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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

    Author(s)
    Evangelou, Evangelos
    Maraganore, Demetrius M
    Annesi, Grazia
    Brijhina, Laura
    Brice, Alexis
    Elbaz, Alexis
    Ferrarese, Carlo
    Hadjigeorgiou, Georgios M
    Krueger, Rejko
    Lambert, Jean-Charles
    Lesage, Suzanne
    Markopoulou, Katerina
    Mellick, George D
    Meeus, Bram
    Pedersen, Nancy L
    Quattrone, Aldo
    Van Broeckhoven, Christine
    Sharma, Manu
    Silburn, Peter A
    Tan, Eng-King
    Wirdefeldt, Karin
    Ioannidis, John PA
    Griffith University Author(s)
    Silburn, Peter A.
    Mellick, George
    Sutherland, Greg T.
    Year published
    2010
    Metadata
    Show full item record
    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 ...
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    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 larger GWA studies and perhaps novel analytical techniques.
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    Journal Title
    American Journal of Medical Genetics. Part B
    Volume
    153B
    Issue
    1
    DOI
    https://doi.org/10.1002/ajmg.b.30980
    Subject
    Genetics
    Clinical sciences
    Neurosciences
    Neurology and neuromuscular diseases
    Publication URI
    http://hdl.handle.net/10072/35521
    Collection
    • Journal articles

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