Abstract

Posttraumatic stress disorder (PTSD) is a complex psychiatric disorder (DSM-V code: 309.81; ICD-10 codes: F43.1). PTSD is an anxiety disorder developed in a person experiencing, witnessing, or learning about an extreme physically or/and psycholog‐ ically distressing event. Its incidence and the number of this disease-affected people are threateningly increasing in contemporary society. Therefore, the development of prognostic strategies and novel efficient methods on early diagnostics and treatment of PTSD is currently considered as one of the most important healthcare problems worldwide. Results of epidemiologic, clinical, and experimental studies suggest implication of both environmental and genetic factors in pathomechanisms of PTSD and that, most probably, PTSD belongs to complex disorders with polygenic inheritance. Whereas the environmental factors triggering PTSD are well defined, less is known about PTSD-associated genetic variations and molecular etiopathomechanisms. Several studies, including our own reports, suggest the involvement of neuro-immune alterations in the pathophysiology of PTSD. These include changes in neuronal plasticity, synaptic connectivity, humoral and cellular immune-mediated responses, and apoptosis rate leading to cognitive deficit and behavioral changes in patients with PTSD accompanied with development of low-grade inflammatory reactions. Currently, many research groups working on elucidation of molecular mechanisms of PTSD are exploring whether these changes have genetic background or are induced by other external or internal environmental factors. © 2015 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. In the present chapter, we provide overview and discussion of the existing data, including our own results, on variations in genes encoding neuro-immune and apoptotic mediators and regulators and related transcription factors in PTSD patients. Potential role of these genetic variations in generation and development of PTSD is considered and the implication of relevant candidate genes in mechanisms responsi‐ ble for disease progression is proposed.

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