Brain disorders (Amsterdam, Netherlands)最新文献

{"title":"The significance of focal pattern in hypsarrhythmia","authors":"Anna Wiedemann,&nbsp;Birgit Stark,&nbsp;Gudrun Gröppel","doi":"10.1016/j.dscb.2025.100188","DOIUrl":"10.1016/j.dscb.2025.100188","url":null,"abstract":"<div><h3>Introduction</h3><div>Infantile Epileptic Spasms Syndrome (IESS) presents a therapeutic challenge and is frequently associated with developmental delay. It is characterized by seizures and hypsarrhythmia on the EEG and has multiple etiologies that influence therapeutic decisions. Severity of hypsarrhythmia serves as an indicator for evaluating treatment efficacy. However, the correlation between clinical symptoms, EEG patterns, and cerebral lesions requires further investigation.</div></div><div><h3>Methods</h3><div>Eighteen infants diagnosed with IESS underwent video-EEG monitoring and MRI. Hypsarrhythmia severity was assessed using the Kramer et al. scoring system. Clinical semiology was evaluated for lateralizing features. Statistical analyses were conducted to examine correlations between EEG findings, clinical symptoms, and cerebral lesions.</div></div><div><h3>Results</h3><div>All infants exhibited hypsarrhythmia and 72.3 % presented with cerebral lesions, predominantly bilateral. Clinical symptoms frequently indicated lateralization, whereas EEG findings demonstrated lateralization in only 22.2 % of cases. No significant correlation was identified between hypsarrhythmia patterns and clinical symptoms or lesions. The severity of hypsarrhythmia was not a reliable predictor of the underlying etiology.</div></div><div><h3>Conclusion</h3><div>This study found no association between hypsarrhythmic patterns and focal semiology or lesions. Given the heterogeneity of IESS, individualized diagnostic approaches remain essential. While the hypsarrhythmia score enhances the comparability of EEG patterns, its utility in determining the underlying etiology appears to be limited.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100188"},"PeriodicalIF":0.0,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143201819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognitive enhancing effect of an extract of Swertia chirata against memory impairment induced by aluminum chloride","authors":"Reena Deshmukh ,&nbsp;Manisha Jaiswal ,&nbsp;Anshita Shukla ,&nbsp;Umesh Patil ,&nbsp;Mukesh Sharma","doi":"10.1016/j.dscb.2025.100190","DOIUrl":"10.1016/j.dscb.2025.100190","url":null,"abstract":"<div><h3>Background</h3><div>The most advanced type of neurodegenerative disease, Alzheimer's disease (AD), significantly reduces cognitive performance. Oxidative stress plays a role in the pathophysiological pathways of several neurodegenerative illnesses. Aluminum is one of the most potent neurotoxins known to cause oxidative stress in neurodegenerative disorders. Since there are currently few therapy options for AD, more alternatives are required. The current investigation aimed to assess the nootropic potential of <em>Swertia chirata</em> in rats.</div></div><div><h3>Materials and Method</h3><div>AlCl3 (100 mg/kg, p.o.) was used to induce amnesia, piracetam (500 mg/kg, p.o.) was employed as a standard, and an ethanolic extract of <em>Swertia chirata</em> (50, 100, 200, 400 mg/kg) was utilized to assess nootropic activity. The Novel Object Recognition test and the elevated plus maze in AlCl3-induced amnesia models were used to evaluate the effects of medications on learning and memory in rats. This impairment is likely due to the increased vulnerability of brain cells to oxidative stress. Numerous studies have demonstrated that certain flavonoid antioxidants reduce oxidative stress-induced neuronal apoptosis.</div></div><div><h3>Results</h3><div><em>Swertia chirata</em> ethanolic extract exhibited longer exploration times for unfamiliar objects compared to familiar ones. Additionally, the ethanolic extract demonstrated a reduction in transfer latency in the elevated plus maze (EPM) in the AlCl3-induced amnesia paradigm, indicating an improvement in cognitive function.</div></div><div><h3>Conclusion</h3><div>In experimental models, the ethanolic extract of Swertia chirata significantly (<em>p</em> &lt; 0.05) reversed AlCl3-induced amnesia and improved learning and memory. The study demonstrated the neuroprotective qualities of the extract. Its anti-inflammatory and antioxidant properties may contribute to its potential in treating cognitive disorders, including dementia and Alzheimer's disease.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100190"},"PeriodicalIF":0.0,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143350766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective effects of apigenin in neurodegeneration: An update on the potential mechanisms","authors":"Ali Mohammadkhanizadeh ,&nbsp;Mohammad Sheibani ,&nbsp;Soroush Taherkhani ,&nbsp;Davood Nourabadi ,&nbsp;Seyed Mahdi Mohamadi-Zarch ,&nbsp;Farnaz Nikbakht ,&nbsp;Yaser Azizi","doi":"10.1016/j.dscb.2025.100189","DOIUrl":"10.1016/j.dscb.2025.100189","url":null,"abstract":"<div><div>Neurodegenerative diseases (NDs) are characterized by the progressive loss of neurons and neuronal connections, leading to cognitive decline, memory impairment, and motor dysfunction. Apigenin, a flavonoid found in various herbs and plants, has garnered significant attention for its neuroprotective properties. This review aims to provide an update on the potential mechanisms by which apigenin exerts its protective effects in neurodegeneration. Apigenin has been shown to possess potent antioxidant activity, which is thought to play a crucial role in its neuroprotective effects. Oxidative stress, resulting from an imbalance between the production of reactive oxygen species (ROS) and the body's antioxidant defenses, is a hallmark of neurodegenerative diseases. Apigenin has been demonstrated to scavenge ROS, thereby reducing oxidative stress and mitigating the damage to neurons. Inflammation is another key feature of neurodegenerative diseases, and apigenin has been found to possess anti-inflammatory properties. Apigenin has been shown to inhibit the production of pro-inflammatory cytokines, such as TNF-α and IL-1β, which are elevated in neurodegenerative diseases. Moreover, apigenin has been demonstrated to suppress the activation of microglia, the resident immune cells in the brain, which are thought to contribute to neuroinflammation. In addition, apigenin has been shown to activate the PI3K/Akt signaling pathway, which is involved in promoting neuronal survival and preventing apoptosis. In this review, we focus on the underlying mechanisms and signaling pathways involved in neurodegenerative disorders, as well as the diverse beneficial effects of apigenin within these pathways. The literature surveyed spans from 1980 to 2024. Also, systematic search was performed in Embase, MEDLINE, Scopus, Web of Science Core Collection, and Google Scholar for relevant references. Our findings highlight the potential mechanisms associated with the neuroprotective effects of apigenin.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100189"},"PeriodicalIF":0.0,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143201821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the role of neuromodulation in neurodegenerative disorders: Insights from Alzheimer's and Parkinson's diseases","authors":"Mega Obukohwo Oyovwi ,&nbsp;Kehinde Henrietta Babawale ,&nbsp;Ejayeta Jeroh ,&nbsp;Benneth Ben-Azu","doi":"10.1016/j.dscb.2025.100187","DOIUrl":"10.1016/j.dscb.2025.100187","url":null,"abstract":"<div><h3>Background</h3><div>Recent studies suggest neuromodulation as a potential therapeutic strategy for neurodegenerative disorders like Alzheimer's disease (AD) and Parkinson's disease (PD), despite their complex pathophysiology and limited treatments' efficacy, requiring further investigation.</div></div><div><h3>Objective</h3><div>This study aims to explore the impact of neuromodulation techniques on the symptoms and progression of AD and PD, focusing on their underlying mechanisms and therapeutic benefits.</div></div><div><h3>Method</h3><div>A comprehensive review of recent literature was conducted, encompassing published articles, results of clinical trials, animal studies, and meta-analyses regarding various neuromodulation techniques, including transcranial magnetic stimulation (TMS), deep brain stimulation (DBS), and transcranial direct current stimulation (tDCS). Data on cognitive function, motor control, and quality of life were extracted and analyzed.</div></div><div><h3>Results</h3><div>Neuromodulation techniques demonstrated promising outcomes in both AD and PD. TMS showed significant improvement in cognitive functions in AD patients, while DBS resulted in substantial relief of motor symptoms and improved quality of life in PD patients. Additionally, mechanisms such as enhanced neuroplasticity, modulation of neurotransmitter systems, and the potential for neuroprotective effects were identified as key contributors to these benefits.</div></div><div><h3>Conclusion</h3><div>Neuromodulation offers potential therapeutic solutions for managing symptoms and slowing neurodegenerative disorders like AD and PD, but further research is needed to understand long-term effects and optimal protocols.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100187"},"PeriodicalIF":0.0,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143387039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Imitation and dyspraxia in autism: Clinical and therapeutic implications","authors":"Leonardo Massoni","doi":"10.1016/j.dscb.2025.100191","DOIUrl":"10.1016/j.dscb.2025.100191","url":null,"abstract":"<div><div>It is known that ASD is often associated with defects in imitating other speech and behaviors as well as with self-other mapping problems, not simply referable to general factors such as memory, spatial reasoning, motor control, or attention. It has also been suggested that disturbances of posture, also known as dyspraxia, as well as impairments in locomotion, facial expression, interests and affect, and inattention to other people's expressions, could be early markers of ASD. Meanwhile, by employing intense interaction, imitation, or “expressive art” therapies, which respond intimately to motor activities, some improvements could be made for these symptoms of ASD.</div><div>Starting from these premises, the aim of this short communication is to discuss some works on the clinical basis and therapeutic perspectives of imitation defects and dyspraxia in autism spectrum disorder.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100191"},"PeriodicalIF":0.0,"publicationDate":"2025-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143201822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of HEPCAM in Jacobsen syndrome: A pediatric case report highlighting white matter abnormalities","authors":"Ghazaleh Ghorbannezhad ,&nbsp;Reza Nejad Shahrokh Abadi ,&nbsp;Farrokh Seilanian Toosi ,&nbsp;Shima Shekari ,&nbsp;Saeedeh Sadat Mirtooni ,&nbsp;Narges Hashemi","doi":"10.1016/j.dscb.2025.100186","DOIUrl":"10.1016/j.dscb.2025.100186","url":null,"abstract":"<div><div>Jacobsen syndrome (JS) is a rare contiguous gene deletion disorder characterized by a deletion at the terminal end of the long arm of chromosome 11. JS has various phenotypic features, such as neurodevelopmental delays and congenital heart defects. Furthermore, deletion mutations in the long arm of chromosome 11 can also give rise to Megalocephalic Leukoencephalopathy (MLC), affecting the HEPCAM gene. The following case report presents a 9-year-old girl with JS and remarkable white matter abnormalities (WMA). Despite the complex clinical presentation with craniofacial anomalies and limb malformations, there were slow partial improvements in the WMAs over time as evidenced by sequential MRI findings. This case adds to the previously documented literature on the topic of white matter abnormalities in the context of Jacobsen syndrome, and showcases these changes after several years.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100186"},"PeriodicalIF":0.0,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143201820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Presentation of paralytic stroke due to hemorrhagic atypical parasagittal meningioma:A case report","authors":"Tie feng Lai ,&nbsp;Hai Yu","doi":"10.1016/j.dscb.2025.100184","DOIUrl":"10.1016/j.dscb.2025.100184","url":null,"abstract":"<div><div>Acute intracranial hemorrhage stemming from meningiomas represents a rare phenomenon. We report on a case of atypical parasagittal meningioma in the left fronto-parietal lobe presenting with right lower extremity paralysis due to intra-tumoral and subdural hemorrhage.Hemorrhagic meningioma in the central gyrus region is rarely reported, the clinical and imaging presentations could closely mimic a ruptured, thrombosed vascular malformation. The vascular proliferation and tumor invasion may play a pivotal role in the spontaneous hemorrhage from meningiomas.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100184"},"PeriodicalIF":0.0,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129814","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitory potential of polyphenolic stilbene derivatives with Glycogen Synthase Kinase-3β (GSK-3β) for Alzheimer's disease: Computational and SAR insights","authors":"Santosh Prasad Chaudhary Kurmi ,&nbsp;Dipanjan Karati","doi":"10.1016/j.dscb.2025.100182","DOIUrl":"10.1016/j.dscb.2025.100182","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a chronic and progressive neurodegenerative disorder. Beta-amyloid plaques and tau protein tangles emerge in the brain as pathological hallmarks of AD. One important enzyme involved in tau phosphorylation, Glycogen Synthase Kinase-3β (GSK-3β), has become a viable therapeutic target for AD. A new approach to AD intervention is provided by polyphenolic stilbene derivatives, which are well-known for their wide range of biological activities and show strong inhibitory capability against GSK-3β. This work uses computational methods, such as molecular docking, binding energy analysis, and structure-activity relationship (SAR) insights, to investigate the inhibitory action of polyphenolic stilbene derivatives. Molecular docking and MD-simulation of the best docked Piceid (C12) compounds were used to analyze the backbone stability and conformational binding affinity with the target protein GSK-3β. The SAR of Piceid and GSK-3β protein was specifically examined as the primary candidate target. Furthermore, binding free energy (MMGBSA), drug-likeness and toxicity, medicinal chemistry parameters were investigated in support to be lead compound for drug discovery. The molecular docking binding affinity of Piceid <strong>(C12)</strong> compound was found -8.8 Kcal/mol which is higher than GSK-3β inhibitor standard compound Laduviglusib <strong>(C18)</strong> has binding energy -8.7 Kcal/mol. These results imply that piceid has potential as an AD treatment because to its favorable interaction profile and high binding affinity.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100182"},"PeriodicalIF":0.0,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129812","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phenethyl isothiocynate attenuates Parkinson's disease and improves performance in hanging wire, rotarod and actophotometer test & dopamine levels in rats via inhibiting HDAC-1","authors":"Nikhil More,&nbsp;Angel Godad","doi":"10.1016/j.dscb.2025.100183","DOIUrl":"10.1016/j.dscb.2025.100183","url":null,"abstract":"<div><div>Parkinson's disease (PD) is a neurodegenerative disorder that affects overall motor activity due to the loss of dopaminergic neurons in the SNpc (Substantia Nigra Pars Compacta) region of the brain. Despite incessant research and development of new therapeutic agents, management of PD is still a troublesome affair. Histone Deacetylase 1 (HDAC-1-1) is an epigenetic regulator which plays an important role in the pathogenesis of PD. In the present study, we hypothesized that Phenethyl isothiocyanate (PEITC), a potent inhibitor of HDAC-1-1, may ameliorate PD. Efficacy of PEITC was evaluated in rotenone-induced PD model in Male Wistar Male rats. Rotenone (2.5mg/kg) was injected intraperitoneally for 28 days to all the groups except Normal Control. The administration of test drug PEITC (5, 10 &amp; 20 mg/kg) and standard drug levodopa with carbidopa was given for 28 days. The animals were subjected to various behavioural parameters to assess motor co-ordination and groups treated with PEITC showed better performance with P&lt;0.05 when compared with rotenone treated group. Further, HDAC-1 levels in brain tissue homogenate and histological analysis were performed. Prophylactic treatment of PEITC attenuated motor dysfunction in dose dose-dependent manner. Furthermore, there was a significant decrease in HDAC-1 levels in brain tissue homogenate in the treatment group. Histological analysis revealed a decrease in neuronal loss and vacuolization. Results of this study suggest potent anti-Parkinsonism activity of PEITC in Rotenone induced rat model of PD.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100183"},"PeriodicalIF":0.0,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129813","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The evolving spectrum of LAMA2 related congenital muscular dystrophy (MDC1)-Case series and review of literature","authors":"Rahul Sinha ,&nbsp;Sonali Singh ,&nbsp;Mona Tiwari ,&nbsp;Zulfikar Luhar ,&nbsp;Ankit Kumar Meena ,&nbsp;Arvinder Wander ,&nbsp;Dharmesh Soneji","doi":"10.1016/j.dscb.2025.100181","DOIUrl":"10.1016/j.dscb.2025.100181","url":null,"abstract":"","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"17 ","pages":"Article 100181"},"PeriodicalIF":0.0,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129815","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}