Post-traumatic stress disorder (PTSD) is characterized by persistent and intrusive memories of traumatic experiences, and general hyper-arousal. Current models of the neural systems involved in PTSD highlight abnormalities in an emotion regulation system involving amygdala hyper-reactivity accompanied by reduced top-down regulation from medial prefrontal regions such as anterior cingulate cortex. However, few previous studies have examined the effects of trauma on functional interactions between the amygdala and medial prefrontal cortex, particularly within the context of engaging and regulating emotional arousal responses. The purpose of the proposed research is to investigate the effects of trauma and PTSD on the brain regions that support and regulate emotional arousal responses to affective stimuli. Environmental factors are uniquely involved in PTSD relative to other psychiatric disorders, as traumatic events serve as a trigger for PTSD, and the intensity and duration of trauma is correlated with symptom severity. In addition, twin studies suggest that heritable factors contribute to vulnerability to the disorder. An additional goal of the proposed research will be to examine gene x environment interaction models of PTSD by focusing on genetic polymorphisms in FKBP5, a gene coding for a co-chaperone in the HPA axis system, as risk alleles have been shown to predict PTSD development after a trauma, and this gene has been studied extensively by our group.
Post-traumatic stress disorder (PTSD) is one of the most universal and severe psychiatric disorders whose incidence continues to rise due to the common exposure to severe trauma in the United States and worldwide. While many are exposed to such trauma, not everyone develops PTSD. Identification of highly vulnerable individuals will permit the use of preventative intervention and likely reduce the burden of chronic PTSD on our healthcare system and society.
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|van Rooij, Sanne J H; Cross, Dorthie; Stevens, Jennifer S et al. (2017) Maternal buffering of fear-potentiated startle in children and adolescents with trauma exposure. Soc Neurosci 12:22-31|
|Stevens, Jennifer S; Kim, Ye Ji; Galatzer-Levy, Isaac R et al. (2017) Amygdala Reactivity and Anterior Cingulate Habituation Predict Posttraumatic Stress Disorder Symptom Maintenance After Acute Civilian Trauma. Biol Psychiatry 81:1023-1029|
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|van Rooij, Sanne J H; Stevens, Jennifer S; Ely, Timothy D et al. (2016) Childhood Trauma and COMT Genotype Interact to Increase Hippocampal Activation in Resilient Individuals. Front Psychiatry 7:156|
|Almli, Lynn M; Stevens, Jennifer S; Smith, Alicia K et al. (2015) A genome-wide identified risk variant for PTSD is a methylation quantitative trait locus and confers decreased cortical activation to fearful faces. Am J Med Genet B Neuropsychiatr Genet 168B:327-36|
|Norrholm, Seth Davin; Glover, Ebony M; Stevens, Jennifer S et al. (2015) Fear load: The psychophysiological over-expression of fear as an intermediate phenotype associated with trauma reactions. Int J Psychophysiol 98:270-275|
|Wingo, Aliza P; Almli, Lynn M; Stevens, Jennifer S et al. (2015) DICER1 and microRNA regulation in post-traumatic stress disorder with comorbid depression. Nat Commun 6:10106|
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