1. Copyright © 2008 American Medical Association. All rights reserved.
From: Association of FKBP5 Polymorphisms and Childhood Abuse With Risk of Posttraumatic Stress Disorder Symptoms in Adults
JAMA. 2008;299(11): doi: /jama
Figure Legend:
SNPs indicate single-nucleotide polymorphisms; PTSD, posttraumatic stress disorder. A, The plot shows the negative log10 of the P value for the main genetic effect (filled circles), the interaction of FKBP5 SNP genotypes and non–child abuse trauma level (open squares), and the interaction of FKBP5 SNP genotypes and child abuse (open triangles) to predict adult PTSD symptoms. The x-axis shows the position of the SNPs on chromosome 6 and the y-axis shows the P value for the respective effects, plotted as the negative log10 of the P value. Dotted line indicates P<.002. B, The position of the FKBP5 gene and its exons (filled rectangles) on chromosome 6 as well as a linkage disequilibrium (LD) plot of all tested SNPs using r2 as the measure of LD is also shown. r2 = 1 indicates complete LD and is depicted by the darkest shade of blue. r2 < 1.0 are printed in the respective square for compared SNPs, with darker shades of blue representing higher levels of LD.
Date of download: 10/8/2017
Copyright © 2008 American Medical Association. All rights reserved.

2. Copyright © 2008 American Medical Association. All rights reserved.
From: Association of FKBP5 Polymorphisms and Childhood Abuse With Risk of Posttraumatic Stress Disorder Symptoms in Adults
JAMA. 2008;299(11): doi: /jama
Figure Legend:
PTSD indicates posttraumatic stress disorder; SNPs, single-nucleotide polymorphisms. Mean serum cortisol concentration with 95% confidence interval (CI) is shown in participants who were tested at baseline and after 0.5 mg of dexamethasone (postdexamethasone suppression). The 4 panels represent the mean cortisol concentrations at baseline and postdexamethasone for individuals without probable PTSD (no PTSD) or with probable PTSD stratified by rs , rs , rs , and rs genotypes. Individuals were categorized as risk allele carriers when they carried the C, A, T, or T alleles of these SNPs, respectively. Carriers of the AA, GG, CC, or CC homozygote genotypes of rs , rs , rs , and rs , respectively, were labeled as carrying the presumed protective genotypes. We found a significant interaction of genotype carrier- and PTSD-status on cortisol suppression (repeated measures analysis of variance: rs , F1,76 = 6.03, P = .02; rs , F1,78 = 8.76, P < .004; rs , F1,79 = 3.95, P = .05; rs , F1,77 = 5.32, P = .02; but also using permutation-based methods on percentage cortisol suppression). Although the risk alleles seem to be associated with less suppression (ie, glucocorticoid receptor resistance) in the no PTSD group, they are associated with greater suppression of cortisol from baseline to postdexamethasone in the group with PTSD. For rs GG carrier with no PTSD and rs CC carrier with no PTSD, the lower bound of the 95% CI had a negative value and was truncated at zero.
Date of download: 10/8/2017
Copyright © 2008 American Medical Association. All rights reserved.