Objective (background) Spermidine (SPD), an endogenous polyamine, has garnered increasing interest for its pleiotropic biological activities and potential benefits for neurological health. This review aims to evaluates the evidence for SPD’s neuroprotective effects in neurological disorders, with particular emphasis on its emerging role in intracerebral hemorrhage (ICH), and to delineate its multifaceted mechanisms of actions Methods We systematically reviewed and synthesized the available preclinical literature on SPD in models of stroke, Alzheimer’s disease (AD), Parkinson’s disease (PD), depression, anxiety, and epilepsy, with a focused analysis on ICH. Key mechanistic studies were examined to identify the core pathways underlying SPD’s neuroprotective actions. Results A core mechanism underlying SPD’s neuroprotective effects is the induction of protective autophagy, primarily through inhibition of the mechanistic target of rapamycin pathway. Additionally, SPD also demonstrates potent anti-neuroinflammatory effects, which consequently reduces the production of pro-inflammatory cytokines such as interleukin-1β, interleukin-6, and tumor necrosis factor-α. Furthermore, SPD alleviates oxidative stress by enhancing antioxidant defenses and helps preserve blood–brain barrier integrity through upregulating tight junction proteins like Zonula Occludens-1. Conclusion Clinical translation of SPD faces key challenges, including limited human pharmacokinetic data and unclear context-dependent mechanisms. Nonetheless, its robust preclinical efficacy and favorable safety profile support SPD as a promising candidate for future neuroprotective strategies.
Objective Hemodynamic forces play a central role in the initiation, growth, and rupture of cerebral aneurysms. Although numerous computational fluid dynamics (CFD)-derived hemodynamic variables have been proposed, inconsistencies in their definitions, interpretation, and application have limited comparisons across studies. This study aimed to systematically organize these variables within a unified computational and biomedical framework. Methods Published computational and experimental studies investigating cerebral aneurysm hemodynamics were systematically analyzed. CFD methodologies, numerical modeling approaches, morphological descriptors, and hemodynamic variables associated with aneurysm initiation, growth, and rupture were evaluated and organized according to their physical meaning, computational characteristics, and reported biological and clinical relevance. Results Hemodynamic variables, including wall shear stress (WSS), oscillatory shear index (OSI), wall shear stress gradient (WSSG), relative residence time (RRT), endothelial cell activation potential (ECAP), helicity, and related metrics, were systematically classified according to their physical interpretation and functional roles. Numerical modeling frameworks, fluid–structure interaction methods, morphological risk factors, and emerging artificial intelligence (AI) applications were also integrated. The proposed framework clarifies relationships among commonly used parameters, resolves inconsistencies in terminology, and provides a structured reference for selecting and interpreting hemodynamic metrics. Conclusions This framework facilitates standardized reporting, improves reproducibility, enables consistent comparisons across studies, and supports future CFD-based investigations and rupture risk assessment in cerebral aneurysms.
Objective Intracerebral hemorrhage (ICH) is a deadly stroke subtype requiring ultra-early bundled interventions. The Mayo Clinic Comprehensive Stroke Center implemented a “ICH Phases” three-tiered communication system to accelerate multidisciplinary care. This article introduces this system and functions as a preliminary small-sample pilot for a larger underway prospective study Methods We conducted a retrospective before-and-after study of spontaneous ICH patients admitted between 2021 and 2025. The pre-implementation cohort included 46 patients (2021–2022), and the post-implementation cohort included 67 patients (2023–2025). Adherence to American Heart Association/American Stroke Association (AHA/ASA) acute ICH quality measures, door-to-CT time, ICH score documentation, antihypertensive treatment initiation, anticoagulation reversal, venous thromboembolism (VTE) prophylaxis, and discharge antihypertensive prescribing were compared before and after the implementation of new system. Results Included were 113 patients (46 pre; 67 post). Post-implementation improvements included: CT acquisition within 25 min (from 34.8% to 68.7%), antihypertensive treatment within 30 min (from 21.1% to 48.2%), anticoagulation reversal within 120 min (from 66.7% to 75.0%), VTE prophylaxis within 24 h (from 71.7% to 91.0%), and discharge antihypertensive prescriptions (from 66.7% to 83.7%). ICH score documentation within 6 h remained high (from 82.6% to 83.6%). Conclusion This structured communication system effectively optimizes multidisciplinary communication and coordination and accelerates hyperacute ICH care.
Despite successful thrombectomy, many patients with large-vessel occlusion stroke remain functionally dependent. The ATTRACTION trial evaluated low-dose tirofiban after successful endovascular reperfusion and showed a modest improvement in 90-day functional independence without a statistically significant increase in symptomatic intracranial haemorrhage. The benefit appeared greater in patients with large-artery atherosclerosis and possibly those with incomplete reperfusion, whereas patients with cardioembolic stroke showed less favourable profiles. Compared with previous negative adjunctive antithrombotic trials, ATTRACTION highlights the importance of timing, dose, and delivery route. Further studies are needed to refine patient selection and balance functional benefit against haemorrhagic risk.
Intracerebral hemorrhage (ICH) remains a devastating disease with high mortality and disability rates, yet effective therapeutic strategies are still limited. Emerging evidence has highlighted that the dynamic crosstalk between microglia and neurons plays a central role in both secondary brain injury and subsequent neural repair. We briefly summarize recent advances regarding how neurons actively modulate microglial phenotypes via soluble mediators and cell–surface signaling axes . We also discuss the dual role of microglia in hematoma clearance, inflammation resolution and tissue remodeling. We propose that targeting microglia–neuron interactions may represent a promising strategy for neuroimmunoregulation and neurorepair after ICH.
