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The stress-related gene  FKBP5  has been related to dysregulated glucocorticoid receptor (GR) signaling, showing increased GR sensitivity in trauma-exposed subjects with post-traumatic stress disorder (PTSD) but not in those without PTSD. However, the neural mechanism underlying the effects of  FKBP5  remains poorly understood. Two hundred and thirty-seven Han Chinese adults who had lost their only child were included. Four  FKBP5  single nucleotide polymorphisms (rs3800373, rs9296158, rs1360780, and rs9470080) were genotyped. All 179 participants were successfully divided into three  FKBP5  diplotype subgroups according to two major  FKBP5  H1 and H2 yin yang haplotypes. Brain average spectral power was compared using a two-way (PTSD diagnosis and  FKBP5  diplotypes) analysis of covariance within four separate frequency bands (slow-5, slow-4, slow-3, and slow-2). Adults with PTSD showed lower spectral power in bilateral parietal lobules in slow-4 and in left inferior frontal gyrus (IFG) in slow-5. There was significant  FKBP5  diplotype main effect in anterior cingulate cortex (ACC) in slow-4 (H1/H1 higher than other two subgroups), and in precentral/postcentral gyri and middle cingulate cortex (MCC) in slow-3 (H2/H2 higher than other two subgroups). Also, there was a significant diagnosis ×  FKBP5  diplotype interaction effect in right parietal lobule in slow-3. These findings suggest that adults with PTSD have lower low-frequency power in executive control network regions. Lower power in ACC and greater power in the motor/sensory areas in  FKBP5  high-risk diplotype group suggest a disturbance of emotional processing and hypervigilance/sensitization to threatening stimuli. The interaction effect of diagnosis ×  FKBP5  in parietal lobule may contribute to PTSD development.

FKBP5 haplotypes and PTSD modulate the resting-state brain activity in Han Chinese adults who lost their only child