Abstract
Post-traumatic stress disorder (PTSD) is increasingly recognized as a neurobiological condition involving persistent neuroinflammation, glial dysfunction, and neuronal injury. Chronic stress induces dysregulation of the hypothalamic-pituitary-adrenal axis, mitochondrial impairment, oxidative stress, and activation of inflammatory signaling pathways, leading to blood-brain barrier (BBB) disruption and progressive neural damage. These processes are reflected in circulating biomarkers that provide insight into underlying molecular pathology. This article focuses on key astroglial and neuronal injury markers-glial fibrillary acidic protein (GFAP), ubiquitin C-terminal hydrolase L1 (UCHL-1), neurofilament light chain (NfL), tau protein, and S100B-as indicators of stress-related brain dysfunction in PTSD. GFAP and S100B reflect astrocyte activation and BBB permeability, while UCHL-1, NfL, and tau indicate neuronal injury, axonal degeneration, and cytoskeletal instability. Accumulating clinical and experimental evidence suggests that altered levels of these biomarkers are associated with symptom severity, cognitive impairment, and neuroinflammatory activity in PTSD, often overlapping with mechanisms observed in neurodegenerative disorders. This review summarizes the current understanding of the biological significance and clinical relevance of these biomarkers and highlights their potential utility for early diagnosis, disease monitoring, and risk stratification. The combined assessment of astroglial and neuronal markers may support a more precise, biologically grounded approach to PTSD and facilitate the development of personalized diagnostic and therapeutic strategies.