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Association of CRP genetic variation with symptomatology, cognitive function, and circulating proinflammatory markers in civilian women with PTSD

大塚 豪士 山梨大学 DOI:info:doi/10.34429/00005018

2021.03.23

概要

(Purpose)
Posttraumatic stress disorder (PTSD) has been associated with increased inflammation. C-reactive protein (CRP) is a marker of systemic inflammation, and recently, single nucleotide polymorphisms (SNPs) in the CRP gene have been associated with increased blood CRP protein levels and illness severity in PTSD patients. However, the mechanism by which the CRP SNPs are involved in PTSD remains unclear. Here we investigated the association of CRP genetic variation with blood proinflammatory protein levels, symptomatology, and cognitive function, and further explored the moderating effect of childhood maltreatment history, in adult patients with PTSD.

(Methods)
Fifty-seven Japanese civilian women with PTSD and 73 healthy control women were enrolled. Three SNPs in the CRP gene, rs2794520, rs1130864, and rs3093059, were genotyped, and analyses focused on rs2794520 (T/C). Serum levels of high-sensitivity CRP (hsCRP), high-sensitivity tumor necrosis factor-α (hsTNF-α), and interleukin-6 were measured. PTSD symptoms were evaluated by the Posttraumatic Diagnostic Scale. Cognitive function was assessed by the Repeatable Battery for the Assessment of Neuropsychological Status. Childhood maltreatment history was assessed by the Childhood Trauma Questionnaire.

(Results)
Patients with the rs2794520 CC/CT genotype, compared to those with TT genotype, showed significantly higher levels of hsCRP (p=0.009) and hsTNF-α (p=0.001), more severe PTSD symptoms (p=0.036), and poorer cognitive function (p=0.018). A two-way analysis of variance revealed a significant genotype-by-maltreatment interaction for more severe PTSD avoidance symptom (p=0.012).

(Discussion)
Our finding of the association of CRP genetic variation with higher blood CRP levels and more severe symptoms in Japanese female patients mostly triggered by interpersonal trauma is consistent with previous studies of PTSD patients among urban African American men and women and veterans with predominantly white men. These results suggest that CRP genetic variation may lead to more severe phenotype of PTSD by causing increased inflammation.

PTSD is associated with wide-ranging cognitive impairments. It is also shown that PTSD patients have hippocampal morphologic abnormalities and increased risk of developing dementia. Neurogenesis in the hippocampus is associated with cognitive function, and inflammation in the brain adversely affects neurogenesis and cognition. The present study is the first, to our knowledge, to show the association between CRP genetic variation and cognitive impairment in patients with PTSD. CRP was originally thought to be a peripheral proinflammatory marker, but it has recently been suggested that CRP may influence the central nervous system. Therefore, the CRP genetic variation can cause increased levels of proinflammatory molecules, thereby leading to neuroinflammation and cognitive dysfunction. Besides cognitive impairment, the more severe PTSD symptoms associated with the CRP polymorphism might also be caused by inflammation in the brain, given the evidence that inflammation can be causally involved in the emergence and maintenance of such symptoms. For instance, animal studies have shown that elevated inflammation impairs extinction of fear memory. In line with this, human studies have demonstrated that increased inflammation is associated with enhanced amygdala activation in response to threatening stimuli.

Effects of environmental factors can be modified by genetic factors, and it is widely accepted that complex gene-environment interactions are involved in the pathogenesis of PTSD. Among a wide variety of environmental factors, childhood maltreatment can be particularly relevant here, as it has been associated with both increased inflammation and risk for PTSD. Supporting this, we observed the significant interaction between rs2794520 genotype and childhood maltreatment severity for PTSD avoidance symptoms, demonstrating an example of gene-environment interaction involved in this disorder. While we are not aware of any previous studies reporting the interaction between CRP genetic variation and childhood maltreatment in PTSD, there are studies that show such interactions for SNPs of other key genes, such as FKBP5 and BDNF. The reason for the specific association with avoidance symptom observed here is not clear, but this may suggest that childhood maltreatment might magnify the CRP genetic effect on this aspect of symptomatology.

(Conclusion)
This study shows significant relationships of the CRP genetic variation with circulating proinflammatory markers, symptom severity, and cognitive dysfunction in a sample of Japanese women with PTSD. We further demonstrate the significant interaction between the CRP polymorphism and childhood maltreatment for more severe PTSD avoidance symptom. These findings may provide an insight into understanding the etiology of PTSD from the inflammatory perspective.

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