New discoveries in brain proteins linked to stress and depression could pave the way for the development of new drugs.

A new study has found a brain protein that linkes stress to depression, paving the way for new drugs to treat depression and anxiety. The study, from the Karolinska Institute, found that a protein previously associated with serotonin function and mood regulation was also involved in the body’s stress response, affecting the release of norepinephrine and epinephrine. This may explain why people who experience severe stress or trauma are more likely to develop depression and anxiety.

New discoveries in brain proteins linked to stress and depression could pave the way for the development of new drugs.

Although both are common mental health conditions, only some people can experience partial relief from symptoms from antidepressants, and unfortunately more people will eventually be diagnosed with anti-treatment depression. Although psychotherapy is possible for the longer category of people, there is still a lack of universally available and very effective solutions.

Antidepressants, like the most popular hallucinogens, act on the brain’s serotonin system. Neurotransmitter serotonin is known to play an important role in a person’s ability to regulate mood. Previous studies at the Karolinska Institute have linked protein p11 to an important component of the overall function as a serotonin neurotransmitter.

Based on the study, the institute’s new study linked the p11 protein to the role of the stress hormone cortisol in the release of certain neuron activity in the brain called the lower pasum. Similarly, this protein affects the release of both the stress hormones noryrophrine and epinephrine.

When mice lacking the p11 protein were exposed to stress, the study found that they experienced more severe stress responses — as seen in humans who had experienced severe stress or trauma. It has previously been determined that p11 protein levels are also low in the brains of people with depression and suicide.

The findings add more fragments to the puzzle of curing depression and anxiety, and the way they may be treated more effectively. Per Svenningsson, the study’s leader, explains.

One promising approach involves enhancing the expression of local p11, which is being tested in several animal models already in a state of depression. Another interesting approach, which requires further study, involves the development of drugs that prevent stress hormone reactions in the brain from starting.