We considered a locus to be replicated when the effect direction was the same in the discovery and replication analyses, and the corresponding one-sided replication P-value was ≤0.002 (i.e. Bonferroni correction).
For replication analyses we included the Sorbs from Germany.
Analyses of these datasets were followed by targeted replication analyses in two independent efforts [29], [30].
To determine the robustness of our model, we performed 2 independent replication analyses.
Interestingly, two subsequent replication analyses of rs8192708 documented associations of decreased AD risk with the minor allele, consistent with our findings [4], [38].
Data from the baseline examination of the population-based ESTHER cohort study previously described in detail [13], [21] were used for replication analyses of the smoking × BMI interaction.
The datasets used for the replication analyses described in this manuscript were obtained from dbGaP through dbGaP accession number phs000166.v2.p1.
Due to the top significance achieved by these two SNPs in our GWAS, our replication analyses in the FHS cohort were focused only on these two SNPs.
In silico replication analyses were carried out in 23,170 women (mean age 54.2 years) of the Women Genome Health Study (WGHS) and 3,078 individuals (69.8% males and mean age 62.7 years) of the PROCARDIS cohort.
In the GWAS and replication analyses, we applied Fisher's exact test to two-by-two contingency three in three genetic models: an allele frequency model, a dominant-effect model, and a recessive-effect model.
Regression analysis was used to examine the association between case-control status (336 cases, 343 controls) and quantitative serum iron measures and 331,060 single nucleotide polymorphism (SNP) genotypes, with replication analyses performed in a sample of 71 cases and 161 controls from a population of white male and female veterans screened at a US Veterans Affairs (VA) medical center.
