titleNon-replication of association for six polymorphisms from meta-analysis of genome-wide association studies of Parkinson's disease: Large-scale collaborative studyen
dc.typejournalArticleen


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