Thinking is a fundamental cognitive process assessed in psychiatric practice through speech and non-verbal signals. While speech is the primary basis for evaluating thought, thinking can occur independently of speech. Disorganized thinking, particularly associated with schizophrenia, involves weakened associations and cognitive disruptions that impact neural networks. Modern definitions of disorganized thinking, rooted in the three-factor model of psychotic disorders, highlight formal disturbances in thought, speech, and behavior. This conceptualization has been substantiated through neuroimaging studies, revealing structural connectivity issues in brain regions responsible for social-emotional processing. Despite its potential, artificial intelligence (AI) has yet to be fully integrated into psychiatric diagnostics, though its success in other medical fields suggests promising applications. AI could enhance psychiatric assessments by analyzing speech, facial expressions, and behavior, offering new diagnostic tools.

In this review scientific papers published on eLibrary, PubMed, Google Scholar were searched and analyzed for all time till 2024 year on the problem of neuropsychiatry, translational neuro-science, biomarkers. The issues of precision psychiatry and targeted therapy of mental disorders are considered. The ways of bridging the gap between theoretical and practical (clinical) psychiatry are discussed.

Parkinson's disease (PD) is a progressively advancing neurodegenerative disorder, the pathogenetic mechanisms of which remain poorly understood. The disease is characterized by the degeneration of dopaminergic neurons in the substantia nigra of the midbrain. Given the improvement in the quality of medical care provided to the population, it is projected that the total number of patients diagnosed with PD worldwide will rise to 8.7 million by 2030. This review addresses the fundamental aspects of neuroinflammation in the context of PD pathogenesis. There is no doubt that pro-inflammatory immunological mechanisms play a critical role in the onset and progression of the disease. Neuronal-derived cells, such as microglia and astrocytes, act as inducers of neuroinflammation, affecting the permeability of the blood-brain barrier to peripheral immune-competent cells. Furthermore, cytokine patterns of the immune response in PD appear to exist. Potential therapeutic approaches for mitigating neuroinflammation in PD, which have been studied in experimental and in vitro models, are also discussed.

Antipsychotic therapy in psychiatric practice can last from several months to many years, which requires the selection of drugs with the greatest effectiveness and the lowest risk of adverse drug reactions for the patient. According to experts, about a quarter of the total variability in response to antipsychotics is of genetic origin. This review analyzes and summarizes the results of domestic and foreign studies of the role of hereditary risk factors that cause a decrease in hepatic metabolism and efflux of antipsychotics due to polymorphism of genes encoding cytochrome P450 isoenzymes and transporter proteins. The key enzymes of antipsychotic metabolism registered for use in Russia and abroad are presented. The prospects of various options for pharmacogenetic testing in reducing the risk of potentially fatal complications in the selection of antipsychotic therapy in clinical practice are assessed.

Schizophrenia is a chronic mental disorder. It is treated with antipsychotics, which have a high risk of adverse drug reactions. Approximately 20-30% of patients with schizophrenia remain resistant to psychopharmacotherapy. Determining the individual predisposition to the response to antipsychotics and antipsychotic-induced adverse drug reactions development is possible using pharmacogenetic testing. Purpose is to present the role of pharmacogenetic testing in optimizing antipsychotic therapy. Materials and methods: The peripheral blood of patients was genotyping using real-time polymerase chain reaction. Results: This case report is about a 30- year-old female patient with paranoid schizophrenia, which had a long history of low effectiveness and poor tolerability of antipsychotics. The treatment was complicated by the pituitary microadenoma presence. According to the PGx results, the patient has a “poor transporter” phenotype, which also explains the high risk adverse drug reactions developing and therapeutic resistance while taking P- glycoprotein substrates antipsychotics. For the treatment, the antipsychotic brexpiprazole was selected, which did not have the P-glycoprotein substrate properties. It made possible to achieve paranoid schizophrenia remission and hyperprolactinemia correction. Conclusion: This case report demonstrates that wider implementation of pharmacogenetic testing into real clinical practice could help significantly improve the efficiency and safety of antipsychotic therapy.