PTSD genes identified by UCLA study

Why do some persons succumb to post-traumatic stress disorder (PTSD) while others who suffered the same ordeal do not? A new UCLA study may shed light on the answer.

UCLA scientists have linked two genes involved in serotonin production to a higher risk of developing PTSD. Published in the April 3 online edition of the Journal of Affective Disorders, the findings suggest that susceptibility to PTSD is inherited, pointing to new ways of screening for and treating the disorder.

“People can develop post-traumatic stress disorder after surviving a life-threatening ordeal like war, rape or a natural disaster,” explained lead author Dr. Armen Goenjian, a research professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA. “If confirmed, our findings could eventually lead to new ways to screen people at risk for PTSD and target specific medicines for preventing and treating the disorder.”

PTSD can arise following child abuse, terrorist attacks, sexual or physical assault, major accidents, natural disasters or exposure to war or combat. Symptoms include flashbacks, feeling emotionally numb or hyper-alert to danger, and avoiding situations that remind one of the original trauma.

Goenjian and his colleagues extracted the DNA of 200 adults from several generations of 12 extended families who suffered PTSD symptoms after surviving the devastating 1988 earthquake in Armenia.

In studying the families’ genes, the researchers found that persons who possessed specific variants of two genes were more likely to develop PTSD symptoms. Called TPH1 and TPH2, these genes control the production of serotonin, a brain chemical that regulates mood, sleep and alertness - all of which are disrupted in PTSD.

PTSD-gene link found in NIU students after shootings
By examining students who were studying at Northern Illinois University when a gunman killed five people and himself, researchers say they have cast light on a link between certain genetic variations and symptoms of post-traumatic stress disorder.

A study released Monday showed that students with particular genetic variations related to the regulation of serotonin - a chemical that affects mood and mental function - displayed PTSD symptoms more frequently than students without the variations.

Researchers drew the conclusion by questioning students about such PTSD symptoms as anxiety and nightmares following Steven Kazmierczak’s shooting spree on Valentine’s Day 2008.

The study could help guide efforts to understand and treat the disorder, said Holly Orcutt, an NIU associate professor of psychology who worked on the study.

“This was my way to make something good out of this senseless tragedy,” said Orcutt, who was off campus when Kazmierczak opened fire in a classroom.

“It’s not just academic for me, certainly. It’s very personal,” she said.

The study, published in this month’s Archives of General Psychiatry, grew out of Orcutt’s prior research on female students’ responses to stress, which she began updating just after the killings.

“We suspect that the gene variants produce less serotonin, predisposing these family members to PTSD after exposure to violence or disaster,” said Goenjian. “Our next step will be to try and replicate the findings in a larger, more heterogeneous population.”

Affecting about 7 percent of Americans, PTSD has become a pressing health issue for a large percentage of war veterans returning from Iraq and Afghanistan. The UCLA team’s discovery could be used to help screen persons who may be at risk for developing PTSD.

In this study, the researchers compared psychological data taken from 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 afterward.

Then researchers compared the psychological data with the genetic variants of the serotonin transporter gene found in students who developed PTSD/acute stress disorder symptoms.

“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,” said Ressler.

The data suggest that some functions of the serotonin transporter gene may mitigate or accentuate response to a severe trauma.

According to the authors, this is consistent with current pharmacological treatment of PTSD with selective serotonin reuptake inhibitors (SSRIs).

“A diagnostic tool based upon TPH1 and TPH2 could enable military leaders to identify soldiers who are at higher risk of developing PTSD, and reassign their combat duties accordingly,” observed Goenjian. “Our findings may also help scientists uncover alternative treatments for the disorder, such as gene therapy or new drugs that regulate the chemicals responsible for PTSD symptoms.”

According to Goenjian, pinpointing genes connected with PTSD symptoms will help neuroscientists classify the disorder based on brain biology instead of clinical observation. Psychiatrists currently rely on a trial and error approach to identify the best medication for controlling an individual patient’s symptoms.

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