Sleep quality disorders in patients with neurological diseases are a common comorbid pathology that leads to mutual aggravation syndromes, accelerating the progression and severity of neurological conditions. Sleep problems speed up the progression of neurological diseases. In turn, these diseases further reduce sleep quality, this creates a “vicious cycle”. The prediction and early diagnosis of sleep quality disorders in patients with neurological profiles require the development of new sensitive and specific biomarkers. Among them, microRNA patterns are the most promising. This report will present the results of preclinical and clinical studies on changes in microRNA expression and their association with sleep quality disorders in experimental animals and humans with various neurological diseases and mental disorders. Additionally, a new personalized approach to assessing the risk of sleep quality disorders in patients with neurological and psychiatric profiles will be presented. This approach evaluates the risk of sleep disorders (low, medium, or high) based on the most thoroughly studied microRNA patterns.

Despite efforts to uncover genome variability confined to the human brain, genome composition of neurons remains a matter of conjecture in health and disease. Still, somatic neurogenomics continuously gives further insights into understanding of mechanisms for devastative psychiatric and neurological disorders. For instance, since somatic genetic mosaicism and genome instability affecting the brain dynamically change during the ontogeny, these phenomena are able to shape individual features of disease manifestation, course, and outcome. This review is dedicated to the involvement of genome instability in the pathogenesis of brain diseases. Genome/chromosome instability and somatic mosaicism mediating brain dysfunction may produce specific (personalized) manifestations and course of a brain disorder via genetic-environmental interactions. Consequently, genome instability in the brain has to be taken into account during the development of personalized therapeutic interventions in a wide spectrum of psychiatric and neurological disorders. Among the latters, the most striking are schizophrenia, Alzheimer’s diseases, and chromosome instability syndromes. Still, neurodevelopmental diseases (e.g., autism and intellectual disability) are to be investigated in the context of brain-specific genome instability.

Phytotherapy, as a traditional medicine method, has diverse therapeutic properties that can be used for disease-modifying therapy of intervertebral disc degeneration (IDD) in humans. Of particular interest are herbal remedies for the correction of chronic inflammation (primarily cytokine imbalance). The aim of this descriptive review is to update knowledge about herbal methods that are promising or traditionally used for the correction of cytokine imbalance in IDD. The results of preclinical and clinical studies and publications of historical interest on the traditional use of herbal remedies in Eastern and Western medicine were analyzed. Most herbal remedies for the correction of cytokine imbalance in IDD have evidence classes C and D, while the number of herbal remedies with evidence classes A and B is still small, despite many years and even centuries of experience in traditional medicine. In recent decades, there has been a trend toward increased research interest in this topic, with a growing number of preclinical studies of herbal remedies in animal models of IDD and arthritis (including arthritis of the facet joints of the spine). This review has demonstrated that traditional herbal medicine has not lost its clinical significance and can be used as a component of disease-modifying therapy for IDD in humans. Planning and conducting new preclinical and clinical studies of herbal remedies for this disease are necessary to increase the level of evidence for their use in clinical practice in accordance with modern requirements.

This study evaluated intravenous administration of allogeneic mesenchymal stem cells (MSCs) transduced with AAV9-ARSA to pigs. The MSCs were modified to overexpress human arylsulfatase A (ARSA). Thirty-five days after treatment, ARSA activity significantly increased in CNS tissues. No hepatotoxicity or systemic inflammation was observed. The results confirm the safety and efficacy of this MSC-based gene therapy for metachromatic leukodystrophy (MLD).

The article studies the clinical manifestations of hepatolenticular degeneration (HLD) in first-degree relatives of patients with genetically confirmed neurological forms of the pathology (a total of 37 representatives from 16 families). Molecular genetic testing was performed using Sanger sequencing. It was found that first-degree relatives in each of the examined families differ only in the severity and timing of the pathology with the same type of mutations in the ATP7B gene, and a clear similarity in the manifestations of the neurological defect. Early manifestation of the neurological defect was confirmed. Its occurrence was noted against the background of signs indicating changes in other organs and systems that mask brain tissue damage and extrapyramidal motor disorders. It has been shown that examination of first-line relatives of patients with neurological forms of HLD allows diagnosing the pathology at the preclinical stage (in 58.8%) or at its initial manifestations (in 35.3%), reducing the delay in diagnosis by 10 years or more. This guarantees early treatment and social adaptation of patients. The conducted studies allow us to recommend practical healthcare to include examination of first-line relatives in the standard of care for patients with HLD for early diagnosis and prevention of unfavorable outcomes.