Post-Traumatic stress disorder (PTSD) is a complex psychiatric condition triggered by exposure to traumatic events. In recent years, the study of epigenetic modifications in the brains of individuals with PTSD has revealed key insights into how trauma affects gene expression without altering the DNA sequence itself. Epigenetic changes, such as DNA methylation and histone modification, can influence gene activity in ways that contribute to the disorder's pathophysiology.
Post-mortem brain studies of individuals with PTSD provide a unique opportunity to analyze these changes in regions involved in fear processing, memory, and emotion regulation, such as the prefrontal cortex, hippocampus, and amygdala. Research has shown that trauma-related epigenetic alterations often involve genes related to the hypothalamic-pituitary-adrenal (HPA) axis, which governs the body's stress response. For example, hypermethylation of the NR3C1 gene, encoding the glucocorticoid receptor, has been observed in PTSD-affected individuals, potentially impairing stress regulation and leading to heightened sensitivity to trauma cues.
Additionally, altered expression of genes linked to inflammation and neuroplasticity has been detected, suggesting that long-term epigenetic shifts may contribute to the enduring nature of PTSD symptoms. These findings offer potential avenues for developing targeted therapies aimed at reversing or mitigating epigenetic changes associated with the disorder, potentially improving outcomes for individuals suffering from PTSD.
Therefore, this research topic seeks to present a comprehensive, up-to-date collection of studies focusing on for individuals suffering from PTSD. We invite contributions in the form of Original Research Articles, Reviews, Mini-Reviews, Systematic Reviews, Perspectives, Commentaries, Data Notes, and Technical Notes. Topics of interest include, but are not limited to:
• Investigate how trauma alters brain structure and function, particularly in the amygdala, hippocampus, and prefrontal cortex, to better understand PTSD’s neural underpinnings.
• Study the role of DNA methylation, histone modification, and non-coding RNAs in regulating stress-related gene expression and their long-term effects on PTSD development.
• Study the role of inflammation and immune system dysregulation in PTSD, and its potential as a target for treatment intervention.
• Research novel drug therapies targeting neurotransmitter systems (e.g., serotonin, glutamate) and epigenetic modifiers for PTSD treatment.
• Explore genetic predispositions to PTSD, focusing on variations in genes related to the HPA axis, serotonin, dopamine, and neuroplasticity.
Keywords:
Post-Traumatic Stress Disorder, Amygdala, Hippocampus, Epigenetic Modifications
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Post-Traumatic stress disorder (PTSD) is a complex psychiatric condition triggered by exposure to traumatic events. In recent years, the study of epigenetic modifications in the brains of individuals with PTSD has revealed key insights into how trauma affects gene expression without altering the DNA sequence itself. Epigenetic changes, such as DNA methylation and histone modification, can influence gene activity in ways that contribute to the disorder's pathophysiology.
Post-mortem brain studies of individuals with PTSD provide a unique opportunity to analyze these changes in regions involved in fear processing, memory, and emotion regulation, such as the prefrontal cortex, hippocampus, and amygdala. Research has shown that trauma-related epigenetic alterations often involve genes related to the hypothalamic-pituitary-adrenal (HPA) axis, which governs the body's stress response. For example, hypermethylation of the NR3C1 gene, encoding the glucocorticoid receptor, has been observed in PTSD-affected individuals, potentially impairing stress regulation and leading to heightened sensitivity to trauma cues.
Additionally, altered expression of genes linked to inflammation and neuroplasticity has been detected, suggesting that long-term epigenetic shifts may contribute to the enduring nature of PTSD symptoms. These findings offer potential avenues for developing targeted therapies aimed at reversing or mitigating epigenetic changes associated with the disorder, potentially improving outcomes for individuals suffering from PTSD.
Therefore, this research topic seeks to present a comprehensive, up-to-date collection of studies focusing on for individuals suffering from PTSD. We invite contributions in the form of Original Research Articles, Reviews, Mini-Reviews, Systematic Reviews, Perspectives, Commentaries, Data Notes, and Technical Notes. Topics of interest include, but are not limited to:
• Investigate how trauma alters brain structure and function, particularly in the amygdala, hippocampus, and prefrontal cortex, to better understand PTSD’s neural underpinnings.
• Study the role of DNA methylation, histone modification, and non-coding RNAs in regulating stress-related gene expression and their long-term effects on PTSD development.
• Study the role of inflammation and immune system dysregulation in PTSD, and its potential as a target for treatment intervention.
• Research novel drug therapies targeting neurotransmitter systems (e.g., serotonin, glutamate) and epigenetic modifiers for PTSD treatment.
• Explore genetic predispositions to PTSD, focusing on variations in genes related to the HPA axis, serotonin, dopamine, and neuroplasticity.
Keywords:
Post-Traumatic Stress Disorder, Amygdala, Hippocampus, Epigenetic Modifications
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.