Aim:
Aim: This study aimed to investigate how the chronicity of PTSD shapes neurobiological functioning by integrating biochemical stress-related biomarkers with morphometric and microstructural brain parameters assessed using magnetic resonance imaging (MRI).

Material and methods:
Materials and Methods: The study included 92 adult male miners and mine rescue workers exposed to life-threatening events. Participants were assigned to three groups: PTSD ≤5 years , PTSD >5 years , and controls without PTSD symptoms . PTSD diagnosis was confirmed using the CAPS-5. MRI was performed on a 1.5 T General Electric Optima 360 scanner and included volumetric T1-weighted imaging, T2-weighted FLAIR, SWAN, and diffusion tensor imaging. Assessed brain parameters included ventricular width, amygdala dimensions, corpus callosum thickness, insular cortex thickness, and lateral fissure width. Biochemical markers were quantified using standard laboratory assays.

Results:
Results: Significant differences across all groups were observed for nearly all biomarkers and structural brain measures (p < 0.001). Early PTSD was characterized by elevated reduced anti-inflammatory, early ventricular enlargement, thinning of the corpus callosum and insular cortex, and reduced amygdala dimensions. Long-term PTSD demonstrated pronounced cortical atrophy, including marked widening of the lateral fissures, significant third-ventricle enlargement, and persistent thinning of the insular cortex and callosal body. Cortisol showed the strongest positive correlation with structural degeneration. Noradrenaline exhibited a potential compensatory effect, demonstrating negative correlations with ventricular width.

Conclusions:
Conclusions: Integrating biomarker profiles with MRI-derived measures provides a robust framework for identifying markers of disease progression and for developing phase-specific therapeutic strategies aimed at mitigating atrophy, modulating stress-response systems, and supporting neuroplasticity.