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These findings support the concept that increased cellular stress responses and altered neuronal signaling are central components of PTSDpathophysiology rather than secondary epiphenomena.
OBJECTIVE Aim: The aim of this review is to summarize current knowledge on the interplay between immune activation and stress-response dysregulation in post-traumatic stress disorder, with particular emphasis on molecular and neurobiological mechanisms. PATIENTS AND METHODS Materials and Methods: This narrative revie...
In conclusion, altered glutamatergic neurotransmission represents a central mechanism in PTSD pathophysiology and its role in synaptic plasticity, neuronal vulnerability, and network dysregulation highlights its potential relevance as a diagnostic and therapeutic target.
These findings support the concept that the processing of pro-inflammatory cytokine maturation and neuroimmune signaling is a central mechanism in PTSD rather than a secondary consequence of stress exposure.
Neuromolecular biomarkers may improve the current symptom-based diagnostic model of PTSD and their integration with clinical assessment tools may support identification of biologically defined subgroups and enable more targeted treatment.
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