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The first aim in our study was to replicate association with the three genome-wide associated SNPs at 7p21.3 in an independent sample of primarily clinical diagnosed FTLD patients (n = 288) and control individuals (n = 595), ascertained in Flanders Belgium.
We apply our approach to a genome-wide analysis of Crohn disease, in which we replicate association with 17 previously identified regions.
We identify and replicate association between SLE and the genomic element containing MECP2 in two independent SLE cohorts from two ethnically divergent populations.
However, we were not able to replicate association between Fibulin-5 polymorphisms and HDL particle size in two independent cohorts, and hence the significance of our finding in GRAPHIC remains doubtful.
We aimed to replicate association of newly identified systemic lupus erythematosus (SLE) loci.
We were also able to replicate association to DCDC2 in our case control analyses across two independent dyslexic samples.
Similar(41)
A major concern is limited statistical power to identify or replicate associations in some studies.
Despite having reasonable power, we could replicate associations of only seven SNPs with various glycaemic phenotypes.
Further, a range of studies have failed to replicate associations between amyloid deposition and clinical measures [ 70], cognition [ 69], FDG-PET [ 71], and hippocampal atrophy in AD [ 69].
A major challenge that many studies face is the often limited statistical power to replicate associations as sample sizes tend to be relatively small.
This limited our ability to replicate associations between some regions of interest (that is, CCR5) and HIV MTCT in this study.
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Justyna Jupowicz-Kozak
CEO of Professional Science Editing for Scientists @ prosciediting.com