The association of latent toxoplasmosis with mental disorders in general and with schizophrenia in particular was noticed in the mid-1950s. In subsequent years, the role of Toxoplasma gondii was established based on its ability to survive for long periods of time in the nerve cells of the brain. The acute manifestations of the infection include psychopathic symptoms resembling those of schizophrenia. In the former USSR, and in other parts of the world, a number of studies were performed with respect to the association of latent toxoplasmosis and schizophrenia. However, with the dissolution of the USSR at the beginning of the 1990s, studies on the subject were halted due to financial problems and have resumed only recently. The reasons for the resumption of such studies in contemporary Russia are related to the progressively increasing incidence of schizophrenia over the last 25–30 years in the country. According to official data, approximately 550 000 persons reported suffering from the disease in 2014. There are reasons to believe that this is only a fraction of the real burden of the disease. Economically, it cost the state no less than approximately US $10 billion. The purpose of the study was to identify the level of toxoplasmosis seroprevalence in patients with verified diagnoses of schizophrenia in comparison to healthy people in Moscow City and in the Moscow region. A total of 155 persons constituted the patients group and 152 healthy people were in the control group. An integrated approach to the diagnosis and comparison of data from the entire spectrum of serological markers of infection was used, including the detection of specific IgM and the determination of IgG concentrations. It was found that among persons with neuropsychiatric disorders, the incidence of cases with latent toxoplasmosis was higher than in the control group. The effect of toxoplasmosis was significant and similar for men and women. Further statistical analyses revealed that among patients with a diagnosis of schizophrenia, the incidence of latent toxoplasmosis was significantly higher than in the control group. These data are in agreement with the results of similar studies in other countries.

Background: Modern medicine has gained considerable knowledge of the pathophysiology of mental disorders at the body, systemic, organ and neurochemical levels of the biological organization of the body. Modern clinical diagnostic of depression has some problem. That is why psychiatric Society to make diagnostics and taxonomy of different types of depression by implemention modern molecular biomarkers in diagnostic procedures. But up to now there were no reliable biomarkers of major depressive disorder (MDD) and other types of depression. Objective: The purpose of this review is to find fundamentals in pathological mechanisms of depression, which could be a basis for development molecular and genetic biomarkers the most feasible for clinic. Method: This review summarizes the published data using PubMed, Science Direct, Google Scholar and Scopus. Results: In this review, we summarized and discussed findings in molecular biology, genetics, neuroplasticity, neurotransmitters, neuroimaging that could increase our understanding of biological foundations of depression and show new directions for development reliable biomarkers. We didn’t find no molecular and genetic biomarkers approved for clinic. But Genome-Wide Association Study method promises some progress in development biomarkers based on SNP in the future. Epigenetic factors also are a promising target for biomarkers. We have found some differences in etiology of different type of atypical and melancholic depression. This knowledge could be the basis for development biomarkers for clinical practice in diagnosis, prognosis and selection of treatment. Conclusion: Depression is not monoetiological disease. Many pathological mechanisms involved in depression, thus up to now there is no approved and reliable biomarker for diagnosis, prognosis and correction of treatment of depression. Structural and functional complexity of the brain, the lack of invasive technology, poor correlations between genetic and clinical manifestation of depression, imperfect psychiatric classification and taxonomy of subtypes of disease are the main causes of this situation . One of the possible way to come over this situation can be to pay attention to the trigger mechanism of disease and its subtypes. Researchers and clinicians should focus their efforts on searching trigger mechanism of depression and different types of it . HPA axis can be a candidate for such trigger in depression caused by stress, because it influences to the main branches of disease: neuroinflammation, activity of biogenic amines, oxidative and nitrozative stress, epigenetic factors, metabolomics etc. But before we shall find any trigger mechanism, we need to create complex biomarker reflecting genetic, epigenetic, metabolomics and other pathological changes in different types of depression. Recently the most encouraging results have been obtained from genetics and neuroimaging. Continuing research in these areas should be forced by using computational , statistical and systems biology approaches, which can allow to get more knowledge about neurobiology of depression. In order to obtain clinically useful tests search for biomarkers should use appropriate research methodologies with increasing samples and identifying more homogeneous groups of depressed patients.

Indications to the use and specific algorithms of substitution and addition of antidepressants in non-effective psychopharmacotherapy of late-onset depressions have been developed. These algorithms of combination therapy suggest the possibilities for choosing the individual combinations of antidepressants.

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