Traumatic brain injury (TBI) is a heterogeneous disease characterized by brain damage and functional impairment caused by external forces. Under the influence of multiple mechanisms, TBI can cause synaptic dysfunction, protein aggregation, mitochondrial dysfunction, oxidative stress, and neuroinflammatory cascade reactions, resulting in a high disability and mortality rate for patients and a heavy burden on families and society. Exosomes are cell-derived vesicles that encapsulate a variety of molecules, including proteins, lipids, mRNAs, and other small biomolecules. Among these, exosomes derived from mesenchymal stem cells (MSCs) have garnered significant attention owing to their therapeutic potential in the nervous system, offering broad clinical applicability. Recent studies have demonstrated that MSC-derived exosome injections in traumatic brain injury models effectively mitigate local inflammatory damage and promote nerve regeneration following injury. Owing to their small size, challenging replication, ease of preservation, and low immunogenicity, MSC exosomes are emerging as a promising therapeutic strategy for traumatic brain injury. This review explores the pathogenesis of traumatic brain injury, the underlying mechanisms of MSC exosome action, and the potential clinical applications of MSC exosomes in the treatment of traumatic brain injury.

Approximately 20%–50 % of individuals with autoimmune encephalitis (AE) demonstrate suboptimal responses to first-line therapies, leading to persistent neurological deficits and the need for second-line interventions. Although rituximab has shown potential as an alternative treatment in AE, the existing evidence remains insufficient. This study systematically evaluated and meta-analyzed the efficacy of rituximab in AE patients who either failed or exhibited inadequate responses to first-line treatments, aiming to refine and optimize therapeutic strategies for AE. A comprehensive search of PubMed, Embase, and the Cochrane Library databases was conducted, covering studies published up to June 10, 2024. In addition, manual cross-referencing of relevant studies was performed using both subject-specific and free-text terms such as “Rituximab,” “Rituxan,” “Mabthera,” “RTX,” “Mab,” “Ma,” “AE,” “encephalitis,” “Anti-NMDAR encephalitis,” and “autoimmune encephalitis.” Data on rituximab's efficacy as a second-line therapy in AE were independently screened and extracted by two researchers. Statistical analyses were conducted using R4.2.1 software to assess the pooled outcomes of the included studies. Analysis of 14 studies involving 277 AE cases revealed an 80 % favorable prognosis rate (0.72–0.89) for rituximab, with superior efficacy in patients under 18 years compared to those over 18 (I² = 65.9 %, 38.7%–81.0 %; p < 0.01). The prognosis rate for patients under 18 was 0.85 (0.76–0.93), while for those over 18, it was 0.72 (0.56–0.88). Furthermore, a disease duration of ≤180 days correlated with a better prognosis than durations exceeding 180 days, with rates of 0.82 (0.69–0.94) and 0.74 (0.61–0.87), respectively. Rituximab demonstrates an 80 % favorable prognosis rate in AE cases unresponsive to first-line treatments, particularly in patients under 18 or those with disease duration ≤180 days.

This investigation is designed to evaluate the effects of rTMS and its varying stimulation parameters and target sites on the therapeutic outcomes for post-stroke lower limb motor impairment and balance, with the objective of pinpointing stimulation locations and parameters that are both reasonable and applicable in clinical practice. An exhaustive search was carried out across the PubMed, MEDLINE, Embase, CENTRAL, and Web of Science databases to identify RCTs that assessed the effectiveness of rTMS in the treatment of lower limb motor impairment following a stroke. Meta-analysis was performed usingR statistical environment (V.4.2.2, www.r-project.org ). The review period encompassed the interval from the databases' origination through to February 18, 2024. Research reveals that applying rTMS to the unaffected motor cortex markedly enhances gait speed in stroke patients,exhibiting a significant effect (SMD: 1.117, 95% CI:0.40, 1.82, I2 = 0.0%). rTMS sessions comprising 1000–1500 pulses (SMD: 0.92, 95% CrI:0.63, 1.21, I2 = 42%, six studies), with a total session count ≥ 10 (SMD: 0.85, 95% CrI:0.53, 1.18, I2 = 54.1%, six studies), and high-frequency rTMS (SMD: 0.83, 95% CrI:0.34, 1.09, I2 = 46.3%, three studies) exhibit significant efficacyin improving lower limb balance and gait post-stroke. The research indicates that rTMS has been instrumental in enhancing the post-stroke prognosis for gait and limb balance. Nevertheless, the therapeutic efficacy of rTMS is subject to the diversity in stimulation locations and parameter settings.

Objective: This study aims to investigate how the E3 ubiquitin ligase LITAF influences mitochondrial autophagy by modulating MCL‐1 ubiquitination, and its role in the development of epilepsy.Methods: Employing single‐cell RNA sequencing (scRNA‐seq) to analyze brain tissue from epilepsy patients, along with high‐throughput transcriptomics, we identified changes in gene expression. This was complemented by in vivo and in vitro experiments, including protein–protein interaction (PPI) network analysis, western blotting, and behavioral assessments in mouse models.Results: Neuronal cells in epilepsy patients exhibited significant gene expression alterations, with increased activity in apoptosis‐related pathways and decreased activity in neurotransmitter‐related pathways. LITAF was identified as a key upregulated factor, inhibiting mitochondrial autophagy by promoting MCL‐1 ubiquitination, leading to increased neuronal damage. Knockdown experiments in mouse models further confirmed that LITAF facilitates MCL‐1 ubiquitination, aggravating neuronal injury.Conclusion: Our findings demonstrate that LITAF regulates MCL‐1 ubiquitination, significantly impacting mitochondrial autophagy and contributing to neuronal damage in epilepsy. Targeting LITAF and its downstream mechanisms may offer a promising therapeutic strategy for managing epilepsy.

Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by impaired neuromuscular junction transmission, leading to fluctuating muscle weakness and fatigue. This condition is driven primarily by autoantibodies targeting the acetylcholine receptor at the neuromuscular junction. These antibodies are predominantly generated through a T‑cell‑dependent pathway, initiating immunomodulatory responses via complement activation. Cytokines and inflammatory mediators also play pivotal roles in the pathogenesis of MG. Recently, increasing attention has been given to the involvement of cytokines in autoimmune diseases. Interleukin‑35 (IL‑35), an immunoregulatory cytokine, is critical in various inflammatory and autoimmune conditions. It modulates immune responses by promoting Treg proliferation, enhancing their immunosuppressive functions, inhibiting Th17 cell differentiation, and reducing proinflammatory cytokine levels. IL‑35 is thus pivotal in the onset and progression of MG. The present review outlines the key functions of IL‑35 in MG pathogenesis and the impact of IL‑35 on the treatment and prognosis of myasthenia gravis, explores its therapeutic potential, and assesses its prognostic value, offering insights into its mechanisms and implications for treatment.