The article provides a comprehensive review of the biological studies on Posttraumatic Stress Disorder (PTSD), covering psychophysiological, structural and functional neuroimaging, endocrinological, genetic, and molecular biological aspects. PTSD is recognized as a major mental disorder caused by exposure to traumatic events, leading to intense fear, helplessness, or horror. The review highlights the explosive growth of biological PTSD literature over the past three decades, emphasizing the need to understand the impact of environmental events at organic, cellular, and molecular levels. Psychophysiological studies have shown heightened emotional reactivity to trauma-related cues, exaggerated startle responses, and increased sensitivity to stimulation in individuals with PTSD. These findings are predictive of PTSD risk and treatment outcomes. Structural neuroimaging studies have identified reduced hippocampal volume and prefrontal cortex volumes in PTSD patients, suggesting impaired fear extinction and emotion regulation. Functional neuroimaging studies reveal altered activity in the amygdala, ventral medial prefrontal cortex (vmPFC), and dorsal anterior cingulate cortex (dACC), which are crucial for fear learning, extinction, and emotion regulation. Neuroendocrinological studies have found abnormalities in catecholamines and cortisol levels, with sympathetic system hyperreactivity and HPA axis dysregulation. Genetic studies have identified multiple gene variants associated with PTSD, including those involved in dopaminergic and serotonergic systems, HPA axis regulation, and neurotrophins. Epigenetic mechanisms, such as DNA methylation and histone deacetylation, also play a role in PTSD development. Animal models have been crucial in identifying candidate brain circuits and cellular/molecular processes involved in PTSD pathophysiology, testing therapeutic targets, and developing interventions. The review underscores the importance of integrating genetic, epigenetic, and molecular information to better understand and treat PTSD.The article provides a comprehensive review of the biological studies on Posttraumatic Stress Disorder (PTSD), covering psychophysiological, structural and functional neuroimaging, endocrinological, genetic, and molecular biological aspects. PTSD is recognized as a major mental disorder caused by exposure to traumatic events, leading to intense fear, helplessness, or horror. The review highlights the explosive growth of biological PTSD literature over the past three decades, emphasizing the need to understand the impact of environmental events at organic, cellular, and molecular levels. Psychophysiological studies have shown heightened emotional reactivity to trauma-related cues, exaggerated startle responses, and increased sensitivity to stimulation in individuals with PTSD. These findings are predictive of PTSD risk and treatment outcomes. Structural neuroimaging studies have identified reduced hippocampal volume and prefrontal cortex volumes in PTSD patients, suggesting impaired fear extinction and emotion regulation. Functional neuroimaging studies reveal altered activity in the amygdala, ventral medial prefrontal cortex (vmPFC), and dorsal anterior cingulate cortex (dACC), which are crucial for fear learning, extinction, and emotion regulation. Neuroendocrinological studies have found abnormalities in catecholamines and cortisol levels, with sympathetic system hyperreactivity and HPA axis dysregulation. Genetic studies have identified multiple gene variants associated with PTSD, including those involved in dopaminergic and serotonergic systems, HPA axis regulation, and neurotrophins. Epigenetic mechanisms, such as DNA methylation and histone deacetylation, also play a role in PTSD development. Animal models have been crucial in identifying candidate brain circuits and cellular/molecular processes involved in PTSD pathophysiology, testing therapeutic targets, and developing interventions. The review underscores the importance of integrating genetic, epigenetic, and molecular information to better understand and treat PTSD.