Genetic Breakthrough in Depression: New Insights for Diagnosis and Treatment

Depression is a serious and widespread mental disorder affecting millions of people worldwide. For a long time, it was believed that external factors such as stress and life circumstances played a key role in the development of depression. However, recent scientific discoveries show that genetic predisposition is also significant. Recent large-scale studies have brought promising results, opening new horizons in the diagnosis and treatment of this disease.

Genetic Trace of Depression: New Research

An international team of researchers, including specialists from the University of Edinburgh, King's College London, the University of Queensland, and the Sydney Brain and Consciousness Center, conducted an extensive study. About five million people from 29 different countries participated. The main goal of the scientists was to study the genetic factors affecting the likelihood of developing depression. The results were impressive: the researchers discovered 293 new genes associated with depression, which is 42% more than previously known. This discovery became possible thanks to the wide geographical coverage of the study and the inclusion of participants of different ethnic backgrounds, including 24% of participants of non-European origin. This approach allowed the identification of about 100 new genetic variants that had not been detected in studies conducted primarily in Europe.

Significance of the Discovery for Diagnosis and Treatment

The discovered genes are linked to important processes in the brain, including neuroinflammation, neurosteroid synthesis, and synaptic function — the structures responsible for transmitting signals between neurons. For example, changes in the DRD2 gene affect dopamine regulation, a neurotransmitter that plays a key role in managing emotions and motivation. This discovery is of immense significance for the development of personalized medicine in psychiatry. By knowing a patient's genetic predisposition, doctors will be able to:

• Conduct early diagnosis and prevention: identify individuals at higher risk of developing depression and offer preventive measures, such as stress management and early medication therapy.
• Develop more effective drugs: discovering new genes opens up possibilities for improving existing medications and developing more precise and effective therapeutic methods.

It is important to emphasize that genetics is not a sentence. While heredity can increase the risk of depression, it is not the only cause. External factors, such as stress, life circumstances, and the social environment, also play an important role.

New Approaches to Studying Serotonin

Alongside genetic research, scientists continue to explore the role of neurotransmitters in the development of depression. Researchers from Guangxi University (China) developed a new fluorescent probe to study serotonin — a neurotransmitter often associated with depression. Their results showed that it is not just the concentration of serotonin but also the ability of neurons to properly produce and release it. The scientists discovered a link between this process and the activity of the mTOR protein, which is involved in cellular signaling mechanisms. Stimulating mTOR activity increased serotonin release in neurons mimicking a depressed state. This discovery may lead to the development of new drugs that target mTOR and improve serotonin production.

Reducing Stigma and Hope for the Future

Recent advances in the genetics and neurobiology of depression not only pave the way for more effective treatment methods but also contribute to reducing the stigma surrounding mental disorders. It is becoming increasingly clear that depression is a condition with biological roots, requiring a thoughtful and professional approach to treatment. While much work remains ahead, recent advances provide hope for the creation of more accurate methods for diagnosing and treating depression, which will improve the quality of life for millions of people around the world.