Post-traumatic stress disorder (PTSD) is a complex psychosocial disorder that develops as a result of extreme events and has a wide-ranging impact on the central nervous system and metabolic pathways. It is now known that chronic stress causes generalized disturbances at the molecular level, which underscores the relevance and necessity of identifying biological markers particularly in the blood – for the diagnosis and subsequent treatment of this condition. A review of the research findings revealed that neuroendocrine dysfunction in PTSD is accompanied by changes in the concentration of the stress hormone cortisol, as well as FK506-binding protein 51 (FKBP51) – a co-chaperone that influences the stress sensitivity of glucocorticoid receptors. In addition, the pathogenesis of the disorder is closely linked to an imbalance in amino acid metabolism and neurotransmitters such as glutamate, glutamine (a precursor), and gamma-aminobutyric acid. Changes in these substances lead to impaired memory consolidation and hyperexcitability. Abnormalities in monoaminergic transmission also play a key role in the pathogenesis of PTSD: emotional instability and hyperreactivity in patients are observed in conjunction with changes in the concentrations of serotonin, norepinephrine, and one of the enzymes involved in their catabolism – platelet monoamine oxidase B (MAO-B). Impaired neuroplasticity, caused by a decrease in brain-derived neurotrophic factor (BDNF) levels, indicates a reduced ability of the brain to recover from traumatic events. Current data show that PTSD is also accompanied by a chronic systemic inflammatory process and oxidative stress. The immune system responds to this by increasing the concentration of pro-inflammatory cytokines and proteins, such as C-reactive protein, interleukin-6, interleukin-1 beta, and tumor necrosis factor-alpha. In this article, we will review current research on the role of these compounds in metabolism within the pathogenesis of PTSD. A comprehensive analysis of these markers may contribute to the development of diagnostic methods for this disorder, as well as to the development of pharmacological treatments.

Ключові слова: кортизол, гамма-аміномасляна кислота (ГАМК), глутамат, нейротрофічний фактор мозку (BDNF), інтерлейкін-6 (ІЛ-6), С-реактивний білок (СРБ), фактор некрозу пухлин альфа (TNF-α), серотонін, норадреналін, глутамін, тромбоцитарна моноаміноксидаза Б (МАО-Б), ін

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