Journal of Neuroscience Research最新文献

Alzheimer's Disease and Frontotemporal Dementia: A Review of Pathophysiology and Therapeutic Approaches 阿尔茨海默病和额颞叶痴呆：病理生理学和治疗方法的综述

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-05-19 DOI: 10.1002/jnr.70046

Sally Kelliny, Xin-Fu Zhou, Larisa Bobrovskaya

{"title":"Alzheimer's Disease and Frontotemporal Dementia: A Review of Pathophysiology and Therapeutic Approaches","authors":"Sally Kelliny, Xin-Fu Zhou, Larisa Bobrovskaya","doi":"10.1002/jnr.70046","DOIUrl":"https://doi.org/10.1002/jnr.70046","url":null,"abstract":"Alzheimer's disease (AD) is a devastating form of dementia, with the number of affected individuals rising sharply. The main hallmarks of the disease include amyloid-beta plaque deposits and neurofibrillary tangles consisting of hyperphosphorylated tau protein, besides other pathological features that contribute to the disease's complexity. The causes of sporadic AD are multifactorial and mostly age-related and involve risk factors such as diabetes and cardiovascular or cerebrovascular disorders. Frontotemporal dementia (FTD) is another type of dementia characterized by a spectrum of behaviors, memory, and motor abnormalities and associated with abnormal depositions of protein aggregation, including tau protein. Currently approved medications are symptomatic, and no disease-modifying therapy is available to halt the disease progression. Therefore, the development of multi-targeted therapeutic approaches could hold promise for the treatment of AD and other neurodegenerative disorders, including tauopathies. In this article, we will discuss the pathophysiology of AD and FTD, the proposed hypotheses, and current therapeutic approaches, highlighting the development of novel drug candidates and the progress of clinical trials in this field of research.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70046","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144085055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Modulation of GABAergic System in a Chicken Retinal Ischemic Model: The Role of Chloride Cotransporters 鸡视网膜缺血模型中gaba能系统的调节：氯共转运体的作用

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-05-12 DOI: 10.1002/jnr.70043

A. A. Nascimento, V. S. Miya-Coreixas, D. S. M. Araújo, T. H. O. Nascimento, G. F. Santos, R. Brito, K. C. Calaza

{"title":"Modulation of GABAergic System in a Chicken Retinal Ischemic Model: The Role of Chloride Cotransporters","authors":"A. A. Nascimento, V. S. Miya-Coreixas, D. S. M. Araújo, T. H. O. Nascimento, G. F. Santos, R. Brito, K. C. Calaza","doi":"10.1002/jnr.70043","DOIUrl":"https://doi.org/10.1002/jnr.70043","url":null,"abstract":"Retinal ischemia is a significant pathological condition that contributes to visual impairment and neuronal cell death in various retinopathies. Evidence suggests that GABA release during ischemic events may exhibit neuroprotective properties, but conflicting findings highlight a potential shift in its effects due to altered chloride ion homeostasis. This study aimed to investigate the role of the GABAergic system in retinal ischemia, focusing on the temporal dynamics of GABA release and its impact on retinal damage. We hypothesized that ischemia-induced changes in GABA transport and chloride ion equilibrium contribute to neuronal damage, which can be mitigated by modulating GABAergic activity. Using an ex vivo chick retina model subjected to oxygen and glucose deprivation (OGD), during different times, we assessed morphological changes, cell death, GABA levels, transporter activity, and the levels of chloride cotransporters NKCC1 and KCC2. Pharmacological interventions, including picrotoxin and bumetanide, were used to evaluate neuroprotective effects. Our results revealed that OGD-induced significant morphological changes and cell death in the retina. GABA levels were reduced in a GAT-1-dependent manner, while picrotoxin and bumetanide demonstrated neuroprotective effects by mitigating retinal swelling and modulating the GABAergic system. Notably, OGD increased NKCC1 content, but not KCC2 levels, indicating a disruption in chloride homeostasis. These findings suggest that ischemia-induced alterations in GABAergic activity and chloride transport contribute to retinal damage. Targeting these pathways with pharmacological agents, such as bumetanide, may offer therapeutic strategies for mitigating ischemic retinal injury. Further research is recommended to explore the clinical applicability of these findings in the ischemic retina.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70043","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143939434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reduced Visual-Cortex Reorganization Before and After Cochlear Implantation Relates to Better Speech Recognition Ability 人工耳蜗植入前后视觉皮层重组减少与语音识别能力提高有关

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-05-08 DOI: 10.1002/jnr.70042

Anna Weglage, Natalie Layer, Jan-Ole Radecke, Hartmut Meister, Verena Müller, Ruth Lang-Roth, Martin Walger, Pascale Sandmann

{"title":"Reduced Visual-Cortex Reorganization Before and After Cochlear Implantation Relates to Better Speech Recognition Ability","authors":"Anna Weglage, Natalie Layer, Jan-Ole Radecke, Hartmut Meister, Verena Müller, Ruth Lang-Roth, Martin Walger, Pascale Sandmann","doi":"10.1002/jnr.70042","DOIUrl":"https://doi.org/10.1002/jnr.70042","url":null,"abstract":"Although a cochlear implant (CI) can partially restore auditory function, CI recipients show alterations not only in auditory but also in visual cortical processing. Yet, it is not well understood how these visual changes relate to the CI outcome and to what extent these changes are induced by auditory deprivation and the limited CI input, respectively. Here, we present a prospective longitudinal electroencephalography study which examined the deprivation- and CI-induced alterations on cortical face processing by comparing visual evoked potentials (VEP) in CI users before and 6 months after implantation. A group of normal-hearing (NH) listeners served as a control. The participants performed a word-identification task and a face-categorization task to study the cortical processing of static and articulating faces in attended and unattended conditions. The CI candidates and CI users showed a reduced visual-cortex activation, a stronger functional connectivity between the visual and auditory cortex, and a reduced attention effect in the (extended) alpha frequency range (8–18 Hz) when compared to NH listeners. There was a positive correlation between the P1 VEP amplitude recorded before implantation and the speech recognition ability after implantation. Our results suggest that the CI users' alterations in cortical face processing are mainly induced by auditory deprivation and not by CI experience. Importantly, these deprivation-induced changes seem to be related to the CI outcome. Our results suggest that the visual P1 amplitude as recorded before implantation provides an objective index of cortical visual reorganization that may help predict the CI outcome.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70042","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143919862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Novel H2S Donor Alleviates Neuroinflammation and Seizures by Inhibiting the C3-C3aR Pathway 一种新型H2S供体通过抑制C3-C3aR通路减轻神经炎症和癫痫发作

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-05-02 DOI: 10.1002/jnr.70041

Yaru Yang, Xutao Wang, Tiantian Wang, Xiao Wang, Honghao Xu, Lian Liu, Shuisheng Lei, Xiao qin Zhu

{"title":"A Novel H2S Donor Alleviates Neuroinflammation and Seizures by Inhibiting the C3-C3aR Pathway","authors":"Yaru Yang, Xutao Wang, Tiantian Wang, Xiao Wang, Honghao Xu, Lian Liu, Shuisheng Lei, Xiao qin Zhu","doi":"10.1002/jnr.70041","DOIUrl":"https://doi.org/10.1002/jnr.70041","url":null,"abstract":"<div>\u0000 \u0000 Both astrocytes and microglia are activated in the epileptic brain. There is an interaction between them through the complement 3 (C3)-C3a receptor (C3aR) pathway, which plays a detrimental role in seizures. Our self-developed novel H2S donor has been found to have anti-seizure effects. However, its mechanism remains to be explored. In the present study, we showed that the novel H2S donor can inhibit the activation of astrocytes and microglia and their interaction through C3-C3aR signaling, which contributed to alleviating microglial neuroinflammation and seizures. In LPS-treated astrocytes and pilocarpine-induced epileptic mice, the H2S donor reduced C3 production in astrocytes and regulated the expression of inflammatory cytokines IL-1β and IL-10 in microglia. The H2S donor also reduced the EEG amplitude of hippocampal epileptic waves and relieved seizures in epileptic mice. These effects of the H2S donor can be reversed by intranasal C3 treatment and mimicked by a C3aR antagonist. These findings provide a novel mechanism underlying the anti-seizure effects of the H2S donor. Therefore, the H2S donor has the potential to be used as a candidate for antiepileptic drugs.\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tubulin Polymerization Promoting Proteins: Functional Diversity With Implications in Neurological Disorders 微管蛋白聚合促进蛋白：功能多样性与神经系统疾病的影响

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-05-02 DOI: 10.1002/jnr.70044

Paloma J. Diaz, Qian Shi, Priscilla Y. McNeish, Swati Banerjee

{"title":"Tubulin Polymerization Promoting Proteins: Functional Diversity With Implications in Neurological Disorders","authors":"Paloma J. Diaz, Qian Shi, Priscilla Y. McNeish, Swati Banerjee","doi":"10.1002/jnr.70044","DOIUrl":"https://doi.org/10.1002/jnr.70044","url":null,"abstract":"Tubulin Polymerization Promoting Proteins (TPPPs) are highly conserved across species but remain poorly understood. There are three TPPP genes in humans, with only one homologous TPPP gene in invertebrates, such as Drosophila and C. elegans. The human TPPP (TPPP1/p25/p25α) is enriched in the brain and shares sequence similarities with the invertebrate TPPPs. TPPP/p25 associates with microtubules and plays a pivotal role in microtubule dynamics, bundling, and polymerization, thereby stabilizing the microtubular network. This is essential for cytoskeletal organization and proper functioning of neurons and glial cells, including axonal growth, regeneration, migration, trafficking, synapse formation, and myelination of axons. However, studies have also uncovered that besides its cytoplasmic/microtubular localization, TPPP/p25 is present in other subcellular compartments, including the mitochondria and nucleus, underscoring the presence of additional novel functions. At the molecular level, TPPP/p25 is predicted to exist as an intrinsically disordered protein and is implicated in neurological and neurodegenerative disorders, including Parkinson's and related disorders and Multiple Sclerosis. In this article, we provide a comprehensive overview of TPPP/p25, highlighting its evolutionary conservation, cellular and subcellular localization, established and emerging functions in the nervous system, interacting partners, potential clinical relevance to human neurological disorders, and conclude with unresolved questions and future areas of study.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 5","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70044","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143897005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Novel Mutation in CNTNAP1 Gene Causes Disorganization of Axonal Domains, Hypomyelination and Severe Neurological Deficits CNTNAP1基因的新突变导致轴突结构域的紊乱、髓鞘化降低和严重的神经功能障碍

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-04-23 DOI: 10.1002/jnr.70040

Lacey B. Sell, Carson Zabel, Sabine Weller Grønborg, Qian Shi, Manzoor A. Bhat

{"title":"A Novel Mutation in CNTNAP1 Gene Causes Disorganization of Axonal Domains, Hypomyelination and Severe Neurological Deficits","authors":"Lacey B. Sell, Carson Zabel, Sabine Weller Grønborg, Qian Shi, Manzoor A. Bhat","doi":"10.1002/jnr.70040","DOIUrl":"https://doi.org/10.1002/jnr.70040","url":null,"abstract":"<div>\u0000 \u0000 CNTNAP1 encodes the contactin-associated protein 1 (Cntnap1) which localizes to the paranodal region in all myelinated axons and is essential for axonal domain organization and the propagation of action potentials. To date, close to 45 reported human CNTNAP1 variants have been identified that are associated with dysregulation and disorganization of the axonal domains, resulting in various forms of congenital hypomyelinating neuropathies in children. Currently, no treatments are available for neuropathies caused by CNTNAP1 variants, highlighting the importance of fully characterizing these mutations and their impact on Cntnap1 functions. To understand the importance of a novel human CNTNAP1 likely pathogenic variant that changes glycine at position 349 to valine in a child who also carries a CNTNAP1 truncation and displayed severe neurological deficits, we used CRISPR/Cas9 methodology and introduced a single nucleotide substitution in the mouse Cntnap1 gene, resulting in glycine at 350 to valine (Cntnap1G350V). Trans-allelic combination of Cntnap1G350V with a Cntnap1 null allele (Cntnap1G350V/−) mimics human pathologies, recapitulating hypomyelination neuropathies associated with CNTNAP1 mutations as well as loss of paranodal junctions and disorganization of axonal domains in myelinated axons. Expression of the wild type Cntnap1 transgene in Cntnap1G350V/− mice rescued the mutant phenotypes and restored all neurological deficits. Our studies demonstrate that GGT (glycine) to GTT (valine) change in human CNTNAP1 creates a recessive loss of function allele and lays the foundation for potential gene therapy studies aimed at treating CNTNAP1-associated hypomyelinating neuropathies in children.\u0000 </div>","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143861880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EXPRESSION OF CONCERN: Lithium Inhibits Aβ-Induced Stress in Endoplasmic Reticulum of Rabbit Hippocampus but Does Not Prevent Oxidative Damage and Tau Phosphorylation 关注表达：锂抑制a β诱导的兔海马内质网应激，但不能防止氧化损伤和Tau磷酸化

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-04-22 DOI: 10.1002/jnr.70031

引用次数: 0

RETRACTION: Effect of growth factors and steroids on transglutaminase activity and expression in primary astroglial cell cultures 回归：生长因子和类固醇对原代星形胶质细胞培养物中转谷氨酰胺酶活性和表达的影响

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-04-22 DOI: 10.1002/jnr.70037

{"title":"RETRACTION: Effect of growth factors and steroids on transglutaminase activity and expression in primary astroglial cell cultures","authors":"","doi":"10.1002/jnr.70037","DOIUrl":"https://doi.org/10.1002/jnr.70037","url":null,"abstract":"RETRACTION: A. Campisi, V. Bramanti, D. Caccamo, G. Li Volti, G. Cannavò, M. Currò, G. Raciti, F. Galvano, F. Amenta, A. Vanella, R. Ientile, R. Avola, “Effect of growth factors and steroids on transglutaminase activity and expression in primary astroglial cell cultures,” Journal of Neuroscience Research 86, no. 6 (2008): 1297–1305, https://doi.org/10.1002/jnr.21579.The above article, published online on 26 November 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley & Sons, Inc. Following publication, concerns were raised by a third party that portions of Figures 1 and 8 were duplicated and manipulated, and that portions of Figure 8 were duplicated from an earlier publication by this research group. Internal investigation confirmed these claims. The publisher attempted to contact the authors and request original data, but the authors did not respond. The retraction has been agreed because of concerns that the images were manipulated, affecting the interpretation of the data and results presented. The authors have been notified of the retraction.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143857178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

RETRACTION: Neuroactive Molecules and Growth Factors Modulate Cytoskeletal Protein Expression During Astroglial Cell Proliferation and Differentiation in Culture 摘编：神经活性分子和生长因子在星形胶质细胞增殖和分化过程中调节细胞骨架蛋白的表达

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-04-22 DOI: 10.1002/jnr.70036

{"title":"RETRACTION: Neuroactive Molecules and Growth Factors Modulate Cytoskeletal Protein Expression During Astroglial Cell Proliferation and Differentiation in Culture","authors":"","doi":"10.1002/jnr.70036","DOIUrl":"https://doi.org/10.1002/jnr.70036","url":null,"abstract":"RETRACTION: V. Bramanti, S. Grasso, D. Tibullo, C. Giallongo, R. Pappa, MV Brundo, D. Tomassoni, M. Viola, F. Amenta, and R. Avola, “Neuroactive Molecules and Growth Factors Modulate Cytoskeletal Protein Expression During Astroglial Cell Proliferation and Differentiation in Culture,” Journal of Neuroscience Research 94, no. 1 (2016): 90-98, https://doi.org/10.1002/jnr.23678.The above article, published online on 15 October 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley & Sons, Inc. Following publication, concerns were raised by a third party that portions of Figures 2B and 3 were duplicated and manipulated, and that most of the images from Figure 2A were duplicated and manipulated from an earlier publication by this research group. Internal investigation confirmed these claims. The publisher attempted to contact the authors and request original data, but the authors did not respond. The retraction has been agreed because of concerns that the images were manipulated, affecting the interpretation of the data and results presented. The authors have been notified of the retraction.","PeriodicalId":16490,"journal":{"name":"Journal of Neuroscience Research","volume":"103 4","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jnr.70036","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143856966","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

EXPRESSION OF CONCERN: Gene Expression Profile Activated by the Chemokine CCL5/RANTES in Human Neuronal Cells 关注表达：趋化因子CCL5/RANTES在人类神经元细胞中激活的基因表达谱

IF 2.9 3区医学

Journal of Neuroscience Research Pub Date : 2025-04-22 DOI: 10.1002/jnr.70038

引用次数: 0