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What does this mean for you?
The new study shows that p11 affects the initial release of the stress hormone cortisol by modulating the activity of specific neurons in the brain area hypothalamus. Through a completely different signaling pathway originating in the brain stem, p11 also affects the release of two other stress hormones, adrenaline and noradrenaline. In addition, the tests showed that mice with p11 deficiency react more strongly to stress, with a higher heart rate and more signs of anxiety, compared to mice with normal p11 levels.
“We know that an abnormal stress response can precipitate or worsen depression and cause anxiety disorder and cardiovascular disease,” says first author Vasco Sousa, a researcher at the Department of Clinical
, Karolinska Institutet.”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.”
The researchers believe that the findings may have implications for the development of new, more effective drugs.
There is a great need for new treatments because current antidepressants are not effective enough in many patients.
“One promising approach involves administration of agents that enhance localized p11 expression, and several experiments are already being conducted in animal models of depression,” says Per Svenningsson, professor at the Department of Clinical Neuroscience, Karolinska Institutet, who led the study.”Another interesting approach which needs further investigation involves developing drugs that block the initiation of the stress hormone response in the brain.”
Vasco C. Sousa, Ioannis Mantas, Nikolas Stroth, Torben Hager, Marcela Pereira, Haitang Jiang, Sandra Jabre, Wojciech Paslawski, Oliver Stiedl, Per Svenningsson. (2020). P11 deficiency increases stress reactivity along with HPA axis and autonomic hyperresponsiveness.
For More Details : Psychology Today