Depression treatment

About 17% of the population suffers from depression. This leads to both economic losses and personal problems. The existing methods of treatment are very limited, as there is resistance to treatment, a low level of response to treatment, and a delay in the effect from treatment to 4-5 months. Therefore, new ways to treat depression are an urgent need in society.

The criteria for depression are complex because the disease is a heterogeneous syndrome. This makes both diagnosis and treatment difficult.

The existing problems do not interfere with progress in the study of the brain regions responsible for depression, the mechanisms of disease development that control mood, emotions that cause anxiety. Researchers have also identified cellular and neurochemical changes that underlie depression and stress. Depression and stress also cause atrophy of neurons in areas of the brain that are responsible for emotions and mood. There is a decrease in the number of synapses, connections between neurons. There is evidence of increased functioning and hypertrophy of areas of the brain that contribute to anxiety and depressed mood. 

There is progress in studying the pathophysiology of the brain in depression. So, in addition to the existing hypothesis about an increased level of functioning of the hypothalamic- pituitary- adrenal system, a hypothesis appeared about neurotrophic changes in chronic stress and depression (atrophy and death of neurons).

Although the development and manufacture of new drugs has proven difficult, evidence has emerged that previously known psychotropic drugs have good antidepressant effects. So antagonists of N-methyl-D- aspartate (ketamine) have a long and rapid antidepressant effect in patients who are resistant to depression therapy.

Also, a muscarinic receptor antagonist, scopolamine has a rapid antidepressant effect. The mechanisms of action of these drugs are completely different from classical monoamine reuptake inhibitors. In addition, the effects of scopolamine and ketamine are dependent on the production of new synapses, which reduce synapse atrophy caused by depression and stress. This leads to the secondary restoration of cortical- limbic connections. Such evidence is a paradigm shift in understanding the mechanisms of treatment for depression, and the emergence of new targets for the treatment of depression.

Research supports the theory of altered plasticity and synapsogenesis that underlie neural network dysfunction in depression. Additional factors that reduce synapsogenesis are increased levels of cytokines, glucocorticoids, and some cytokines.

Post-mortem studies of the brain of patients with depression revealed changes associated with the regulation of mood. They were observed in the prefrontal cortex, hippocampus, amygdala, and basal ganglia. The study of cerebral blood flow and its neuroimaging revealed areas with increased and weakened activity. These data led to the construction of a functional diagram of depression. This disease also decreases the volume of the hippocampus and prefrontal cortex. The decrease is proportional to the severity of depression, the duration of the illness, and the time of treatment. Postmortem studies also show a decrease in the size of neurons, a decrease in glia, and tissue atrophy in the prefrontal cortex. Stress leads to hypertrophy of neurons in the amygdala, which contributes to an increase in anxiety and emotionality in depression. Increased tonsil function and hypertrophy are the result of decreased function of the prefrontal cortex and atrophy, as this area of ​​the brain suppresses the activity of the amygdala and contributes to the development of depression. Decreased function and atrophy of neurons in the prefrontal cortex contribute to dysfunction of the subcallosal cortex and basal ganglia.

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