Study Links Genes to PTSD After NIU Campus Shootings
Certain variations in a gene that regulate serotonin have been associated with several stress-related syndromes including post-traumatic stress disorder (PTSD), according to a recent study conducted with Northern Illinois University students.
Serotonin, a neurotransmitter, is a contributor of feeling of well-being and happiness.
One of the critical questions surrounding PTSD is why some individuals are at risk for developing the disorder following a trauma, while others appear to be relatively resilient, says lead author, Kerry Ressler, who is a professor in the Dept. of Psychiatry and Behavioral Sciences at Emory University School of Medicine.
It is known that genetic heritability is one component of the differential risk for PTSD, but the mechanisms remain relatively unknown.
On Feb. 14, 2008, Steven Kazmierczak shot multiple people on the campus of Northern Illinois University in DeKalb, Illinois, killing 5 and wounding 21.
In this study, the researchers were able to look at college students who had been interviewed for a study prior to a 2008 mass shooting on the Northern Illinois University campus, and then were interviewed afterwards.
The researchers used these prospective psychological data to examine the association between variants in the serotonin transporter gene promoter region of the brain, and PTSD/acute stress disorder symptoms that developed in the aftermath of exposure to the shooting.
We believe that the strength of this study is the availability of the same validated survey measure to assess PTSD symptoms prior to and after a shared acute traumatic event, explains Ressler, who is also a researcher at the Yerkes National Primate Research Center at Emory.
The data suggest that differential function of the serotonin transporter may mediate differential response to a severe trauma. This is interesting because the gene product is the target for the first-line treatment for PTSD, the selective serotonin reuptake inhibitors (SSRIs). Additionally, variants in the gene have previously been shown to be associated with different risk for depression following life stress.
The researchers concluded that when examined in a relatively homogeneous sample with shared trauma and known prior levels of child and adult trauma, this serotonin transporter genotype may serve as a useful predictor of risk for PTSD-related symptoms in the weeks and months following trauma.
Ressler said this is one of likely a number of genes that will ultimately be found to contribute to risk and resilience. As more of these gene pathways are understood, it is hoped that such findings will contribute to improved treatment and prevention as well as better prediction of risk for PTSD following traumatic exposure.
In recent years, PTSD has gained increasing recognition as a major public health issue. While PTSD has always been associated with combat veterans, it is generally accepted that any civilian trauma, including sexual or physical assault, childhood abuse, motor vehicle accident, or other type of disaster, can also lead to the disorder in at-risk individuals. The lifetime prevalence of PTSD has been estimated to be 6.8 percent among adult Americans.
The research, published in Archives of General Psychiatry, was funded by grants from the Joyce Foundation, the Burroughs Wellcome Fund, the National Institute of Child Health and Human Development and the National Institute of Mental Health.
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