Background: Multiple sclerosis (MS) is an immune-mediated inflammatory disease of the central nervous system characterized by demyelination and axonal damage. This chronic neurological disorder affects millions worldwide and poses a significant economic and social burden. Current therapeutic strategies for MS primarily focus on mitigating neuroinflammation but do not effectively reverse demyelination. The GABA_B receptor is expressed in oligodendrocytes and immune cells. GABA_B receptors appear to play a role in modulating immune cells and promoting remyelination of damaged neurons. However, the effects of GABA_B-receptor modulation in animal models of MS remain largely unexplored. Therefore, this study evaluates the therapeutic role of GABA_B receptor activity in rats with experimental autoimmune encephalomyelitis (EAE) to mimic MS in humans. Methods: EAE was induced in rats by immunization with 200 μg myelin oligodendrocyte glycoprotein (35-55) peptide in complete Freund’s adjuvant containing killed Mycobacterium tuberculosis. Additionally, rats received injections of 200 ng pertussis toxin on the day of immunization and 48 h later. The EAE rats were treated with normal saline, CGP-55845, baclofen, or CGP-55845 + baclofen, i.p. Myelination in the lumbar spinal cord was assessed in control rats at 18- and 35-day postinduction. Results: CGP treatment significantly enhanced remyelination in EAE rats. This was evidenced by significant improvements in body weight and EAE clinical scores, as well as favorable histological changes. The observed increase in myelin expression in CGP-treated animals suggests that CGP-55845 promotes both remyelination and oligodendrocyte differentiation. Conclusions: Our results suggested that the selective GABA_B receptor antagonist CGP-55845 plays a significant role in promoting neural stem cell proliferation, particularly oligodendrocyte cells and remyelination in the EAE model of MS

Elderly individuals with dementia experience significant cognitive and emotional impairments, motivating research into technology-driven therapies to improve their quality of life. However, the effectiveness of such systems is often limited by poor-quality electroencephalographic (EEG) data, which can be distorted or incomplete due to artefacts. This study introduces a novel brain-computer interface (BCI)-based rehabilitation framework that combines neural network-assisted EEG data restoration with personalised therapy modules. The proposed method employs a multilayer perception (MLP) enhanced with a custom activation function to reconstruct missing EEG values by modelling spatial and temporal dependencies among adjacent electrodes. Experimental evaluation on benchmark EEG datasets shows that the proposed approach reduces Mean Absolute Error (MAE) by 15% and increases the Correlation Coefficient (CC) by 10% compared to traditional imputation techniques such as mean substitution and k-nearest neighbours (KNN). The restored EEG data are further integrated into a generative AI-powered rehabilitation system that delivers adaptive treatments through virtual reality (VR) environments and social interaction activities. By incorporating patient-specific affective profiles and preferences, the system dynamically personalises interventions such as cognitive games, reminiscence sessions, and immersive simulations. Overall, this framework bridges computational neuroscience and patient-centred healthcare, highlighting EEG imputation as a core technology for next-generation intelligent dementia care solutions, particularly in rural and resource-limited settings.

Deficiencies in immune protection (both congenital and acquired through life) significantly influence a human’s life quality. Primary minor immunodeficiencies (PMDs) are more common in the population than classical immunodeficiencies and place a high burden on society. However, the evidence on PMDs is not systematized. The aim of the current research became the analysis and synthesis of the evidence on etiology, epidemiology, diversity, clinical manifestations, diagnosis, and treatment of PMD in humans to synthesize a scientific concept. In this way, the systematic review of publications from PubMed and SCOPUS databases has been conducted by the keywords. The time of analysis was the period from 1960 to 2025. Out of 2937 primary publications, 424 that met the selection criteria were included in the final list. As a result, terminology, genetic heterogeneity, epidemiology, spectrum of manifestation, structuring of clinical syndromes, and classification of PMD were clarified due to the current research. A distinction is made between PMD and classical immunodeficiencies. The algorithms of diagnostics and immunotherapeutic interventions were considered. The scientific concept of PMD diagnosis and treatment was proposed, which presents PMDs as a universal natural model of the development of different human immune-dependent pathologies on a population scale. PMDs, by their prevalence in the population, diversity, and degree of clinical manifestation, can explain the development of the entire described spectrum of immunodependent diseases in humans. The proposed PMD concept can allow optimizing the clinical management of patients with associated immunodependent pathology using an integrative personalized multidisciplinary approach with the availability of etiology estimation and etiotropic treatment providing.