Neuroscience
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Mitochondrial dysfunction is a pivotal factor in the pathogenesis of neurodegenerative disorders, driving neuronal degeneration through mechanisms involving oxidative stress, impaired energy production, and dysregulated calcium homeostasis. Agmatine, an endogenous polyamine derived from arginine, has garnered attention for its neuroprotective properties, including anti-inflammatory, anti-oxidative, and antiapoptotic effects. Recent studies have highlighted the potential of agmatine in preserving mitochondrial function and mitigating neurodegeneration, making it a promising candidate for therapeutic intervention. ⋯ Despite promising findings, challenges such as optimizing agmatine's pharmacokinetics, determining optimal dosing regimens, and elucidating its precise molecular targets within mitochondria remain to be addressed. Future research directions should focus on developing targeted delivery systems for agmatine, investigating its interactions with mitochondrial proteins, and conducting well-designed clinical trials to evaluate its therapeutic efficacy and safety profile in neurodegenerative disorders. Overall, agmatine emerges as a novel therapeutic agent with the potential to modulate mitochondrial homeostasis and alleviate neurodegenerative pathology, offering new avenues for treating these debilitating conditions.
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In the context of EEG-based emotion recognition tasks, a conventional strategy involves the extraction of spatial and temporal features, subsequently fused for emotion prediction. However, due to the pronounced individual variability in EEG and the constrained performance of conventional time-series models, cross-subject experiments often yield suboptimal results. To address this limitation, we propose a novel network named Time-Space Emotion Network (TSEN), which capitalizes on the fusion of spatiotemporal information for emotion recognition. ⋯ TSEN exhibits high accuracy and low variance in cross-subject emotion prediction tasks, effectively reducing individual differences among different subjects. Additionally, TSEN has a smaller parameter count, enabling faster execution.
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Intracerebral hemorrhage is a kind of hemorrhagic stroke resulting from bleeding in the brain parenchyma. SUMOylation is one of post-translational protein modifications based on covalent binding of small ubiquitin-like modifier (SUMO) peptide. Although SUMOylation has been reported to play neuroprotective roles in ischemic stroke, the role of SUMOylation in the pathology of intracerebral hemorrhage remains unclear. ⋯ For in vitro study, phagocytic activity of microglial BV-2 cells was examined using erythrocytes obtained from mouse blood. We found that both TAK-981 and small interfering RNA-mediated knockdown of SUMO2/3 inhibited erythrophagocytosis by BV-2 cells. These results suggest that SUMOylation by SUMO2/3 promotes hematoma clearance via regulation of CD36 expression in microglia and contributes to the recovery from pathology of intracerebral hemorrhage.
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This study investigated the clinical predictive value of cerebrospinal fluid (CSF) γ-aminobutyric acid (GABA) and serum neuron-specific enolase (NSE) and microRNA-155 (miR-155) for post-stroke epilepsy (PSE) in patients with cerebral infarction (CI). A total of 69 CI patients with PSE and 84 with non-post-stroke epilepsy (N-PSE) were retrospectively enrolled, with their clinical baseline data (CI type) and the National Institute of Health Stroke Scale (NIHSS) score collected. CSF GABA and serum NSE and miR-155 expression levels were determined, with their clinical value further assessed. ⋯ Briefly, CSF GABA was reduced while serum NSE and miR-155 were elevated in PSE patients. GABA and NSE combined with miR-155 had high diagnostic value for PSE occurrence in CI patients. Lowly-expressed GABA or highly-expressed NSE and miR-155 were independent risk factors for PSE in CI patients, which could provide effective guidance for the clinical diagnosis and management of PSE.