Boosting the activity of a protein in the brain may provide a therapeutic benefit to those with post-traumatic stress disorder (PTSD).
Pawel Licznerski, PhD and Ronald Duman, PhD, both of Department of Psychiatry at Yale School of Medicine, New Haven, Conn., and colleagues performed a whole-genome expression screen on the post-mortem brains of six patients with PTSD. Expression of the protein serum and glucocorticoid regulated kinase 1 (SGK1) in the prefrontal cortex of these subjects was less than 80% that seen in control brains, the researchers reported in the journal PLOS Biology.
The researchers then looked at rats. Rodents with lower SGK1 activity had higher levels of learned helplessness in response to a shock than those with higher levels. When SGK1 expression was lowered in the rats, it led to several PTSD-type behaviors, leading to the idea that reduced SGK1 activity likely contributes to PTSD.
However, boosting activity of SGK1 may help to reduce the symptoms of PTSD, according to the authors. This could potentially provide new targets for developing medications to treat PTSD. The researchers caution that further postmortem studies are needed to confirm the findings.
PTSD impacts 5% of the overall U.S. population, but more than 10% of veterans.
People with post-traumatic stress disorder (PTSD) have reduced activity of the protein serum and glucocorticoid regulated kinase 1 (SGK1) in their prefrontal cortices, and experimentally reducing the protein’s activity in rats leads to PTSD-like behavior, according to a new study in PLOS Biology.
The study by Pawel Licznerski, Ronald Duman and colleagues of the Department of Psychiatry at Yale University publishing in the Open Access journal PLOS Biology on Oct. 27th, suggests that augmenting activity of SGK1 may be therapeutic in PTSD.