Skip to main content
. Author manuscript; available in PMC: 2013 Jun 1.
Published in final edited form as: Mol Psychiatry. 2012 Nov 13;18(6):700–707. doi: 10.1038/mp.2012.152

Table 3.

Results of genetic association testing using 30 gene-wide SNPs in CRHR1

(A) Multiple regression analysis of overall genetic models with exon 6 SNPs fixed
Phenotype
Anxioustemperament Hippocampus
P = P =
Additive NS 0.001
D-major 0.014 0.008
D-minor 0.034 0.028
(B) Multiple regression analysis testing 30 SNPs simultaneously with exon6 SNPs fixed in model
Phenotype
Anxioustemperament
Hippocampus
P= Geneticmodel P= Geneticmodel
SNP5886 0.043 D-minor NS
SNP9009 NS 0.044 D-minor
SNP2107 0.017 D-major 0.017 D-major
SNP0879 0.012 D-minor 0.021 Add., D-minor
SNP4820 NS 0.048 D-minor
SNP5137 NS 0.015 D-minor

Abbreviations: CRHR1, corticotrophin-releasing hormone receptor 1; SNP, single nucleotide polymorphism.

After taking linkage disequilibrium into account, 30 SNPs were assessed for association with anxious temperament (AT) and hippocampal metabolism using a multiple regression approach. The SNPs that showed significant association in the previous seven SNP analysis were held fixed in the model (SNP4805, SNP5043 and SNP5094). (A) The significance of the full model for each of the three alternative models (additive (Add.), dominance-major (Dmajor) and dominance-minor (D-minor)) was assessed for AT and hippocampal metabolism. (B) For each multiple regression model that was significant, the partial regressions (SNPs) were assessed. When multiple models were significant for the same SNP, the lowest P-value is presented.

Bolded P-values represent P≤0.05.