scholarly journals Performance Comparison of Two Gene Set Analysis Methods for Genome-wide Association Study Results: GSA-SNP vs i-GSEA4GWAS

2012 ◽  
Vol 10 (2) ◽  
pp. 123 ◽  
Author(s):  
Ji-sun Kwon ◽  
Jihye Kim ◽  
Dougu Nam ◽  
Sangsoo Kim
Keyword(s):  
Association Study ◽  
Genome Wide Association Study ◽  
Performance Comparison ◽  
Genome Wide Association ◽  
Gene Set Analysis ◽  
Gene Set ◽  
Analysis Methods ◽  
Genome Wide ◽  
Study Results

scholarly journals Replication of celiac disease UK genome-wide association study results in a US population

2009 ◽  
Vol 18 (21) ◽  
pp. 4219-4225 ◽  
Author(s):  
C.P. Garner ◽  
J.A. Murray ◽  
Y.C. Ding ◽  
Z. Tien ◽  
D.A. van Heel ◽  
...  
Keyword(s):  
Celiac Disease ◽  
Association Study ◽  
Genome Wide Association Study ◽  
Genome Wide Association ◽  
Genome Wide ◽  
Study Results

scholarly journals Genome-wide association study results for educational attainment aid in identifying genetic heterogeneity of schizophrenia

2017 ◽  
Author(s):  
V. Bansal ◽  
M. Mitjans ◽  
C.A.P. Burik ◽  
R.K. Linnér ◽  
A. Okbay ◽  
...  
Keyword(s):  
Educational Attainment ◽  
Association Study ◽  
Genetic Heterogeneity ◽  
Genome Wide Association Study ◽  
Genome Wide Association ◽  
Clear Pattern ◽  
Replication Cohort ◽  
Genome Wide ◽  
Study Results ◽  
Higher Educational Attainment

ABSTRACTHigher educational attainment (EA) is negatively associated with schizophrenia (SZ). However, recent studies found a positive genetic correlation between EA and SZ. We investigated possible causes of this counterintuitive finding using genome-wide association study results for EA and SZ (N = 443,581) and a replication cohort (1,169 controls; 1,067 cases) with deeply phenotyped SZ patients. We found strong genetic dependence between EA and SZ that cannot be explained by chance, linkage disequilibrium, or assortative mating. Instead, several genes seem to have pleiotropic effects on EA and SZ, but without a clear pattern of sign concordance. Genetic heterogeneity of SZ contributes to this finding. We demonstrate this by showing that the polygenic prediction of clinical SZ symptoms can be improved by taking the sign concordance of loci for EA and SZ into account. Furthermore, using EA as a proxy phenotype, we isolate FOXO6 and SLITRK1 as novel candidate genes for SZ.

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