U. MICHIGAN (US)—Post-traumatic stress disorder (PTSD) may be caused by actual alterations in the body’s immune system triggered by exposure to a disturbing event.
“We think we have uncovered a key biological step in the process that leads to PTSD,” says Monica Uddin, assistant research scientist in the department of epidemiology at the University of Michigan.
PTSD is a severe anxiety disorder that develops in some people who have been exposed to events involving the threat of serious injury or death.
“Diseases in general, and psychiatric diseases in particular, involve an interplay between social and biological factors. In the case of PTSD, traumatic events can get under your skin and literally alter your biology, with significant physical and mental consequences,” she says.
The researchers used data from the Detroit Neighborhood Health Study, a five-year project funded by the National Institutes of Health. They examined more than 14,000 genes using DNA from blood samples provided by 100 Detroit residents.
Twenty-three of those individuals suffered from post-traumatic stress disorder. Numerous genes were identified—most of them involved in regulating the immune system—that appeared to be more active in people with PTSD.
Previous studies have posited a link between altered immune function and PTSD. The new findings support that model and go a step further by identifying a specific biochemical reaction that may be involved.
The biochemical reaction is a process called DNA methylation, in which methyl groups (CH3 groups) are added to some of the molecular letters that spell out the genetic code. DNA methylation can alter gene activity, typically reducing it.
For technical reasons, the research team could not directly measure gene activity in the study, so they used methylation patterns as a proxy for gene activity and compared the signatures found in PTSD sufferers to those without the disorder.
Methylation levels of immune-related genes were lower in the PTSD group, suggesting increased activity in those genes. That finding supports a model for PTSD in which exposure to a traumatic event changes gene expression, which in turn alters immune-system activity, leading to the disorder.
“To the best of our knowledge, there have been no studies to date that have documented differences in epigenetic methylation patterns among persons with versus without PTSD,” the authors write.
The findings have potential implications for the treatment. Since DNA methylation states are changeable, it’s conceivable that genes identified in this study could become targets for new drug therapies to treat PTSD, Uddin says.
Researchers from Wayne State University, Harvard University, and the University of Tubingen Medical School in Germany contributed to the research, which received support from the National Institutes of Health, the Robert Wood Johnson Health, Society Scholars Small Grant Program, and from the universities involved.
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