IntroductionIn schizophrenia, there are disorders in all sensory modalities, but the regularities of their occurrence, their pathogenesis and attitude towards cognitive functions are not sufficiently studied.ObjectivesExamine the interrelation between the dysfunctions in different analysers (olfactory and visual) and their dependence on the duration of the disease and the severity of psychotic symptoms and cognitive deficit in schizophrenic patients (F20 according to ICD 10 criteria).MethodsAll subjects were determined the threshold of olfactory sensitivity to n-butanol, the ability to discriminate against odors and the amount of error in comparing the same sections. Cognitive functions were evaluated using the BACS scale.ResultsThe inverse correlation between the value of the visual assessment error and the reduction of the threshold of olfactory sensitivity (r=- 0.56; p < 0.05) and the inverse correlation between the value of the visual assessment error and the ability to discriminate smells (0.64; p < 0.05) were revealed. There are no significant correlations between the duration of the disease and sensory disturbances. Olfactory and visual disturbances in schizophrenic patients were connected with cognitive functions ((r=-0,62; p< 0,05 and r=-0,84, p< 0,001 accordingly).ConclusionsThe data confirm that sensory impairments have a common pathogenesis and are closely related to cognitive deficits. Sensory and cognitive deficits in schizophrenia may be the result of top-down regulation failure.DisclosureNo significant relationships.
Summary. Mental disorders are clinically heterogeneous chronic diseases resulting from complex interactions between genotype variants and environmental factors. Epigenetic processes, such as DNA methylation and post-translational histone modification, determine the interpretation by the body at the cellular and tissue levels of various environmental factors. Given that epigenetic modifications are environmentally sensitive, stable and reversible, epigenetic research in psychiatry may be a promising approach to better understanding and treating mental illness. This review discusses the clinical opportunities and challenges posed by epigenetic research in psychiatry. Using individual examples, the main conclusions are drawn that confirm the role of adverse life events, alone or in combination with genetic risk, in the epigenetic programming of neuropsychiatric systems. Further epigenetic studies show encouraging results in the use of methylation changes as diagnostic markers of disease manifestations and provide predictive tools for assessing progression and response to treatment. The potential for the use of targeted epigenetic pharmacotherapy, combined with psychosocial methods, in the context of the personalized medicine of the future in psychiatry is discussed next. It concludes with a discussion of methodological limitations that can make it difficult to interpret epigenetic data in psychiatry. They mainly arise due to the heterogeneity of individuals, both at the level of the whole organism and at the level of tissues, and require new strategies to better assess the biological significance of epigenetic data and their translational use in psychiatry. Overall, we believe that epigenetics can provide new insights and a more comprehensive understanding of the etiology and pathogenesis of mental illness, and should ultimately improve the nosology, treatment and prevention of mental disorders.
According to modern data, about a third of patients suffering from schizophrenia are considered treatment resistant. The metabolism of about 20% of medicines and mainly psychotropic drugs is caused by the isoenzyme CYP2D6. This article presents the data of the CYP2D6 gene study as biomarkers for the treatment resistant schizophrenia. The study included 130 patients, men (65.4%) and women (34.6%) aged 18 to 60 years with schizophrenia. Based on the results, we found no effect of rs1065852 and rs3892097 polymorphisms gene CYP2D6 on treatment resistant schizophrenia.
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