Vol 41, No 1 (2024)

There is no single model for the pathogenesis of schizophrenia, but neuroinflammation is considered a key mechanism in the development of this disease. The aim of the study: to analyze and summarize the literature data on the role of neuroinflammation markers in schizophrenia. Using the keywords “neuroinflammation”, “cytokines”, “chemokines”, “microcirculation”, “microglia”, “neurodestruction”, “schizophrenia”, articles for the period 1990–2003 in the PubMed and e-Library.ru databases were searched. The review discusses an integrated approach to the concept of neuroinflammation in schizophrenia, taking into account known and promising markers. Studies, including those of the authors of the article, indicate a significant role of microcirculation disorders and endothelial dysfunction, cytokines and chemokines, neurodestruction in the mechanisms of development and course of schizophrenia. The presented results require more detailed development to establish new neurobiological and pathogenetic functions of neuroinflammation in schizophrenia.

Ciliary neurotrophic factor (CNTF) is a pluripotent neurotrophic factor with high neuroprotective potential, a neurocytokine that has demonstrated potential in the therapy of neurodegenerative, psychiatric and metabolic diseases. Preclinical data support the general concept of its potential neuroprotective and trophic effects, and recent clinical data support the potential role of CNTF in the treatment of neurodegeneration and obesity. A number of data indicate the involvement of CNTF in stress reactivity and the pathogenesis of affective disorders. Data from studies of CNTF levels in invasive (blood) and non-invasive (tears) human biomaterials suggest the possibility of its use as a biomarker for certain brain diseases, although more research is needed to confirm this.

The aim of the study was investigation of the peculiarities of the conformational changes of serum albumin in patients with anxious and melancholic depression. Albumin conformation was measured by the method of the subnanosecond laser time resolved fluorescence spectroscopy. Anxious depression was followed with the significant decrease of the values of the three amplitudes on the serum albumin in comparison with controls. In the melancholic depression the values of all three amplitudes on serum albumin molecules were significantly elevated in comparison with controls. These results are clearly indicated that anxious and melancholic depression are followed by differently directed changes in serum albumin conformation.

The involvement of inflammation, disturbances of glutamate metabolism and oxidative stress in the pathogenesis of schizophrenia and affective disorders has been proven by numerous studies. It seems relevant to assess the role of these systems in the development of prodromal stages of schizophrenia in juvenile patients with depression. The aim of this study was to investigate the connection between markers of inflammation, energy and glutamate metabolism, and antioxidant defense with the clinical features of patients with adolescent depression. 74 males aged 16–25 years with a first depressive episode (F32.1–2, F32.38, F32.8) were observed: 32 subjects with attenuated positive symptoms, 22 persons with attenuated negative symptoms, 20 individuals without attenuated schizophrenia symptoms. The control group included 57 mentally healthy adults aged 16–25 years. The activity of leukocyte elastase and α1-proteinase inhibitor, the level of autoantibodies to S100B and myelin basic protein in plasma and the activity of cytochrome c-oxidase, glutamate dehydrogenase, glutathione reductase and glutathione-S-transferase in platelets were determined. Within each clinical group, differences in the profiles of immunological and biochemical parameters were identified. Division of patients into clusters according to all biological parameters showed different level of inflammation and changes of glutamate metabolism and antioxidant defense related to the features of psychopathological symptoms. The results confirm the connection of the studied metabolic systems and their different involvement to the development of adolescent depression with different psychopathological structure, which is important to assess the role of these systems in the trajectory of the disease and early therapeutic correction.

Many individuals with schizophrenia also suffer from metabolic syndrome (MetS), which is a major risk factor for the development of cardiovascular diseases associated with a heavy burden of disease, as well as with premature death of patients. This study investigated the expression of 7 genes potentially important for the development of metabolic syndrome. QuantiGene Plex 2.0 technology was used to measure how 7 studied genes (DRD3, GHRL, FTO, LEPR, INSIG2, GSTP1, ABCB1 (MDR1)) were expressed by leukocytes in 60 recently admitted patients with schizophrenia who had been on treatment with antipsychotic drugs. The preliminary results of our study show a change in the expression of the FTO gene in schizophrenia male with metabolic disorders, however, further studies are needed to determine the role of disturbances in the expression of this gene in the development of the metabolic syndrome in patients with schizophrenia.

The possibility of transferring exosomes of neural (NSC) and mesenchymal (MSC) mouse stem cells labeled with the fluorescent dye PKH26 into the cerebral cortex and hippocampus after their intranasal administration to mice, and the accumulation and localization of exosomes in cultured brain cells of various types, and also the effect of exosomes of NSCs and MSCs on the parameters of the cell cycle and the level of apoptosis of cultured NSCs after irradiation at a dose of 4 Gy. The accumulation of exosomes obtained from the culture medium of NSCs and MSCs from the adipose tissue of C57BL/6 mice was shown both in the hippocampus and in the cerebral cortex after their intranasal administration to syngeneic mice. Exosomes were found predominantly in the perinuclear region of brain cells. When culturing NSCs and differentiated from NSCs neurons and astrocytes, exosomes accumulate more intensively in astrocytes and are also localized in the perinuclear region of cells, and in astrocytes also in the cytoplasm. Exosomes accumulated most intensively in astrocytes. When studying the effect of stem cell exosomes on the cell cycle of irradiated NSCs, it was shown that the cultivation of NSCs irradiated at a dose of 4 Gy in the presence of exosomes of both NSCs and mouse MSCs does not lead to the restoration of cell cycle parameters, but provides a decrease the number of apoptotic cells in 24 h after exposure.