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.

Public Health Relevance

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.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32MH101976-01A1
Application #
8716219
Study Section
Special Emphasis Panel (ZRG1)
Program Officer
Chavez, Mark
Project Start
2014-05-02
Project End
2017-05-01
Budget Start
2014-05-02
Budget End
2015-05-01
Support Year
1
Fiscal Year
2014
Total Cost
Indirect Cost
Name
Emory University
Department
Psychiatry
Type
Schools of Medicine
DUNS #
City
Atlanta
State
GA
Country
United States
Zip Code
30322
Powers, Abigail; Stevens, Jennifer S; van Rooij, Sanne J H et al. (2017) Neural correlates and structural markers of emotion dysregulation in traumatized civilians. Soc Cogn Affect Neurosci 12:823-831
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
Wingo, A P; Almli, L M; Stevens, J S et al. (2017) Genome-wide association study of positive emotion identifies a genetic variant and a role for microRNAs. Mol Psychiatry 22:774-783
Kilaru, V; Iyer, S V; Almli, L M et al. (2016) Genome-wide gene-based analysis suggests an association between Neuroligin 1 (NLGN1) and post-traumatic stress disorder. Transl Psychiatry 6:e820
Stevens, Jennifer S; Ely, Timothy D; Sawamura, Takehito et al. (2016) CHILDHOOD MALTREATMENT PREDICTS REDUCED INHIBITION-RELATED ACTIVITY IN THE ROSTRAL ANTERIOR CINGULATE IN PTSD, BUT NOT TRAUMA-EXPOSED CONTROLS. Depress Anxiety 33:614-22
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

Showing the most recent 10 out of 15 publications