Common pathogenetic mechanisms in affective disorders and multiple sclerosis: role of interleukin imbalance in the progression of comorbid pathology

Relevance. Among many comorbid pathologies, it is of considerable interest to study and compare the pathogenetic mechanisms of neurological and mental disorders that combine the clinical manifestations of multiple sclerosis (MS) and affective disorders. The high MS prevalence, economic and social significance of the disease, heterogeneity of clinical symptoms, an unfavorable progressive course, as well as the frequent combination of this pathology with various forms of hypothymic disorders determine the relevance of studying the common pathogenetic mechanisms for the development of this comorbid pathology, which is necessary for the development of effective and safe preventive medical activities. The purpose of the review is to determine the common immunopathological mechanisms of affective disorders and multiple sclerosis, to analyze the role of cytokine status imbalance in the mutual increase in the severity of clinical symptoms in comorbid pathology, and to identify prognostic markers of disease progression. Materials and methods. On the basis of electronic Russian and foreign databases for the period 2017–2022, a theoretical analysis of the pathophysiological mechanisms of autoimmune CNS damage in MS and affective disorders was carried out. In order to search for literary sources, the following resources were used: https://elibrary.ru/, https://www.ncbi.nlm.nih.gov/pubmed/, https://cyberleninka.ru/. 10 Russian and 25 foreign sources were cited. Results. The mechanisms of development of mental affective disorders and multiple sclerosis have common pathogenetic features and are characterized by a violation of pro-inflammatory cytokine reactions and autoimmune nature of changes in the structures of the central nervous system (CNS). The similarity of immunological disorders underlying the pathogenesis of various forms of multiple sclerosis and affective disorders is of undoubted interest in terms of developing common approaches to the prevention and treatment of detectable interleukin status imbalance in neurological and mental diseases. Conclusion. Identification of mutually reinforcing changes in interleukin status and determination of the features of the course of immune imbalance in multiple sclerosis and hypothymic disorders in various pathologies of the mental sphere are necessary for a deeper understanding of neuroimmune interactions.