Multiple sclerosis (MS) is a chronic autoimmune disease characterized by pathological processes of demyelination, subsequent axonal loss, and neurodegeneration within the central nervous system. Despite the availability of numerous disease-modifying therapies that effectively manage this condition, there is an emerging need to identify novel therapeutic targets, particularly for progressive forms of MS. Based on contemporary insights into disease pathophysiology, ongoing efforts are directed toward developing innovative treatment modalities. Primarily, monoclonal antibodies have been extensively investigated for their efficacy in influencing specific pathological pathways not yet targeted. Emerging approaches emphasizing cellular mechanisms, such as chimeric antigen receptor T cell therapy targeting immunological cells, are attracting increasing interest. The evolving understanding of microglia and the involvement of ferroptotic mechanisms in MS pathogenesis presents further avenues for targeted therapies. Moreover, innovative treatment strategies extend beyond conventional approaches to encompass interventions that target alterations in microbiota composition and dietary modifications. These adjunctive therapies hold promise as complementary methods for the holistic management of MS. This narrative review aims to summarize current therapies and outline potential treatment methods for individuals with MS.

Ischaemic stroke is the most prevalent stroke subtype, accounting for 80–90% of all cases worldwide, and remains a leading cause of morbidity and mortality. Its pathophysiology involves complex molecular cascades, with oxidative stress playing a central role. During cerebral ischaemia, reduced blood flow deprives neurons of essential oxygen and nutrients, triggering excitotoxicity, mitochondrial dysfunction, and excessive production of reactive oxygen and nitrogen species (RONS). Not only do these species damage cellular components, but they also activate inflammatory pathways, particularly those mediated by the transcription factor nuclear factor kappa-B (NF-κB). The pro-inflammatory milieu intensifies neuronal damage, compromises blood–brain barrier integrity, and exacerbates reperfusion-induced damage. Recent findings highlight the importance of the gut microbiota in modulating stroke outcomes, primarily through metabolic and immunological interactions along the gut–brain axis. Dysbiosis, characterised by reduced microbial diversity and an imbalance between beneficial and harmful strains, has been linked to increased systemic inflammation, oxidative stress, and worse prognoses. Specific gut-derived metabolites, including short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO), appear to either mitigate or intensify neuronal injury. SCFAs may strengthen the blood–brain barrier and temper inflammatory responses, whereas elevated TMAO levels may increase thrombotic risk. This narrative review consolidates both experimental and clinical data demonstrating the central role of oxidative stress in ischaemic stroke pathophysiology and explores the gut microbiota’s ability to modulate these damaging processes. Therapeutic strategies targeting oxidative pathways or rebalancing gut microbial composition, such as antioxidant supplementation, dietary modulation, probiotics, and faecal microbiota transplantation, present promising paradigms for stroke intervention. However, their widespread clinical implementation is hindered by a lack of large-scale, randomised trials. Future efforts should employ a multidisciplinary approach to elucidate the intricate mechanisms linking oxidative stress and gut dysbiosis to ischaemic stroke, thereby paving the way for novel, mechanism-based therapies for improved patient outcomes.

Cognitive impairment is a major healthcare challenge worldwide, with vascular cognitive impairment (VCI) being its second leading cause after Alzheimer’s disease. VCI is a heterogeneous group of cognitive disorders resulting from various vascular pathologies. Therefore, it is particularly difficult to determine its underlying cause and exact molecular basis. Nevertheless, the current understanding of the pathophysiological processes underlying VCI has changed and evolved in the last decades. The aim of this narrative review is to summarize the current state of knowledge on VCI pathogenesis and to analyze the potential role of the gut microbiota in this process, considering the most recent scientific reports and in accordance with the current understanding of these processes. Chronic cerebral hypoperfusion, which results in impaired blood supply, i.e., oxygen and nutrient deficiency, is the main underlying mechanism of VCI. Furthermore, chronic cerebral hypoperfusion triggers a cascade of molecular changes, starting with an energy imbalance, leading to glutamate excitotoxicity, acidotoxicity, and oxidative stress. Also, all of the above provoke the activation of microglia and the release of pro-inflammatory cytokines that recruit systemic immune cells and lead to their infiltration into the central nervous system, resulting in neuroinflammation. Blood–brain barrier dysfunction may occur at various stages of chronic cerebral hypoperfusion, ultimately increasing its permeability and allowing potentially toxic substances to enter the brain parenchyma. Gut microbiota and their metabolites, which have been identified in numerous inflammatory conditions, may also influence the pathophysiological processes of VCI.

Introduction: Hemodialysis patients are at higher risk of developing cognitive impairment, but the pattern of affected cognitive domains is still undetermined. Little is also known about the symptoms of depression and anxiety in hemodialysis patients. Methods: In this cross-sectional study, we included 74 consecutive adult patients undergoing hemodialysis. Cognitive functions were assessed using the Addenbrooke Cognitive Test III. In addition, all patients were screened for symptoms of depression and anxiety using the Hospital Anxiety and Depression Scale. Results: The mean age of hemodialysis patients was 65.69 ± 14 years. Among the patients, there were 27% and 31% of patients with mild cognitive impairment and suspected dementia, respectively. In the group of patients with suspected dementia, all cognitive functions had significantly lower values compared to these functions in incognitively unimpaired and mild cognitive impairment patients. The most impaired domain was verbal fluency, which reflects impairments in executive function. Depression and anxiety symptoms were observed in 28% and 22% of patients, respectively. Patients with anxiety symptoms had higher levels of endogenous creatinine, parathyroid hormone, and hemoglobin, as well as decreased creatinine clearance, being younger and less educated. No factors contributing to the occurrence of depressive symptoms were found. Conclusion: Cognitive dysfunction is a significant problem in hemodialysis patients. Our study showed that the prevalence of cognitive impairment and depression and anxiety symptoms in hemodialysis patients was high. The domain of executive functions was most affected. Furthermore, creatinine, parathyroid hormone, hemoglobin levels, creatinine clearance, and education affected the anxiety scale score.

As the world’s population continues to age, social patterns are changing, making aging a notable public health challenge. With aging as the major risk factor for cognitive decline, the global prevalence of dementia is projected to triple in the next 25 years. In light of the growing body of evidence of the involvement of microbiota in health and pathology, its role in age-related cognitive decline should be explored. Therefore, the aim of this narrative review is to thoroughly analyze the ways in which microbiota might affect the aging process and age-related cognitive decline. Overall, aging is a complex phenomenon manifested at systemic, cellular and molecular levels. According to recent studies, gut microbiota composition may influence age-related changes through the gut-brain axis. One mechanism involves dysbiosis-related chronic systemic inflammation, leading to the blood-brain barrier disruption and subsequent neuroinflammatory processes. In addition to inflammaging, gut microbiota may induce oxidative stress, which is another key factor in brain aging. Finally, not only gut microbiota, but also microbiota colonizing the oral cavity may be associated with age-related neurodegenerative diseases.

Background: Cognitive impairment (CI) in patients with chronic kidney disease, including those treated with renal replacement therapy, is a growing problem worldwide. Objectives: The study aimed to assess the prevalence of CI and associated factors in patients undergoing peritoneal dialysis (PD). Methods: In this cross-sectional study, 18 consecutive patients with PD therapy and 15 controls were evaluated for CI using the Addenbrooke’s Cognitive Examination III (ACE III) test. Results: The prevalence of CI was 33% in patients and 27% in the control group and was not statistically significant. A higher prevalence of CI was found in subjects aged ≥65 years old than in those <65 years old (p = 0.02), but only in the control group. The prevalence of CI in PD patients over and under 65 years of age did not differ statistically significantly (p = 0.12). Memory and verbal fluency were the most affected cognitive domain in PD patients with CI (p = 0.00, p = 0.04, respectively). There was a significant correlation between higher educated PD patients and the ACE III test results. The duration of dialysis did not affect the results of the cognitive screening test. Conclusions: CI is a growing problem in the course of chronic kidney disease and dialysis therapy. It seems that cognitive problems may occur in patients undergoing PD at a younger age than in the general population with particularly affected memory and verbal fluency. Higher educated patients score better on the cognitive screening test.