Phytomedicine, Journal Year: 2024, Volume and Issue: 135, P. 156222 - 156222
Published: Nov. 9, 2024
Language: Английский
Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 12, 2025
Language: Английский
Citations
0
CNS Neuroscience & Therapeutics, Journal Year: 2025, Volume and Issue: 31(2)
Published: Feb. 1, 2025
ABSTRACT Background Epilepsy, a prevalent neurological disorder, is distinguished by episodic abnormal discharges of neurons within the brain, resulting in transient brain dysfunction. Prior research has identified novel form cell death termed ferroptosis, which intricately linked to initiation and progression epilepsy. It been demonstrated that astaxanthin (AST) can inhibit ferroptosis enhancing activity nuclear factor erythroid 2‐related 2 (Nrf2), thereby providing cytoprotection. Therefore, this study aims investigate whether AST alleviate neuronal epilepsy activating Nrf2/GPX4 pathway, exerting neuroprotective effect. Methods By constructing kainic acid (KA)‐induced mouse model KA‐induced HT22 model, we employed behavioral testing, Western blot analysis, quantitative real‐time reverse transcription qRT‐PCR, ferroptosis‐related assay kits, immunofluorescence staining, other methods. These methodologies were utilized protective effects underlying mechanisms on epileptic mice neurons. Results Our results demonstrate pretreatment alleviates behaviors cognitive impairments mitigates indicators such as lipid peroxidation mitochondrial morphological alterations. This effect appears be mediated activation signaling axis. In vitro studies further revealed confers neuroprotection against death, an abrogated Nrf2 inhibitor. Hence, properties are significantly associated with modulation Nrf2‐mediated corroborated bioinformatics analyses. Conclusion The effectively inhibits both vivo models via pathway. finding suggests holds promise potential therapeutic agent for treatment
Language: Английский
Citations
0
Advanced Healthcare Materials, Journal Year: 2025, Volume and Issue: unknown
Published: April 30, 2025
Abstract Epilepsy is a prevalent chronic neurological disorder characterized by seizures resulting from an imbalance between excitatory and inhibitory neurons. While pharmacotherapy remains the standard treatment, traditional faces significant challenges, including poor brain penetration, high drug resistance rates, providing only symptomatic relief, rather than addressing underlying causes for comprehensive cure. Recently, neurovascular complex (NVC) has gained attention its critical role in development progression of epilepsy. Simultaneously, various innovative bio‐nanotechnology systems have emerged, specifically designed to enhance delivery across enable precise targeting within lesion. Herein, this review begins outlining core NVC involved epilepsy breaking it down into four key components: blood‐brain barrier (BBB), neurons, glial cells, microenvironment. The viability improve therapy analyzed. Next, systems, detailing their design principles, construction strategies, preclinical evaluations are highlighted. Finally, prospects next‐generation nanotechnologies challenges that must be overcome effective clinical translation discussed. Overall, aims guide more efficient bio‐nano therapies, ultimately enhancing treatment outcomes patients.
Language: Английский
Citations
0
Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15
Published: Aug. 6, 2024
Patients with epilepsy face heightened risk of post-ictal cardiorespiratory suppression and sudden unexpected death in (SUDEP). Studies have shown that neuroinflammation, mediated by the activation microglia astrocytes, may be a cause or consequence seizure disorders. Kcnj16 (Kir5.1) knockout rats (SS kcnj16−/− ) are susceptible to repeated audiogenic seizures recapitulate features human SUDEP, including ventilatory suppression, which worsens seizure-induced mortality. In this study, we tested hypothesis neuroinflammation within key brainstem regions contribute control breathing. Audiogenic were elicited once/day for up 10 days groups adult male SS rats, from frozen biopsies pre-Bötzinger complex/nucleus ambiguus (preBötC/NA), Bötzinger complex (BötC), raphe magnus (RMg) subjected cytokine array. Several cytokines/chemokines, IL-1α IL-1ß, increased selectively preBötC/NA after 3 5 fewer changes other tested. additional underwent seizures, quantified microglial (IBA-1+) cell counts morphology, specifically region, showed counts, area, volume consistent activation. To further test role inflammation physiological responses seizure-related mortality, treated anakinra (IL-1R antagonist), ketoprofen (non-selective COX inhibitor), saline before (1/day), breathing was measured before, during, each seizure. Remarkably, IL-1R antagonism mitigated on 7–10 but failed prevent whereas treatment exacerbated compared prevented These data demonstrate region respiratory following functionally differentially pathophysiological consequences seizures.
Language: Английский
Citations
3
Epilepsia Open, Journal Year: 2024, Volume and Issue: 9(5), P. 1962 - 1967
Published: Aug. 16, 2024
Abstract This case report presents a 38‐year‐old male patient who, after febrile infection, developed super‐refractory status epilepticus and multiorgan failure, died in 2 weeks despite the best possible intensive care. Autopsy revealed findings suggestive of hemophagocytic lymphohistiocytosis (HLH). shows that rare immunological cause such as HLH may infection‐related epilepsy syndrome (FIRES), complications care can mask physiological laboratory changes HLH. Plain Language Summary man intractable epileptic activity requiring treatment. During care, showed signs multiple organ damage (HLH), which is immune system regulation disorder leading to persistent inflammatory state damages. an like underlie treatment resistant fever‐related seizures.
Language: Английский
Citations
3
Cells, Journal Year: 2025, Volume and Issue: 14(2), P. 94 - 94
Published: Jan. 10, 2025
Epilepsy is a chronic neurological disorder marked by recurrent seizures, significantly impacting individuals worldwide. Current treatments are often ineffective for third of patients and can cause severe side effects, necessitating new therapeutic approaches. Glial cells, particularly astrocytes, microglia, oligodendrocytes, emerging as crucial targets in epilepsy management. Astrocytes regulate neuronal homeostasis, excitability, synaptic plasticity, playing key roles maintaining the blood-brain barrier (BBB) mediating neuroinflammatory responses. Dysregulated astrocyte functions, such reactive astrogliosis, lead to abnormal activity seizure generation. They release gliotransmitters, cytokines, chemokines that may exacerbate or mitigate seizures. Microglia, innate immune cells CNS, contribute neuroinflammation, glutamate excitotoxicity, balance between excitatory inhibitory neurotransmission, underscoring their dual role promotion protection. Meanwhile, primarily involved myelination, also modulate axonal excitability neuron-glia network underlying pathogenesis. Understanding dynamic interactions glial with neurons provides promising avenues novel therapies. Targeting these improved control better clinical outcomes, offering hope refractory epilepsy.
Language: Английский
Citations
0
New discovery., Journal Year: 2025, Volume and Issue: unknown, P. 1 - 8
Published: March 10, 2025
Febrile infection-related epilepsy syndrome (FIRES) is a severe epileptic with unclear etiology and pathogenesis, difficult treatment, as well generally poor prognosis. This more common in school-age children previously normal physical examinations, often induced by fever, rapid onset, mainly manifesting status epilepticus refractory epilepsy. Due to the limited treatment options, most FIRES patients are resistant multiple antiepileptic drugs, condition explosive refractory, resulting review provides detailed of latest research progress on FIRES. It comprehensively examines diagnostic methods, approaches for FIRES, focus medication timing biological agent selection, providing reference clinical diagnosis
Language: Английский
Citations
0
Epilepsia, Journal Year: 2025, Volume and Issue: unknown
Published: April 28, 2025
Abstract Objective Mild malformations of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE) are brain lesions associated focal and characterized by increased density, heterotopic neurons, hypomyelination the white matter. Although previous studies have implicated somatic mutations SLC35A2 gene, cellular molecular mechanisms underlying MOGHE pathogenesis remain elusive. To address this gap, study aimed to systematically characterize cell type composition alterations at resolution using single‐nucleus multiomic profiling. Methods We performed sequencing obtain paired gene expression chromatin accessibility profiles >31 000 nuclei from gray matter regions compared results publicly available neurotypical control datasets. Results The analysis two patients revealed significant alterations, including presence neurons disease‐specific oligodendrocyte populations within subcortical MOGHE‐specific oligodendrocytes were upregulation synaptic functions enhanced neuron communication, denoting a possible role support mediation glia–neuron interactions disease. On other hand, genes neuronal migration Wnt signaling pathway, suggesting mechanism their atypical localization. Significance This high‐resolution mapping clinical samples unveils glial affected disease provides novel insights into pathophysiological MOGHE.
Language: Английский
Citations
0
Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 254, P. 155146 - 155146
Published: Jan. 19, 2024
Language: Английский
Citations
2
Neuroscience & Biobehavioral Reviews, Journal Year: 2024, Volume and Issue: 162, P. 105731 - 105731
Published: May 18, 2024
Fragile X messenger ribonucleoprotein 1 (FMRP) is a widely expressed RNA binding protein involved in several steps of mRNA metabolism. Mutations the FMR1 gene encoding FMRP are responsible for fragile syndrome (FXS), leading genetic cause intellectual disability and autism spectrum disorder, X-associated tremor-ataxia (FXTAS), neurodegenerative disorder aging men. Although mainly neurons, it also present glial cells its deficiency or altered expression can affect functions with implications pathophysiology brain disorders. The review focuses on recent advances role subtypes, astrocytes, oligodendrocytes microglia, FXS FXTAS, describes how absence reduced these impact neuronal functions. We will briefly address radial effects neural development gliomas speculate other
Language: Английский
Citations
2