Protein affects stress and the development of depression
Persistent stress is associated with many health risks, although the stress response can differ significantly from person to person and the underlying mechanisms remain unclear. According to a recent study, a special protein in the brain could have a significant influence on the stress response and also on the risk of anxiety disorders and depression.
Stress has all kinds of negative health effects and also seems to be a direct trigger for depression and anxiety. (Image: Nicola_Del_Mutolo / Stock.Adobe.com)
The p11 protein appears to play an important role in the stress response and in the development of depression and anxiety, according to the result of the new study with the participation of researchers from the Karolinska Institutet in Sweden. The study was published in the English language journal “Molecular Psychiatry”.
Effects of stress
Some people develop an abnormal or chronic stress response after trauma or severe stress. This increases the risk of other illnesses such as depression and anxiety. So far, however, it is not clear what mechanisms play a role or how the stress response is regulated.
What role does the p11 protein play?
A certain protein in the brain is particularly important for the function of the mood-regulating substance serotonin and for the release of stress hormones, at least in mice, the researchers report. Depressed people and suicide victims have lower levels of the p11 protein in their brains, and lab mice with reduced p11 levels exhibit behavior similar to depression and anxiety, experts say.
How does p11 affect stress hormones?
The new study now shows that p11 influences the initial release of the stress hormone cortisol in mice by modulating the activity of certain neurons in the hypothalamus region of the brain. Through a completely different signaling path that originates from the brainstem, p11 also influences the release of two other stress hormones, adrenaline and norepinephrine.
Consequences of p11 deficiency
Additionally, tests showed that compared to mice with normal p11 levels, mice with p11 deficiency were more susceptible to stress, which was linked to a higher heart rate and more signs of anxiety, explains the research team.
Research on humans would be desirable
“We know that an abnormal stress response can trigger or worsen depression and cause anxiety disorders and cardiovascular disease. It is important to know whether the link between p11 deficiency and the stress response we observe in mice can also be established in humans, ”said study author Vasco Sousa of the Karolinska Institutet in a Press release.
Current antidepressants are often not effective enough
The researchers hope the results of their investigation could have an impact on the development of new, more effective drugs. There is a great need for new therapies because current antidepressants are not effective enough for many people. One promising approach is the administration of active ingredients that increase localized expression of p11, the researchers report. Experiments are already being carried out on animal models of depression using this approach.
“Another interesting approach that needs to be explored is the development of drugs that block the onset of the hormonal stress response in the brain,” adds study author Professor Per Svenningsson. (as)
Author and source information
This text conforms to the requirements of specialized medical literature, medical directives and current studies and has been verified by health professionals.
Vasco C. Sousa, Ioannis Mantas, Nikolas Stroth, Torben Hager, Marcela Pereira et al .: P11 deficiency increases stress reactivity with the HPA axis and autonomic hyper-reactivity, in molecular psychiatry (published October 1 2020), Molecular PsychiatryKarolinska Institutet: New clues on the link between stress and depression (published October 2, 2020), Karolinska Institutet
This article is provided for informational purposes only and should not be used for self-diagnosis or self-treatment. It cannot replace a visit to the doctor.