Inflammatory cytokines have been implicated as crucial contributors to the onset and progression of non-alcoholic fatty liver disease (NAFLD). The exact mechanisms by which interleukins (ILs) contribute to NAFLD may vary, and ongoing research is aimed at understanding the specific roles of different ILs in the pathogenesis of this condition. In addition, variations in environmental factors and genetics in each individual can influence the onset and/or progression of NAFLD. The lack of clinical studies related to the potential therapeutic properties of IL-1 inhibitors currently does not allow us to conclude their validity as a therapeutic option, although preclinical studies show promising results. Further studies are needed to elucidate their beneficial properties in NAFLD treatment.

The existing literature highlights the presence of numerous coagulation factors and markers. Elevated levels of coagulation factors are associated with both existing and newly diagnosed cases of atrial fibrillation (AF). However, this article summarizes the role of coagulation in the pathogenesis of AF, which includes fibrinogen and fibrin, prothrombin, thrombomodulin, soluble urokinase plasminogen activator receptor, von Willebrand factor, P-selectin, D-dimer, plasminogen activator inhibitor-1, and platelet activation. Coagulation irregularities play a significant role in the pathogenesis of AF.

Background: Multiple sclerosis (MS) pathology is characterized by acute and chronic inflammation, demyelination, axonal injury, and neurodegeneration. After decades of research into MS-related degeneration, recent efforts have shifted toward recovery and the prevention of further damage. A key area of focus is the remyelination process, where researchers are studying the effects of pharmacotherapy on myelin repair mechanisms. Multiple compounds are being tested for their potential to foster remyelination in different clinical settings through the application of less or more complex techniques to assess their efficacy. Objective: To review current methods and biomarkers to track myelin regeneration and recovery over time in people with MS (PwMS), with potential implications for promyelinating drug testing. Methods: Narrative review, based on a selection of PubMed articles discussing techniques to measure in vivo myelin repair and functional recovery in PwMS. Results: Non-invasive tools, such as structural Magnetic Resonance Imaging (MRI) and Positron Emission Tomography (PET), are being implemented to track myelin repair, while other techniques like evoked potentials, functional MRI, and digital markers allow the assessment of functional recovery. These methods, alone or in combination, have been employed to obtain precise biomarkers of remyelination and recovery in various clinical trials on MS. Conclusions: Combining different techniques to identify myelin restoration in MS could yield novel biomarkers, enhancing the accuracy of clinical trial outcomes for remyelinating therapies in PwMS.

Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an emerging autoimmune demyelinating disorder distinct from multiple sclerosis and AQP4-IgG-positive neuromyelitis optica. Despite increasing recognition, no therapies are currently approved for MOGAD, and treatment remains empirical, with significant variability in clinical response and access to care. This review explores the evolving treatment landscape of adult MOGAD, with a focus on immunotherapies under active clinical investigation: azathioprine, tocilizumab, satralizumab, and rozanolixizumab. For each agent, we discuss mechanisms of action, pharmacokinetics, dosing, safety, and efficacy based on clinical trials and observational data. Literature was identified through PubMed and ClinicalTrials.gov, including ongoing phase 2/3 studies (MOGwAI, TOMATO, METEOROID, and cosMOG). Targeted immunotherapies have the potential to transform MOGAD management. In the next five years, one or more of these agents may achieve regulatory approval, particularly if biomarker-driven strategies and trial designs are refined. Addressing unmet needs in pediatric populations and low-resource settings will be essential to ensure equitable, personalized treatment.

Objective: To evaluate the real-world effectiveness and safety of eculizumab in patients with AQP4-IgG–positive neuromyelitis optica spectrum disorder (NMOSD) and to identify predictors of disability outcomes. Methods: This multinational, retrospective cohort study analyzed data from 46 patients across 26 centers. The outcomes included the annualized relapse rate (ARR), relapse-free status, change in expanded disability status scale (EDSS) scores, and adverse events. To identify predictors of EDSS improvement or worsening, patients were stratified into subgroups (improved vs. stable/worsened) at each follow-up time point and compared based on demographic, clinical, and radiological variables. Results: This retrospective cohort study included 46 patients with AQP4-IgG-positive NMOSD from 26 centers, followed for a mean of 27.3 months. The mean ARR significantly decreased from 1.1 in the 2 years pre-treatment to 0.1 during eculizumab therapy. The relapse-free rate increased from 6.5% pre-treatment to 80.4%. Mean EDSS scores improved from 4.2 at baseline to 3.6 at 24 months. The presence of area postrema syndrome was associated with a favorable prognosis, while the presence of spinal attacks was associated with a poor prognosis at 12 months. Adverse events occurred in 7 patients (18.9%), leading to permanent discontinuation in only two. Conclusion: Eculizumab demonstrated robust real-world effectiveness in reducing relapse rates and stabilizing disability, with an acceptable safety profile. Clinical outcomes may be influenced by attack phenotype, underscoring the importance of early intervention.