Journal of Neurorestoratology最新文献

{"title":"Letter to Editor: Authors' response to “Respondence of ‘Brain iron deposition and whole-exome sequencing of non-Wilson's disease hypoceruloplasminemia in a family’”","authors":"Min Xu, Jian-Zhong Yi, Xiao-Ping Wang","doi":"10.1016/j.jnrt.2024.100155","DOIUrl":"10.1016/j.jnrt.2024.100155","url":null,"abstract":"","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 4","pages":"Article 100155"},"PeriodicalIF":3.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000627/pdfft?md5=7c590c63c0cd37f723a13ec4acdef07b&pid=1-s2.0-S2324242624000627-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142150633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GsMTx4 ameliorates spinal cord injury by regulating microglial polarization through the Piezo1/NFκB/STAT6 pathway","authors":"Weiwei Zheng ,&nbsp;Peng Zhang ,&nbsp;Hui Che ,&nbsp;Yu Zhang ,&nbsp;Xing Yang ,&nbsp;Yixin Shen","doi":"10.1016/j.jnrt.2024.100144","DOIUrl":"10.1016/j.jnrt.2024.100144","url":null,"abstract":"<div><h3>Objective</h3><p>Inflammatory reactions are recognized as pivotal in spinal cord injury (SCI), with the anti-inflammatory role of polarized microglia crucial in mitigating such injury. The present study aimed to determine the protective effects of GsMTx4 on functional recovery in a mouse model of SCI and investigate the role of GsMTx4 in cytokine-induced microglial activation and associated molecular mechanisms.</p></div><div><h3>Methods</h3><p>We assessed the effects of GsMTx4 on motor function in a mouse model of SCI, including neuronal survival and activated microglia in the vicinity of the injury after SCI. We also investigated the effects of GsMTx4 on expression of relevant inflammatory factors involved in cytokine-induced microglial activation and the associated signaling pathways.</p></div><div><h3>Results</h3><p>GsMTx4 effectively promoted functional recovery in mice and alleviated nerve damage after SCI. Additionally, GsMTx4 facilitated the transition of microglia from the M1 phenotype to the M2 phenotype, suppressed microglial activation, and reduced the expression of corresponding inflammatory mediators. These effects may involve modulation of neurogenic inflammation through the Piezo1/NFκB/STAT6 pathway, at least in part.</p></div><div><h3>Conclusion</h3><p>GsMTx4 safeguards against SCI by regulating microglial polarization, potentially via the Piezo1/NFκB/STAT6 pathway, offering initial evidence supporting the potential therapeutic efficacy of GsMTx4 for treatment of SCI.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 4","pages":"Article 100144"},"PeriodicalIF":3.1,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000512/pdfft?md5=bfe78d8fe1add4d4db5e0233b5e29251&pid=1-s2.0-S2324242624000512-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142128501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of chronic restraint stress-and lipopolysaccharide-induced mouse models of depression: Behavior, c-Fos expression, and microglial and astrocytic activation","authors":"","doi":"10.1016/j.jnrt.2024.100130","DOIUrl":"10.1016/j.jnrt.2024.100130","url":null,"abstract":"<div><p>Depression is a mental disease that involves a variety of complex physiological mechanisms. A wide range of methods have therefore been used to establish mouse models of depression, and there are currently many ways to develop such mouse models. The present study aimed to compare the effects of various model induction methods and assesses their different effects. To this end, C57BL/6J mice were divided into three experimental groups: the chronic restraint stress (CRS) group received 6 hours of daily confinement within restraint tubes over a 3-week period; the chronic lipopolysaccharide (C-LPS) administration group received daily intraperitoneal injections of 0.5 mg/kg LPS for 1 week; and the acute LPS (A-LPS) administration group received a singular intraperitoneal injection of 0.83 mg/kg LPS. A corresponding control group was established for each experimental condition. Following mouse model establishment, depression-like behaviors were assessed through the forced swimming and tail suspension tests; anxiety-related behaviors were evaluated using the open field test and elevated plus maze. Furthermore, the expression of the immediate early gene c-Fos, ionized calcium-binding adapter molecule 1 (IBA1), and glial fibrillary acidic protein (GFAP) was examined via immunofluorescence. Longer immobility durations during the forced swimming and tail suspension tests were observed across all model groups (<em>p</em> &lt; 0.05), indicating depression-like behaviors. Furthermore, the CRS and C-LPS group, but not the A-LPS group, showed significant anxiety-like behaviors in the elevated plus maze (<em>p</em> &lt; 0.05). All model groups also exhibited significant increases in both time and distance explored within the central area of the open field test (<em>p</em> &lt; 0.05). The activation of GFAP- and IBA1-positive cells in the cerebral cortex and hippocampus was also markedly pronounced in all experimental groups, suggesting the association of neuroinflammatory responses with induced depressive states. The present findings contribute to our understanding of the pathophysiology of stress-induced and neuroinflammatory-associated depression, and will help researchers to choose suitable depression models for their investigations.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100130"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000378/pdfft?md5=7a7c7c0bf937867ee601b6849c8cef0f&pid=1-s2.0-S2324242624000378-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141411565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The 2023 yearbook of Neurorestoratology","authors":"","doi":"10.1016/j.jnrt.2024.100136","DOIUrl":"10.1016/j.jnrt.2024.100136","url":null,"abstract":"<div><p>Remarkable advancements have been made in understanding the pathogenesis of Alzheimer's disease, Parkinson's disease, and other neurological disease; in our depth of understanding neurorestorative mechanisms such as anti-inflammatory processes, immune regulation, neuromodulation, neovascularization/neural repair, and neuroprotection; and in clinical neurorestorative treatments. Multiple types of cell therapies have been reported, with some positive outcomes. Diverse forms of neurostimulation and neuromodulation as well as brain–computer interfaces have shown good therapeutic outcomes in clinical applications. Further, therapeutic neurorestorative surgery and pharmaceutic therapy have been very impressive. These fundamental achievements are helpful for understanding the pathogenesis of neurological diseases and the mechanisms of neurorestoration. Patients with neurological impairments have benefited from therapeutic progress, but some of these therapies still require confirmation in higher-level randomized clinical trials.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100136"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000433/pdfft?md5=f1d96797a2736929de41d950264bc2f4&pid=1-s2.0-S2324242624000433-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141393554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potential of diverse brain–computer interface signal acquisition techniques in neurorestoratology","authors":"Yike Sun,&nbsp;Xiaogang Chen,&nbsp;Xiaorong Gao","doi":"10.1016/j.jnrt.2024.100138","DOIUrl":"10.1016/j.jnrt.2024.100138","url":null,"abstract":"","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100138"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000457/pdfft?md5=200a9ecbc680128773cf688f67fcfbcc&pid=1-s2.0-S2324242624000457-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141846734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of ultrashort wave on neuronal damage and heat shock protein 70 expression after cerebral ischemia-reperfusion injury in rats","authors":"Jing Yin ,&nbsp;Jiaxin Sun ,&nbsp;Wenbin Li ,&nbsp;Yongmei Fan ,&nbsp;Zhang Lei","doi":"10.1016/j.jnrt.2024.100132","DOIUrl":"10.1016/j.jnrt.2024.100132","url":null,"abstract":"<div><h3>Background</h3><p>Ultrashort wave (USW) therapy has been reported to alleviate cerebral ischemia/reperfusion (IR) injury, however the underlying mechanisms remain elusive. The aim of this study was to observe the effect of non-thermal USW therapy on neuronal damage and expression of heat shock protein 70 (HSP70) after cerebral IR in rats.</p></div><div><h3>Methods</h3><p>Focal ischemia-reperfusion (IR) was induced in Sprague–Dawley rats by middle cerebral artery occlusion/reperfusion (MCAO/R). The Ninety-two rats (both male and female) were screened using the Zea-Longa 5 grade evaluation. Included rats were then randomly divided into blank, sham, model 1-day, model 3-day, model 7-day, USW 1-day, USW 3-day, or USW 7-day groups. All rats in the model groups received sham USW treatment, while rats in the USW groups received USW treatment, for 1, 3, or 7 days. We assessed the National Institutes of Health Stroke Scale, brain infarction volumes, ultrastructural damage scores using electron microscopy, and HSP70 expression by western blotting between the different groups.</p></div><div><h3>Results</h3><p>USW treatment reduced the National Institutes of Health Stroke Scale, infarction volume, and ultrastructural neuronal damage, and increased expression of HSP70, in the hippocampal CA1 region.</p></div><div><h3>Conclusions</h3><p>Non-thermal USW therapy may improve neurological function, decrease infarction volume, and reduce neuronal damage by increasing HSP70 expression following cerebral IR injury.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100132"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000391/pdfft?md5=5a7ce8f6cc1ae34e6325b8a2ba31324f&pid=1-s2.0-S2324242624000391-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141408613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Virtual reality as a non-conventional rehabilitation for stroke: A comprehensive review","authors":"Muhammad Altaf Hussain ,&nbsp;Asim Waris ,&nbsp;Syed Omer Gilani ,&nbsp;Shafaq Mushtaq ,&nbsp;Amit N. Pujari ,&nbsp;Niaz B. Khan ,&nbsp;Mohammed Jameel ,&nbsp;Gulrux Daminova ,&nbsp;M. Ijaz Khan","doi":"10.1016/j.jnrt.2024.100135","DOIUrl":"10.1016/j.jnrt.2024.100135","url":null,"abstract":"<div><p>Stroke survivors often experience debilitating neural, physical, and cognitive impairments, particularly affecting upper limb functions. Conventional rehabilitations, though effective, are perceived as slow and monotonous by stroke survivors. This review explores the potential of Virtual Reality (VR) as an engaging rehabilitation approach to address such limitations. Our findings show that VR-based rehabilitations can be beneficial in restoring post-stroke upper limb functions and improving routine life of survivors. Moreover, VR offers adaptability, and user-friendliness across age groups. However, further research with larger sample size studies and stronger evidence base is needed to definitively establish the effectiveness of VR in post-stroke rehabilitation.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100135"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000421/pdfft?md5=f9d81b9c5501e98f86e5d1bfa979843a&pid=1-s2.0-S2324242624000421-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142006311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PRP and other techniques for restoring function across peripheral nerve gaps","authors":"Damien P. Kuffler","doi":"10.1016/j.jnrt.2024.100131","DOIUrl":"10.1016/j.jnrt.2024.100131","url":null,"abstract":"<div><p>Restoring function to peripheral nerves with a gap is challenging, with &lt;50% of patients undergoing nerve repair surgery recovering function. Sensory nerve grafts (autografts) are the clinical “gold standard” for bridging nerve gaps to restore sensory and motor function. They have significant limitations and restore meaningful function only across short gaps when repairs are performed soon after trauma and patients are young. When the value of any of these variables is large, the extent of recovery decreases precipitously, and when two or all are simultaneously large, there is little to no recovery. The extent of restored meaningful recovery has not increased in almost 70 years. Thus, novel techniques are needed that enhance both the extent of recovery and the percentage of patients who recover meaningful recovery. This paper reviews the limitations of autografts and other materials used to repair nerves. It also examines autologous platelet-rich plasma (PRP), a promising nerve gap repair technique that induces recovery in clinical settings where autografts are ineffective, including when the values of all three variables are simultaneously large.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100131"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S232424262400038X/pdfft?md5=582f62d527b387398931b96d9c29d834&pid=1-s2.0-S232424262400038X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141405536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correct understanding of brain–computer interfaces","authors":"Yunfa Fu,&nbsp;Xiaogang Chen,&nbsp;Yong Hu","doi":"10.1016/j.jnrt.2024.100139","DOIUrl":"10.1016/j.jnrt.2024.100139","url":null,"abstract":"","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100139"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2324242624000469/pdfft?md5=6754e03b1872bf83ada4ffd71eeebd9e&pid=1-s2.0-S2324242624000469-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141838571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances in STXBP1 encephalopathy research and translational opportunities","authors":"","doi":"10.1016/j.jnrt.2024.100134","DOIUrl":"10.1016/j.jnrt.2024.100134","url":null,"abstract":"<div><p><em>STXBP1</em> encephalopathy (<em>STXBP1</em>-E) is a rare neurodevelopmental disorder that includes epilepsy; it is caused by <em>de novo STXBP1</em> mutations. In clinical settings, pharmaceutical interventions to treat <em>STXBP1</em>-E predominantly concentrate on seizure control. However, effective treatments for seizure recurrence, treatment resistance, and common comorbidities remain scarce. Patients with <em>STXBP1</em>-E display a wide range of pathogenic variations that manifest as loss-of-function, gain-of-function, or dominant-negative effects. However, recent studies have primarily investigated the pathogenic mechanisms resulting from loss-of-function mutations using <em>STXBP1</em> haploinsufficiency models. This approach fails to accurately assess the impact of disease-causing mutations. Moreover, to evaluate new syntaxin-binding protein 1 (STXBP1)-targeting drugs, novel models that incorporate disease-causing mutations or even the genetic backgrounds of patients are needed. Here, we discuss the clinical symptoms of <em>STXBP1</em>-E and the relationship between this disorder and <em>STXBP1</em> mutations. We also review recent progress toward understanding the biological function of STXBP1 and its deficiency-induced cellular defects. We then discuss recent discoveries concerning the pathogenesis of <em>STXBP1</em>-E and the limitations and challenges associated with the current research model. Additionally, we underscore the value of leveraging stem cell technology to study the pathogenic mechanisms of <em>STXBP1</em>-E, and review stem cell transplantation as a potential approach for treating this disorder. We also discuss potential future research directions that need to be resolved.</p></div>","PeriodicalId":44709,"journal":{"name":"Journal of Neurorestoratology","volume":"12 3","pages":"Article 100134"},"PeriodicalIF":3.1,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S232424262400041X/pdfft?md5=f7a8b09795703d81f7a217f44f1e9bba&pid=1-s2.0-S232424262400041X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141393922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}