Understanding the genetic architecture of schizophrenia provides insight into the etiologic heterogeneity of the disease and helps to address a number of important issues related to the limitations of current genetic research. However, despite data based on large cohorts, assessing the risks of schizophrenia based on genetic data is currently difficult due to a number of factors. To a significant extent, this is due to ethnic diversity. This is especially relevant for the population of the Russian Federation, which is multiethnic in nature. As a result of significant migration and active interethnic mixing, the population of Russia is a complex ethnic conglomerate. At the same time, the genetic basis of mental illness in the multiethnic and multicultural population of the Russian Federation remains insufficiently studied. Objective: to propose a project for a model with high predictive values adapted to the Russian population based on the analysis of population genetic studies of schizophrenia. Results: The proposed project is aimed at integrating several cohorts of patients with schizophrenia and healthy volunteers into a single database of microarray genotyping, as well as the subsequent study of polygenic risk scores for schizophrenia in the Russian population. As a result of the project, a GWAS with a minimally sufficient cohort size will be performed in the Russian population for the first time, as well as a study of schizophrenia PRS, compiled on the basis of genome-wide association studies in European and East Asian cohorts and adapted to the multiethnic Russian cohort. A meta-predictor of schizophrenia risk based on polygenic scales will also be developed and validated, and a model for assessing the risk of schizophrenia adapted to the Russian population will be developed.

Tardive tardive dyskinesia (TD) is a serious, often disabling movement disorder caused by dopamine receptor blocking drugs, including antipsychotics. TD is quite common, but controlling risk factors can, in theory, reduce the likelihood of iatrogenic development. TD has a colossal negative impact on all areas of a patient's life, including physical and psychological well-being, social satisfaction, and the course of the underlying mental illness. Currently, there is no standard treatment approach. However, specialists have treatment options that can significantly alleviate the condition. One such drug is amantadine sulfate (PК-Merz), which has demonstrated sufficient efficacy and safety in this patient population.

A number of metabolic disorders (hyperglycemia, dyslipidemia, obesity) are an urgent problem in psychiatry due to the fact that patients with severe mental disorders have a higher risk of developing them, which is associated both with the impact of psychopharmacotherapy and with individual characteristics of the patient and requires a personalized approach in the selection of treatment. Cariprazine, aripiprazole and brexpiprazole, are allocated to a separate class of III generation antipsychotics, and belong to partial dopamine agonists. This class of drugs has a lower risk of developing metabolic complications, but it also has a pronounced heterogeneity in terms of safety and efficacy, which necessitates further, more targeted studies of their metabolic effects. Material and methods: the analysis of the features of the development of hyperglycemia, weight gain, dyslipidemia in patients receiving aripiprazole, brexpiprazole, aripiprazole according to the results of data from randomized controlled studies. Results and discussion: It was found that brexpiprazole is probably associated with a higher risk of weight gain and blood triglyceride levels, and cariprazine with a higher risk of hyperglycemia, but in general a low risk of developing metabolic effects during therapy with third-generation antipsychotics was revealed. Their favorable effect on the lipid spectrum was revealed: cariprazine leads to a decrease in LDL cholesterol, and aripiprazole and brexpiprazole — to an increase in HDL cholesterol, which generally makes them the drugs of choice for patients with an increased risk of developing metabolic disorders.

This article presents a narrative review of the key theoretical and clinical approaches to understanding personality disorders. It traces the historical evolution of the concept, from early psychiatric descriptions to its current formulations in the DSM-5 and ICD-11 classifications. The review discusses differences in the definition of personality disorders and evaluates the advantages and disadvantages of categorical versus dimensional diagnostic systems. Special attention is given to comparing psychodynamic, cognitive-behavioral, and neurobiological models, including their influence on treatment strategies. The article provides a detailed analysis of neurobiological models of personality disorders, including data on structural and functional brain changes, neurochemical imbalances, and genetic factors, as well as their potential for the development of biomarkers and individualized therapies. Furthermore, it outlines the principles of psychotherapeutic interventions according to different theoretical frameworks—from psychoanalytically oriented therapy and schema therapy to dialectical behavior therapy. The review also examines the possibilities and limitations of pharmacotherapy, including current data on its efficacy and applicability across various types of personality pathology. This comprehensive overview aims to present the current state of the field and may be of interest to professionals in psychiatry and psychotherapy, as well as researchers exploring the development of integrative models for the diagnosis and treatment of personality disorders.

Neurochemical disorders following asthenia (A) in various parts of the brain are considered. For the first time, A presented as synaptic autoidosis caused by the imbalance of neurotransmitters (and other) systems in the brain structures responsible for emotional-volitional behaviour, motivation, cognitive and motor activity. We presented the hypothesis that choline replenishment with parallel enhancement of antioxidant activity with gincolydes can reduce A autocoidosis, and ameliorate A clinical symptoms. 40 patients with similar clinical course A (mild and moderate cognitive disorders, asthenic symptoms, etc.), received composition of choline strong which includes choline as such (550 mg), and standardized GINKGO biloba (60 mg) in a single capsule BID, for the period of 60 days. Evaluation of the Spielberg tests, depression (Beck Scale), the A and MOCA tests, as well as the Schulze test, and general clinical indicators, after processing the results showed a significant improvement in patient’s condition.

The study of the prognostic role of individual components of family relationships at different stages of remission in patients with depressive and anxiety neurotic disorders seems to be significant in the context of preventing adverse forms of the course of the disease in this population. The aim of the study was to determine the significance of the psychological characteristics of the microsocial environment of patients with depressive and anxiety neurotic disorders in the formation of remission 1 year after discharge. The study involved 50 patients (17 men, 33 women aged 18 to 61 years) and 50 relatives (16 men, 34 women aged 21 to 67 years). One year after the discharge 49 patients (17 men, 32 women) were available for examination. The microsocial predictors of remission at different stages of its formation are emotional support, order and hierarchy of the family system, a positive attitude of relatives towards the treatment process, the general orientation of the family towards active leisure and a variety of social ties. While the severity of negative feelings or indifference to the patient, the open manifestation of negative feelings in the family is predictively associated with less favorable dynamics of the condition and a greater degree of severity of symptoms in patients 1 year after discharge. Effective treatment of patients with depressive and anxiety neurotic disorders requires a comprehensive, personalized strategy that includes sociocentric interventions in the family and social context.

Pharmacogenetic markers are a promising tool for a personalized approach to treating alcohol dependence (AD). Previous studies using dominant models have identified several associations between polymorphisms in dopamine system genes and the efficacy of disulfiram and cyanamide therapy, but they did not allow for an evaluation of the influence of individual genotypes. Objective: To study the associations of specific genotypes from a pathogenetic panel of pharmacogenetic markers with the efficacy of disulfiram and cyanamide for stabilizing remission in patients with AD. Methods: The pharmacogenetic study was based on a 12-week, double-blind, randomized, comparative, placebo-controlled clinical trial on the efficacy and tolerability of disulfiram and cyanamide in AD therapy. The study included 150 detoxified patients with AD (mean age 40.65±1.09 years, 19.3% women) who were randomized into three treatment groups: disulfiram, cyanamide, and placebo. The genetic panel included 15 polymorphic loci in 9 genes related to the dopamine and opioid systems, as well as the aldehyde dehydrogenase enzyme cluster. Results: The homozygous CC genotype of rs1800955 in the dopamine receptor type 4 (DRD4) gene was associated with longer retention in the treatment program for patients receiving cyanamide (tendency at the border of significance, p=0.052). At the same time, the homozygous AA genotype of rs6275 in the dopamine receptor type 2 (DRD2) gene was associated with a higher risk of rapid dropout from therapy in the placebo group (p=0.015). Conclusion: Preliminary pharmacogenetic markers for the efficacy of alcohol dependence treatment have been identified at the level of specific genotypes. This approach is optimal for the practical application of pharmacogenetic research in clinical medicine. After validation, these markers can be used for patient stratification and the optimization of personalized therapy.

Aim — to find the predictors of high BMI values among socio-demographic, clinical-biological and anamnestic parameters in patients with severe mental disorders. Materials and methods: The study collected socio-demographic, clinical-anamnestic, anthropometric and clinical-biological data of 103 patients with diagnoses within the headings F31, F32, F33, F20 to analyze their impact on the body mass index (BMI). Results: Several regression models were obtained and tested for the total sample. The best model showed an association of increased BMI with a larger number of exacerbation episodes, a diagnosis of schizophrenia, moderate severity of psychopathological symptoms (PANSS) and global clinical impression (CGI), patient age, higher levels of insulin, cholesterol, triiodthyronine (free T3), absolute lymphocyte count, and platelet-to-lymphocyte ratio (PLR). Factors influencing BMI in patients with affective pathology and schizophrenia were assessed separately. Conclusion: Models for different nosological groups partially had similar features. The common parameters were the number of exacerbation episodes, moderate severity of the disease, the patient's age, and high cholesterol. For affective patients, the age of the initial visit to a psychiatrist was another significant indicator for the BMI. For patients with schizophrenia, the indicators are the presence of cardiovascular pathology, the duration of the disease, higher levels of insulin, triglycerides, and PLR.

Objective. The aim of the study was to study the influence of impulsivity on the severity of symptoms and the effectiveness of therapy for generalized anxiety disorder (GAD), taking into account the factor of comorbid mental disorders. Materials and methods. The study included 153 patients with GAD, including 36 patients with concomitant mental disorders. Psychometric assessment of symptoms of anxiety and depression was carried out using the Hospital Anxiety and Depression Scale (HADS), symptoms of impulsivity — on the Barratt Impulsivity Scale. The following information was collected about the patients: demographic data, information about psychopharmacotherapy and the effectiveness of treatment. To assess the impact of impulsivity, two groups of patients were compared: with clinically significant impulsivity (total Barratt score above 70) and without it (total Barratt score below 70) in the general group of patients and in a subgroup without comorbid mental disorders that directly affect the level of impulsivity. Results. Increased level of impulsivity is associated with a greater severity of symptoms of anxiety and depression on the HADS scale in the general sample of patients, however, when taking into account the influence of comorbid diagnoses, there was no significant effect of the level of impulsivity on symptoms. Among the individual characteristics of impulsivity, only the association with attention deficit and increased score on the HADS anxiety scale was revealed. Impulsivity had no effect on the effectiveness of therapy. Conclusion. The results of the study show that the symptoms of impulsivity in GAD are largely due to concomitant pathology, whereas in isolated GAD the effect of impulsivity on symptoms is minimal. No significant effect of impulsivity on the therapeutic response was found in this study.

In a cross-sectional study, 120 patients with anxiety disorders (episodic anxiety [EA]: F40, F41.0; generalized anxiety: F41.1) and comorbid subdepressive symptomatology participated and were divided into two equal groups. The aim was to identify specific psychotherapy targets for patients with risky alcohol consumption levels. Patients with generalized anxiety disorder (GAD) showed significantly higher anxiety levels on the HAM-A scale (p<0.001) and higher rates of risky alcohol consumption (41.6% vs. 13.4% in the episodic anxiety group). Episodic anxiety is characterized by symptomatic targets (muscle tension, sleep disturbances, somatovegetative dysfunctions). In GAD, emotional-cognitive targets predominate (high anxiety, catastrophizing, low tolerance for uncertainty, hypercontrol, using alcohol as an anxiolytic). Patients with GAD demonstrate predominantly avoidant behavior and deficits in problem-solving skills; individuals with EA tend toward excessive preventive coping. Factor analysis identified three aspects of dysfunction correlating with alcohol use: neuroticism — strong correlation with alcohol consumption in both groups (p<0.001); anankastic traits — significant correlation, especially in the episodic anxiety group; sensitivity — very strong correlation in the episodic anxiety group (p<0.001), noticeable also in the GAD group. Significant correlations between personality components (agreeableness, neuroticism, openness, extraversion, conscientiousness) and alcohol consumption level were identified, specific to each group. Based on these findings, priority therapy targets were defined across domains: symptomatic — relaxation training, normalization of sleep, management of hyperventilation; emotional — reducing anxiety and fears, correcting anhedonia, substituting alcohol with adaptive regulation strategies; cognitive — correcting catastrophizing thinking, increasing tolerance for uncertainty, addressing dysfunctional beliefs about the usefulness of worry/ hypercontrol; behavioral — overcoming avoidance, developing problem-solving skills, modifying coping strategies, assertiveness training; personality — building adequate self-esteem, reducing neuroticism and sensitivity. For subdepressive symptoms, additional targets from interpersonal therapy were added (loss experiences, role conflicts, deficits).

Schizophrenia is a severe multifactorial mental disorder. Recently, there has been a significant increase in studies of potential peripheral biomarkers that can determine the development of a particular clinical form, type of course and the development of metabolic syndrome in patients with schizophrenia for the prognosis and effective treatment of this disease. The aim of this work was to study the concentrations of serum potential biomarkers myeloperoxidase (MPO), cathepsin D, plasminogen activator inhibitor type 1 (PAI-1) in schizophrenia, taking into account the clinical heterogeneity of the disease. A comprehensive clinical and biological examination of 212 patients (119 men and 93 women) of ethnic Russian patients with schizophrenia (F20), who had long-term use of antipsychotic therapy, was conducted. The control group consisted of 30 healthy donors, matched by gender and age to patients with schizophrenia. The concentration of cathepsin D, MPO and PAI-1 was measured in the blood serum using xMAP technology on Magpix and Luminex 200 analyzers (Luminex, USA). Statistical processing of the results was performed using the SPSS 23.0 program. It was shown that the concentration of MPO and PAI-1 is significantly higher in the group of patients with schizophrenia compared to the group of healthy individuals (p = 0.001 and p = 0.002, respectively). As a result of the study, correlation relationships between the concentrations of the studied serum biomarkers and the clinical heterogeneity of schizophrenia (duration of the disease, leading symptoms, type of course) were not found. The concentrations of cathepsin D and PAI-1 in the blood serum positively correlate with the body mass index (p = 0.0001 and p = 0.004, respectively). Thus, we have obtained pilot data that elevated serum MPO and PAI-1 concentrations can be used as biomarkers of schizophrenia, and elevated concentrations of cathepsin D and PAI-1 can be used as antipsychotic-induced increases in body mass index in schizophrenia.