After nearly a decade of sending troops into harms way, the U.S. is now coping with the aftermath that those situations can create for our armed forces, like posttraumatic stress disorder (PTSD). So it’s nice to see progress made towards understanding that condition. While many people are exposed to traumatic events, only a fraction will develop PTSD. So why does it plague some and not others? The search for genetic and molecular variations involved in PTSD risk has uncovered that DNA methylation may something to do with it.
PTSD and DNA Methylation
A polymorphism in the promoter of the serotonin transporter (SLC6A4) locus is associated with its decreased expression and with PTSD risk. Since DNA methylation also regulates the expression of this gene, researchers from Harvard, Columbia, and Michigan examined whether SLC6A4 methylation plays a role in PTSD risk. The team deployed DNA microarrays and Pyrosequencing to measure the DNA methylation levels in a subsample of the Detroit neighborhood health study (DNHS) and in the process revealed a few new facts:
- As expected, the risk of PTSD increased with exposure to increasing numbers of traumatic events.
- SLC6A4 methylation and genotype were not directly associated with PTSD.
- However, methylation of SLC6A4 modified how the number of traumatic events affected the risk for PTSD.
- Specifically, higher levels of methylation provided a protective effect against developing PTSD and lower levels of methylation were associated with increased risk for PTSD after exposure to multiple traumatic events.
Early identification of people at increased risk for developing PTSD has the potential to significantly improve their mental health care. These new results indicate that DNA methylation may play a role in this particular mental disorder and may also provide molecular markers for identifying at-risk patients. Of course, further studies are needed to validate the findings.
Get a handle on how DNA modification modifies the risk for PTSD, at Depression and Anxiety, May 2011.