Researchers get to the roots of chronic stress and depression

A study provides clues about the common molecular origins of chronic stress and depression. The discovery could inform new treatments for mood disorders. Millions of years ago, our ancestors evolved the physiological responses needed to survive in the face of sudden threats from rivals and predators.

The release of hormones, including epinephrine (adrenaline), noradrenaline (norepinephrine), and the steroid hormone cortisol, trigger these “fight-or-flight” stress responses. However, sustained or chronic stress that does not resolve when the immediate threat passes is a major risk factor for the development of mood disorders such as anxiety and depression.

Traumatic experiences, for example, in military combat, can also damage the body’s ability to regulate its stress responses, causing post-traumatic stress disorder. People with these mood disorders have abnormally high and sustained stress hormone levels, which puts them at an increased risk of developing cardiovascular disease. Researchers, suspected that a protein called p11 plays a pivotal role in damping down stress responses in healthy brains after an acute threat has passed.

Serotonin signal boost Their previous research found that p11 enhances the effect of the hormone serotonin, which regulates mood and has a calming effect. Unusually low levels of p11 have been found in the brains of people with depression and in individuals who died by suicide. Mice with reduced p11 levels also show depression and anxiety-like behaviors. In addition, three different classes of antidepressants that are effective in humans increase levels of this protein in the animals’ brains. Now the researchers have discovered that reduced p11 levels in the brains of mice make the animals more sensitive to stressful experiences. The scientists also demonstrated that the protein controls activity in two distinct stress signaling pathways in the brain. It reduces not only the release of cortisol via one pathway but also adrenaline and noradrenaline via the other.

Therefore, it is important to find out whether the link between p11 deficiency and stress response that we see in mice can also be seen in patients.

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