An international team of scientists have discovered possible molecular mechanisms for the brain switching from anxiety to depression. In the long term, this discovery may lead to the creation of new, more effective drugs for the treatment of human mental disorders. The work was published in the journal Progress in Neuro-Psychopharmacology and Biological Psychiatry .
A group of scientists from Russia, China, the Netherlands and Brazil tested the hypothesis of the existence in the brain of a mechanism responsible for conjugating disparate symptoms into a single disease. Thus, the symptoms of depression – decreased appetite or depressed mood – can occur in many people, but only a few specific symptoms combine to form a disease. As an experimental model in the study of anxiety states, mice are often used under conditions of chronic social stress. The two males are planted in a cage, where they begin to fight, after which they are separated by a transparent partition with holes through which they can feel each other, but cannot contact. They are left for the whole day, and then the manipulations are repeated for many days in a row – as a result, “winners” and “losers” appear, the state of which is of interest for the study of anxiety and depression. According to the model, after about 10 days, the “vanquished” develop anxiety, and after 20 days, depression.
Scientists wondered how one pathology passes into another, and suggested that unique genes may be responsible for this. Such switch genes cannot be detected by classical methods, because they are not responsible for any symptom, but only for switching one pathology to another. To experimentally prove the hypothesis, the scientists performed genome-wide screening of mice brain gene activity in two key areas: the prefrontal cortex , which is responsible for long-term planning and social behavior, and the hippocampus, which is responsible for memory.
“Our discovery is this: We found out what happens on day 15 in a model of transition from experimental anxiety to depression-like state in mice. At this point, molecular mechanisms begin to activate in the brain that are not associated with neurotransmitters (as in anxiety) or inflammation (as in depression). These mechanisms are associated with the cellular skeleton and astrocytes , the side glial cells in the brain that are increasingly associated with mental illness. Thus, we have shown that when in mice one pathology of the brain turns into another, unique cellular mechanisms are activated, in fact acting as a “switch”, which can launch the vector of pathogenesis either in one direction (anxiety) or in another direction (depression). , – said the head of the study, leading researcher at UrFU and professor at St. Petersburg State University Alan Kaluev .
In about 70% of people with chronic anxiety, the disorder can develop into depression over time. At the same time, traditional antidepressant therapy helps 30–40% of people. The number of diagnosed cases is growing every year, and fundamentally new drugs for depression do not appear. Therefore, the mechanisms discovered by scientists can become a target for the creation of fundamentally new classes of psychotropic drugs.