International Journal of Neuroscience最新文献

{"title":"Nerve growth factor and angiotensin converting enzyme 2 levels in children with neurodevelopmental disorders.","authors":"Melike Kevser Gul, Murside Sahin, Esra Demirci, Sevgi Ozmen, Reyhan Tahtasakal, Elif Funda Sener","doi":"10.1080/00207454.2023.2257871","DOIUrl":"10.1080/00207454.2023.2257871","url":null,"abstract":"<p><strong>Objective: </strong>Neurodevelopmental disorders (NDDs) are the most common psychiatric disorders in childhood, and there are many factors in their etiology. In recent years, many biomarkers have been studied to elucidate the etiology of these disorders. In this study, it was aimed to investigate the levels of nerve growth factor (NGF) and angiotensin converting enzyme 2 (ACE2) in attention deficit hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and intellectual disability (ID).</p><p><strong>Methods: </strong>The study included 74 children with NDDs (the number of patients in ADHD, ASD and ID groups were 24, 25 and 25 respectively) and 30 healthy controls (HCs). Serum NGF and ACE2 levels were studied with ELISA kits, also complete blood count (CBC), levels of fasting glucose and serum lipids were assessed.</p><p><strong>Results: </strong>ACE2 levels were found to be lower in NDD group than HCs in girls. In boys with ASD, triglyceride levels were significantly higher than other groups. Also a positive correlation was found between ACE2 and NGF levels when all sample assessed together.</p><p><strong>Conclusions: </strong>This study is a premise for investigating ACE2 and NGF in NDDs. The role of these markers in ADHD, ASD, ID and other NDDs and their associations with gender should be assessed by studies in which both larger sample groups and more disorders.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1235-1241"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10578273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction.","authors":"","doi":"10.1080/00207454.2020.1783748","DOIUrl":"10.1080/00207454.2020.1783748","url":null,"abstract":"","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1424"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38073613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Translation and validation of the Persian version of the Stroke Self-Efficacy Questionnaire in stroke survivors.","authors":"Alia Saberi, Sajjad Saadat, Fatemeh Dadar, Mozaffar Hosseininezhad, Kasra Sarlak, Samaneh Ghorbani Shirkouhi, Nasim Athari, Nima Broomand Lomer","doi":"10.1080/00207454.2023.2273776","DOIUrl":"10.1080/00207454.2023.2273776","url":null,"abstract":"<p><strong>Background: </strong>The Stroke Self-Efficacy Questionnaire (SSEQ) is a self-report scale that measures stroke survivors' self-efficacy and covers specific domains of functioning after stroke.</p><p><strong>Objectives: </strong>We aimed to determine the validity and reliability of the Persian version of the SSEQ.</p><p><strong>Methods: </strong>This descriptive cross-sectional study included 124 stroke patients in the sub-acute phase (between 2 weeks and 3 months of stroke onset). The original SSEQ was translated to Persian and back-translated to English. Demographic, neurologic examination, 'Persian Stroke Self-Efficacy Questionnaire (SSEQ-P)', and 'General Self-Efficacy Scale' (GSE-10) data were collected. The reliability of the questionnaire was evaluated by test-retest assessment among 30 people with stroke at an interval of two weeks. Factor analysis was used to assess the validity of SSEQ-P. Cronbach's alpha assessed internal consistency in all participants. Statistical analysis was performed by SPSS software version 23 and SmartPLS version 3.</p><p><strong>Results: </strong>In this study, the mean of SSEQ scores was 87.99 ± 37.09. Content Validity Ratio (CVR) and Content Validity Index (CVI) were favorable. Convergent validity of the questionnaire was reported (<i>r</i> = 0.669) using GSE. Factor loadings of items in SSEQ ranged from 0.41 to 0.92. Validity indices (AVE = 0.75, SRMR = 0.07) showed that the single-factor model of the present study owns a favorable fit. Test-retest reliability and Cronbach's alpha values of SSEQ in the present study were calculated at 0.80 and 0.97, respectively.</p><p><strong>Conclusions: </strong>The Persian version of the SSEQ depicted acceptable reliability and validity and can be utilized to evaluate the self-efficacy of patients with stroke.HIGHLIGHTSStroke Self-Efficacy Questionnaire (SSEQ) is a self-report scale that measures stroke survivors' self-efficacy.The Persian version of the SSEQ demonstrated acceptable reliability and validity and can be used in stroke patients.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1365-1371"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49677311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential role of thoracolumbar fascia in younger middle-aged patients with chronic low back pain.","authors":"S Gumruk Aslan, S Koylu Uyar, E Gurcay","doi":"10.1080/00207454.2023.2251671","DOIUrl":"10.1080/00207454.2023.2251671","url":null,"abstract":"<p><strong>Aim: </strong>This study aimed to quantitatively assess the thickness of the thoracolumbar fascia (TLF) and lumbar multifidus muscle through ultrasound imaging in younger-middle aged individuals, both those experiencing chronic low back pain (LBP) and those without LBP. Additionally, the study sought to explore the potential significance of these anatomical structures in relation to clinical and sonographic findings.</p><p><strong>Method: </strong>A cross-sectional study was conducted involving a cohort of 50 participants, divided into two groups: chronic LBP group (Group LBP, <i>n</i> = 30) and a group without LBP (Group control, <i>n</i> = 20). Participants from both groups underwent assessments pertaining to pain characteristics (intensity and quality), functional impairment, and kinesiophobia. The thicknesses of the thoracolumbar fascia and lumbar multifidus muscle were measured using ultrasonography.</p><p><strong>Results: </strong>Among participants with chronic LBP, the thoracolumbar fascia displayed a statistically significant increase in thickness on the left side, whereas the lumbar multifidus muscle exhibited reduced thickness on the left side. Notably, positive correlations were observed between the thickness of the thoracolumbar fascia and scores from the Numerical Rating Scale (NRS) for pain intensity (<i>r</i> = 0.472, <i>p</i> = 0.008) as well as the McGill Pain Questionnaire (MPQ) (<i>r</i> = 0.547, <i>p</i> = 0.002). Moreover, a positive correlation was established between the thickness of the lumbar multifidus muscle and the modified Schober test (<i>r</i> = 0.174, <i>p</i> = 0.040). However, the thickness of the lumbar multifidus muscle demonstrated a negative correlation with age (r = -0.304, <i>p</i> = 0.032). Multiple logistic regression analysis did not identify any significant predictors for the presence of LBP based on demographic or clinical variables.</p><p><strong>Conclusions: </strong>Individuals afflicted with chronic LBP exhibited pronounced thickening of the thoracolumbar fascia and attenuation of the lumbar multifidus muscle in comparison to asymptomatic counterparts. Notably, increased thickness of the thoracolumbar fascia corresponded to heightened pain intensity, while reduction in lumbar multifidus muscle thickness was associated with decreased lumbar flexion ability. These findings underscore the importance of incorporating tailored regimens targeting both fascial and muscular components in the rehabilitation of individuals with LBP.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1198-1204"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10173687","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Probable eculizumab-associated hepatotoxicity in a patient with neuromyelitis optica: a case report.","authors":"Koc Emine Rabia, Turan Ömer Faruk, Saridas Furkan, Elhamida Sarra Lazrak, Pinar Acar Ozen, Aslı Tuncer","doi":"10.1080/00207454.2023.2253361","DOIUrl":"10.1080/00207454.2023.2253361","url":null,"abstract":"<p><strong>Objectives: </strong>Neuromyelitis optica (NMO) is an inflammatory, autoimmune and demyelinating disease of the central nervous system and is often characterized by attacks of severe optic neuritis and long segment myelitis. Identifying the disease-specific pathogenic anti-AQP4 autoantibody in NMOSD has allowed the development of highly effective disease-modifying drugs in the treatment phase. Eculizumab is a humanized antibody that binds to complement C5 and inhibits the formation of the C5b-induced membrane attack complex. It is approved for treating many diseases in which tissue damage is accompanied by complement (such as neuromyelitis optica, myasthenia gravis, autoimmune hemolytic anemia and paroxysmal hemoglobinuria).</p><p><strong>Methods: </strong>We present a patient diagnosed with NMO who developed possible drug-induced liver injury three months after the start of eculizumab treatment.</p><p><strong>Result: </strong>After discontinuing eculizumab treatment, liver function tests gradually regressed in a month.</p><p><strong>Conclusions: </strong>Eculizumab-associated hepatotoxicity is a previously unreported adverse event in NMOSD patients. Therefore, patients should be monitored for liver function tests during eculizumab treatment, and care should be taken for hepatotoxicity. If hepatotoxicity is detected while under eculizumab treatment, patients should be investigated for other drug use, complementary food supplementation, or possible autoimmune hepatitis, and other potential causes should be excluded.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1205-1209"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10474359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhancement of hippocampal-dependent spatial memory by Ashwagandha (<i>Withania somnifera</i>) characterized by activation of NMDA receptors against monosodium glutamate-induced neurotoxicity in rats.","authors":"Rawand H Al-Dmour, Nafe M Al-Tawarah, Nesrin Mwafi, Banan M Alkhataybeh, Khaled M Khleifat, Amjad Tarawneh, Anas O Satari, Sahem M Alkharabsheh, Layla Albustanji","doi":"10.1080/00207454.2023.2255372","DOIUrl":"10.1080/00207454.2023.2255372","url":null,"abstract":"<p><strong>Background and aim: </strong>Monosodium glutamate (MSG) is used in food-additives, and the Food and Drug Administration has placed it under intense scrutiny following several reports that it causes glutamate neurotoxicity. Ashwagandha (ASH) roots are traditionally used for memory enhancement. This study aimed to evaluate the nootropic activity of ASH as well as its therapeutic anti-amnesic activity against MSG-induced hippocampal-dependent spatial memory impairment and hippocampal-NMDAR modulation.</p><p><strong>Method: </strong>A total of 36 rats were divided equally into six groups (<i>n</i> = 6 in each group); the rats in the normal and negative groups were administered daily doses of normal saline and MSG (300 mg/kg), respectively, for 21 days. Two nootropic groups were administered ASH at 300 and 500 mg/kg o.p., respectively, for 21 days. Two other treatment groups were administered daily doses of MSG 300 mg/kg o.p. as well as 300 mg/kg and 500 mg/kg o.p. of ASH for 21 days. The rats' spatial memory was assessed for five days using the MWM. Additionally, NMDAR were measured quantitatively by immunohistochemistry.</p><p><strong>Results: </strong>We found that the rats in the nootropic groups showed significantly enhanced nootropic activity characterized by improved hippocampal-dependent spatial memory, as well as increases in the level of NMDAR in the Cornu Ammonis 1 region of their hippocampus. Moreover, we elucidated the therapeutic potential of ASH to protect against the depression of spatial memory caused by MSG-induced neurotoxicity.</p><p><strong>Conclusion: </strong>Further, we elucidated a strong correlation between NMDAR-positive cells in the hippocampus and enhancement of spatial learning induced by long-term administration of ASH as well as a strong correlation between NMDAR positive cells in the hippocampus and depression of spatial learning induced by long-term administration of ASH and MSG.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1220-1228"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10669316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Histone demethylases in neurodevelopment and neurodegenerative diseases.","authors":"Haiying Wang, Beiyi Guo, Xiaoqiang Guo","doi":"10.1080/00207454.2023.2276656","DOIUrl":"10.1080/00207454.2023.2276656","url":null,"abstract":"<p><p>Neurodevelopment can be precisely regulated by epigenetic mechanisms, including DNA methylations, noncoding RNAs, and histone modifications. Histone methylation was a reversible modification, catalyzed by histone methyltransferases and demethylases. So far, dozens of histone lysine demethylases (KDMs) have been discovered, and they (members from KDM1 to KDM7 family) are important for neurodevelopment by regulating cellular processes, such as chromatin structure and gene transcription. The role of KDM5C and KDM7B in neural development is particularly important, and mutations in both genes are frequently found in human X-linked mental retardation (XLMR). Functional disorders of specific KDMs, such as KDM1A can lead to the development of neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). Several KDMs can serve as potential therapeutic targets in the treatment of neurodegenerative diseases. At present, the function of KDMs in neurodegenerative diseases is not fully understood, so more comprehensive and profound studies are needed. Here, the role and mechanism of histone demethylases were summarized in neurodevelopment, and the potential of them was introduced in the treatment of neurodegenerative diseases.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1372-1382"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71412174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of pyridoxine or cobalamin supplementation on apoptosis and cell cycle progression in a human glioblastoma cell line.","authors":"Carolina A Martínez-Mendiola, José A Estrada, Luis Á Zapi-Colín, Gerson G Contreras-Chávez, Irazú Contreras","doi":"10.1080/00207454.2023.2263815","DOIUrl":"10.1080/00207454.2023.2263815","url":null,"abstract":"<p><p>Glioblastoma is the most aggressive type of brain tumor, with current therapies failing to significantly improve patient survival. Vitamins have important effects on cellular processes that are relevant for tumor development and progression.</p><p><strong>Aim: </strong>The present study explored the effect of pyridoxine or cobalamin supplementation on the viability and cell cycle progression of human glioblastoma cell line U-87 MG.</p><p><strong>Method: </strong>Cell cultures were treated with increasing concentrations of pyridoxine or cobalamin for 24-72 h. After supplementation, cell viability and cell cycle progression were assessed by spectrophotometry and flow cytometry. Analysis of Bcl-2 and active caspase 3 expression in supplemented cells was performed by western blot.</p><p><strong>Result: </strong>The results show that pyridoxine supplementation decreases cell viability in a dose and time dependent manner. Loss of viability in pyridoxin-supplemented cells is probably related to less cell cycle progression, higher active caspase 3 expression and apoptosis. In addition, Bcl-2 expression did not appear to be altered by vitamin supplementation, but active caspase 3 expression was significantly increased in pyridoxine-, but not cobalamin-supplemented cells, furthermore, cobalamin inhibited the pyridoxine cytotoxicity in the cell viability assay when combined.</p><p><strong>Conclusion: </strong>The results suggest that pyridoxine supplementation promotes apoptosis in human glioblastoma-derived cells and may be useful to enhance the effect of cytotoxic therapies in vivo.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1320-1331"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41130294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interactome analysis implicates class II transactivator (CIITA) in depression and other neuroinflammatory disorders.","authors":"Kishore Nagasubramanian, Krishnakant Gupta","doi":"10.1080/00207454.2023.2279502","DOIUrl":"10.1080/00207454.2023.2279502","url":null,"abstract":"<p><strong>Purpose: </strong>Inappropriate inflammatory responses within the nervous system (neuroinflammation) have been implicated in several neurological conditions. Class II transactivator (CIITA), a principal regulator of the major histocompatibility complex II (MHCII), is known to play essential roles in inflammation. Hence, CIITA and its interactors could be potentially involved in multiple neurological disorders. However, the molecular mechanisms underlying CIITA-mediated neuroinflammation (NI) are yet to be understood.</p><p><strong>Materials and methods: </strong>In this regard, we analyzed the potential involvement of CIITA and its interactome in the regulation of neuroinflammation. In the present study, using various computational tools, we aimed (1) to identify NI-related proteins, (2) to filter the critical interactors in the CIITA-NI network, and (3) to analyze the protein-disease interactions and the associated molecular pathways through which CIITA could influence neuroinflammation.</p><p><strong>Results: </strong>CIITA was found to interact with P T GS2, GSK3B, and NR3C1 and may influence depressive disorders. Further, the IL4/IL13 pathway was found to be potentially underlying the CIITA-interactomemediated effects on neurological disorders. Moreover, CIITA was found to be connected to genes associated with depressive disorder through IL4, wherein CIITA was found to be potentially involved in depressive disorders through IL-4/IL-13 and hippo pathways. However, the present study is based on the existing data on protein interactomes and could be re-evaluated as newer interactions are discovered. Also, the functional mechanisms of CIITA's roles in neuroinflammation must be evaluated further.</p><p><strong>Conclusion: </strong>Notwithstanding these limitations, the results presented here, could form a basis for further experimental studies to assess CIITA as a potential therapeutic target in managing depression and other neuroinflammatory disorders.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1153-1171"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71481423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insights into the advances in therapeutic drugs for neuroinflammation-related diseases.","authors":"Bozhi Luo","doi":"10.1080/00207454.2023.2260088","DOIUrl":"10.1080/00207454.2023.2260088","url":null,"abstract":"<p><p>Studies have shown that neurodegenerative diseases such as AD and PD are related to neuroinflammation. Neuroinflammation is a common inflammatory condition that can lead to a variety of dysfunction in the body. At present, it is no medications specifically approved to prevent or cure neuroinflammation, so even though many drugs can temporarily control the neurological symptoms of neuroinflammation, but no one can reverse the progress of neuroinflammation, let al.one completely cure neuroinflammation. Therefore, it is urgent to develop new drug development for neuroinflammation treatment. In this review, we highlight the therapeutic advancement in the field of neurodegenerative disorders, by focusing on the impact of neuroinflammation treatment has on these conditions, and the effective drugs for the treatment of neuroinflammation and neurodegenerative diseases and their latest research progress are reviewed according to the related signaling pathway, as well as the prospect of their clinical application is also discussed. The purpose of this review is to enable specialists to better understand the mechanisms underlying neuroinflammation and anti-inflammatory drugs, promote the development of therapeutic drugs for neuroinflammation and neurodegenerative diseases, and further provide therapeutic references for clinical neurologists.</p>","PeriodicalId":14161,"journal":{"name":"International Journal of Neuroscience","volume":" ","pages":"1256-1281"},"PeriodicalIF":1.7,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10656877","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}