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  •   University of Thessaly Institutional Repository
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
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  •   University of Thessaly Institutional Repository
  • Επιστημονικές Δημοσιεύσεις Μελών ΠΘ (ΕΔΠΘ)
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ.
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Non-replication of association for six polymorphisms from meta-analysis of genome-wide association studies of Parkinson's disease: Large-scale collaborative study

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Author
Evangelou, E.; Maraganore, D. M.; Annesi, G.; Brighina, L.; Brice, A.; Elbaz, A.; Ferrarese, C.; Hadjigeorgiou, G. M.; Krueger, R.; Lambert, J. C.; Lesage, S.; Markopoulou, K.; Mellick, G. D.; Meeus, B.; Pedersen, N. L.; Quattrone, A.; Van Broeckhoven, C.; Sharma, M.; Silburn, P. A.; Tan, E. K.; Wirdefeldt, K.; Ioannidis, J. P. A.
Date
2010
DOI
10.1002/ajmg.b.30980
Keyword
Genome-wide association
Meta-analysis
Parkinson's disease
marker
adult
aged
allele
article
controlled study
female
gene replication
genetic polymorphism
genetic susceptibility
human
major clinical study
male
marker gene
Parkinson disease
priority journal
risk
signal transduction
single nucleotide polymorphism
Genome-Wide Association Study
Humans
Polymorphism, Genetic
Metadata display
Abstract
Early 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.
URI
http://hdl.handle.net/11615/27391
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  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [9728]

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