Previous studies have demonstrated an increased risk of developing Parkinson’s disease (PD) in patients with type 2 diabetes mellitus (T2DM), as well as more severe and rapid motor and non-motor deterioration in diabetic PD patients compared to their non-diabetic counterparts. Additional research has suggested that diabetic subjects treated with glucagon-like peptide-1 (GLP-1) receptor agonists exhibit a reduced incidence of PD compared to those receiving other anti-diabetic medications. GLP-1 receptor agonists are FDA-approved therapies for T2DM, and recent studies have explored their potential as repurposed treatments for neurodegenerative diseases, including PD, AD, and ALS, as well as cerebrovascular disorders. This systematic review aims to assess the available literature on the efficacy and safety profiles of GLP-1 receptor agonists in PD management. A comprehensive search of PubMed, Scopus, CENTRAL, Web of Science, Embase, and ClinicalTrials.gov was conducted to identify relevant studies. The primary outcomes of this review include motor impairment in PD, as assessed by MDS-UPDRS Part III, as well as motor complications (Part IV) and motor experiences of daily living (Part II), and the incidence of gastrointestinal and systemic side effects. Meta-analysis showed that GLP-1 receptor agonists significantly improved motor function, as reflected by MDS-UPDRS Part III scores in the ON state (mean difference = − 2.88; p = 0.01; I² = 30%), although they were associated with a higher incidence of adverse events across all safety outcomes. Findings and conclusions of this review will contribute to a clearer understanding of the therapeutic potential of GLP-1 receptor agonists in PD, guiding future clinical research and treatment strategies.

Huntington’s disease (HD) is a progressive neurodegenerative disease resulting from a mutation in the huntingtin (HTT) gene and characterized by progressive motor dysfunction, cognitive decline, and psychiatric disturbances. Currently, no disease-modifying treatments are available. Recent research has developed therapeutic agents that may have the potential to directly target the disease pathology, such as gene silencing or clearing the mutant protein. However, these agents are limited by their inability to cross the blood-brain barrier (BBB), preventing optimal therapeutic effects. Although various techniques have been explored to overcome the BBB, focused ultrasound (FUS) has emerged as a promising non-invasive therapeutic modality offering the potential for targeted intervention in neurodegenerative diseases, including HD. Preclinical studies demonstrated the safety and efficacy of FUS in delivering therapeutic agents, such as siRNAs and AAV vector-based gene therapy, resulting in significant reductions in mutant HTT expression and improvements in motor function in HD mouse models. Furthermore, the safety profile of FUS-induced BBB opening has been established in clinical trials on human patients of neurodegenerative diseases other than HD, showing no adverse effects on brain structure or function. This review provides a comprehensive overview of the current state of FUS research in HD and connects existing evidence from neurodegenerative disease studies with its promise in establishing disease-modifying therapies for HD. Graphical Abstract

Background: There is limited evidence regarding the safety and efficacy of tenecteplase 0.25 mg/kg in patients with acute ischemic stroke in the extended time window, either with large vessel occlusion or not. Therefore, we aim to assess its safety and efficacy for these patients. Methodology: We searched PubMed, Scopus, and Web of Science for randomized controlled trials that compared tenecteplase 0.25 mg/kg with the best medical management. Our primary efficacy outcomes included favorable and excellent functional outcomes, measured via the modified Rankin score (mRS), and early neurological improvements. Primary safety outcomes were mortality and symptomatic intracranial hemorrhage rates. Subgroup analyses were performed based on mRs, and the inclusion of patients eligible for mechanical thrombectomy in addition to TNK. Results: Our search found nine randomized controlled trials, of which 8 were included in the meta-analysis. A total of 3068 patients were included. Tenecteplase 0.25 mg/kg did not differ from the control group in achieving excellent functional outcomes and favorable functional outcomes ( P values: 0.15 and 0.69), while there was significant improvement in early neurological improvement ( P value: 0.02). Symptomatic intracranial hemorrhage was statistically higher in the tenecteplase 0.25 mg/kg group ( P value 0.008). Subgroup analyses indicated that patients with mRS 0–1 who receive TNK 0.25 mg/kg do better than those with mRS 0–2. Better results for TNK 0.25 mg/kg were observed in studies that excluded patients eligible for mechanical thrombectomy in addition to TNK. Conclusions: TNK 0.25 mg/kg appears to significantly achieve early neurological improvement with no effect in achieving excellent or favorable functional outcomes; however, it showed a significant increase in symptomatic intracranial hemorrhage. Patients who performed endovascular thrombectomy after administering TNK 0.25 mg/kg had statistically significantly higher rates of symptomatic intracranial hemorrhage; on the other hand, current evidence endorses the use of tenecteplase 0.25 mg/kg in patients with ischemic strokes whose baseline mRs ranges from 0 to 1. Further RCTs are necessary to validate these findings. Prospero registration number : CRD42025636473.

This systematic review and meta-analysis aimed to evaluate the safety and effectiveness of magnetic resonance-guided focused ultrasound (FUS) subthalamotomy in patients with Parkinson’s disease (PD), focusing on improvements in motor symptoms, quality of life (QoL), medication burden, and adverse events (AEs). Following PRISMA and Cochrane guidelines, a comprehensive search was conducted across PubMed, Cochrane CENTRAL, Scopus, and Web of Science up to November 2025. Studies were included if they assessed the safety or efficacy of unilateral or bilateral FUS-STN in PD. Data extraction and risk of bias assessment were independently conducted by two reviewers. Meta-analyses at six months used a random effects model to pool mean differences (MD) with 95% confidence intervals (CI). Five studies ( n = 75) were included. FUS-subthalamic nucleus (STN) significantly reduced Movement Disorder Society-Sponsored Unified PD Rating Scale, Part III (MDS-UPDRS-III) scores at six months (MD: -11.05; 95% CI: [-14.68, -7.42]; P < 0.00001), with greater effects off-medication ( P = 0.0009). Treated-side scores improved (MD: -10.67; 95% CI: [-13.41, -7.92]), while untreated-side scores did not. Significant improvements were also seen in MDS-UPDRS-II (MD: -3.58; 95% CI: [-4.84, -2.32]; P < 0.00001), PD Questionnaire-39 (PDQ-39) (MD: -8.55; 95% CI: [-13.51, -3.58]; P = 0.0007), and levodopa equivalent daily dose (LEDD) (MD: -111.63 mg; 95% CI: [-162.52, -60.74]; P < 0.0001). Common AEs included dyskinesia (9.2%), gait disturbance (6.9%), and dysarthria (6.4%). FUS-STN significantly improves motor function, daily living activities, and QoL (PDQ-39) and reduces dopaminergic medication burden in PD patients with asymmetrical symptoms. AEs were generally mild and manageable, supporting its role as a safe, effective, and non-incisional alternative to conventional surgical options.

Background: Hemophilia A and B are inherited bleeding disorders in which outcomes are shaped by factor levels, inhibitor development, inter-individual pharmacokinetics, and progressive joint disease. With the emergence of extended half-life therapies, non-factor therapies, and gene therapy, there is an increasing need for biomarkers to support diagnosis, risk stratification, treatment selection, and monitoring. Methods: We conducted a narrative review of English-language studies indexed in PubMed, Scopus, Web of Science, and Google Scholar (January 2000 to October 2025). We prioritized primary studies, trials, registries, and assay-validation reports on diagnostic, prognostic, predictive, or monitoring biomarkers in hemophilia A/B; guidelines were used for context. Results: Established biomarkers include FVIII/FIX activity assays, inhibitor testing (Bethesda/Nijmegen-modified), F8/F9 genotyping, and imaging-based joint assessment. Emerging candidates include global hemostasis assays (thrombin generation, viscoelastic testing), PK/PD metrics for prophylaxis individualization, and exploratory inflammatory/angiogenic and tissue-turnover markers linked to arthropathy. Conclusions: Evidence for biomarkers in hemophilia is heterogeneous, and many non-traditional markers remain exploratory; standardized assays and prospective multicenter validation with clinically meaningful endpoints are needed before routine adoption. Limitation: This narrative synthesis was conducted in English and did not include a formal risk-of-bias assessment.