Journal of Molecular Neuroscience最新文献

The Progress of Cognitive Dysfunction Impairment Caused by Temporal Lobe Epilepsy. 颞叶癫痫所致认知功能障碍的研究进展。

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-21 DOI: 10.1007/s12031-025-02365-0

Qianqian Wang, Yanguang Geng, Xin Li, Yunhua Hao, Shuqi Huang

引用次数: 0

More Than Three Decades After Discovery of the Neuroprotective Effect of PACAP, What Is Still Preventing Its Clinical Use? 在发现PACAP的神经保护作用30多年后，是什么阻碍了它的临床应用？

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-21 DOI: 10.1007/s12031-025-02366-z

Asma Cherait, Xavier Xifró, Dora Reglodi, David Vaudry

引用次数: 0

Cerebrospinal Fluid-Derived Genomic Alterations Tracking Glioma. 脑脊液衍生的基因组改变追踪神经胶质瘤。

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-20 DOI: 10.1007/s12031-025-02361-4

Zhongyuan Zhu, Yanjiao Yu, Fuzhong Liu, Xiaosong Yang, Zijie Zhou, Zhengquan Zhu, Zifeng Wang, Ji Zhang

{"title":"Cerebrospinal Fluid-Derived Genomic Alterations Tracking Glioma.","authors":"Zhongyuan Zhu, Yanjiao Yu, Fuzhong Liu, Xiaosong Yang, Zijie Zhou, Zhengquan Zhu, Zifeng Wang, Ji Zhang","doi":"10.1007/s12031-025-02361-4","DOIUrl":"10.1007/s12031-025-02361-4","url":null,"abstract":"Diffuse gliomas are aggressive brain tumors known for heterogeneity and frequent oncogenic mutations. Our study harnessed circulating tumor DNA (ctDNA) in cerebrospinal fluid (CSF) as a less invasive method for disease monitoring and guiding therapeutic interventions. Through targeted sequencing of ctDNA from CSF and matched blood and tumor tissue samples, we aimed to identify glioma-associated somatic alterations and DNA fragmentations. The identified glioma-associated mutations from ctDNA in CSF and genome DNA of the resected tumor were compared, revealed a broad genetic alteration spectrum within CSF ctDNA, closely reflecting the genomic profiles of corresponding tumor samples. And we found 91.67% (11/12) of tissue samples analyzed by next-generation sequencing (NGS), a minimum of one tumor-specific mutation was present. Also, at least one tumor-specific mutation was detected in 91.67% of serial CSF ctDNA samples (11/12). In some patients, CSF sequencing showed higher mutation detection rate compared to tissue sequencing. Moreover, the average mutation frequencies were similar between CSF and tumor tissue samples. These results support that CSF ctDNA is a reliable candidate for detecting glioma-specific alterations for molecular profiling, complements the histopathological, molecular and imaging defect, and can be adopted into clinical practice.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 3","pages":"79"},"PeriodicalIF":2.8,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332236","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}

引用次数: 0

The Astrocyte Elevated Gene- 1 Expression and other Risk Factors for Different Varieties of Diabetic Optic Neuropathy in Egyptian Patients with Diabetic Retinopathy. 埃及糖尿病视网膜病变患者不同类型糖尿病视神经病变星形胶质细胞基因- 1表达升高及其他危险因素

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-19 DOI: 10.1007/s12031-025-02372-1

Noha Rabie Bayomy, Sameh Mohamed Elgouhary, Eman Masoud Abd El Gayed, Karema Abdelhady Diab, Mai A Kamel, Nashwa Mahmoud Mouhamed Muharram

{"title":"The Astrocyte Elevated Gene- 1 Expression and other Risk Factors for Different Varieties of Diabetic Optic Neuropathy in Egyptian Patients with Diabetic Retinopathy.","authors":"Noha Rabie Bayomy, Sameh Mohamed Elgouhary, Eman Masoud Abd El Gayed, Karema Abdelhady Diab, Mai A Kamel, Nashwa Mahmoud Mouhamed Muharram","doi":"10.1007/s12031-025-02372-1","DOIUrl":"10.1007/s12031-025-02372-1","url":null,"abstract":"To assess the role of the mRNA and protein expression of Astrocyte Elevated Gene- 1 (AEG-1) and other possible risk factors for diabetic optic neuropathy (DON) in Egyptian patients with diabetic retinopathy (DR). This case-control study constituted 450 diabetic patients divided into three groups: Group 1 included 150 DR patients with any sign of DON (diabetic papillopathy (DP), non-arteritic anterior ischemic optic neuropathy (AION), and optic atrophy (OA)). Group 2 included 150 DR patients without any sign of DON. Group 3 included 150 sex and age-matched diabetic patients without any sign of DR or DON. The expression level of AEG-1 mRNA was assessed by real-time PCR. Serum AEG-1 was determined by ELISA. Multivariate logistic regression analysis was conducted to assess the DON risk factors. The mRNA expression of the AEG-1 gene and AEG-1 protein levels were significantly increased (P < 0.001) in diabetic patients with (group 1) than without (group 2) DON. ROC curve analysis showed that the mRNA level of the AEG-1 gene exhibited a 70% specificity and a 79.33% diagnostic sensitivity. The diagnostic sensitivity of the serum concentration of AEG-1 was 84.67%, while the specificity was 70%. Multivariate regression analysis showed that the risk factors for DON were 2hpp blood sugar, HbA1c, serum cholesterol, AEG-1 gene's mRNA expression, and AEG-1 protein. Serum cholesterol, the AEG-1 gene's mRNA expression, and the AEG-1 protein are risk factors for all varieties of DON. While the blood glucose levels favour the development of DP, control of diabetes favours the occurrence of AION. Lastly, diabetes duration is more related to the presence of OA.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 3","pages":"78"},"PeriodicalIF":2.8,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178977/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144332237","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}

引用次数: 0

Ferroptosis: Disease Associations and Therapeutic Target Exploration. 上睑下垂：疾病关联及治疗靶点探索。

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-14 DOI: 10.1007/s12031-025-02369-w

Hailing Wang, Liwei Jia, Rui Yin, Shujun Xu, Xin Meng

{"title":"Ferroptosis: Disease Associations and Therapeutic Target Exploration.","authors":"Hailing Wang, Liwei Jia, Rui Yin, Shujun Xu, Xin Meng","doi":"10.1007/s12031-025-02369-w","DOIUrl":"https://doi.org/10.1007/s12031-025-02369-w","url":null,"abstract":"Ferroptosis, a distinct form of cell death, is transforming the understanding of complex diseases such as cancer, neurodegenerative disorders. Driven by iron accumulation and lipid peroxidation, ferroptosis offers significant therapeutic potential by selectively targeting diseased cells. Ferroptosis is closely associated with renal impairment, metabolic disease, and neurological disorders. The current focus is on understanding the signaling pathways of ferroptosis to precisely regulate the ferroptosis mechanism. For example, ferroptosis increases intracellular selenium content and synergistically activates transcription factors transcription factor AP-2 gamma and specificity protein 1 to promote glutathione peroxidase-4 expression (GPX4). Despite its broad therapeutic potential, significant challenges remain, particularly in uncovering the detailed molecular mechanisms of ferroptosis and minimizing off-target effects. However, in the past two years, there has been a few comprehensive reviews on the exploration of therapeutic targets related to ferroptosis in disease treatment. This article provides a summary of the current understanding of ferroptosis mechanisms, its links to various diseases, and the exploration of potential therapeutic targets. By elucidating the complex molecular pathways of ferroptosis and highlighting its role in disease progression, we gain new insights for potential therapeutic strategies. This underscores the substantial theoretical significance of targeting ferroptosis for treatment purposes.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":"76"},"PeriodicalIF":2.8,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293081","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}

引用次数: 0

Salicylaldehyde Benzoylhydrazone Protects Against Ferroptosis in Models of Neurotoxicity and Behavioural Dysfunction, In Vitro and In Vivo. 水杨醛苯甲酰腙在体外和体内对神经毒性和行为功能障碍模型的铁下垂有保护作用。

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-14 DOI: 10.1007/s12031-025-02371-2

Niamh C Clarke, Ellen McCabe, Lasse D Jensen, Bernadette S Creaven, Derek A Costello

{"title":"Salicylaldehyde Benzoylhydrazone Protects Against Ferroptosis in Models of Neurotoxicity and Behavioural Dysfunction, In Vitro and In Vivo.","authors":"Niamh C Clarke, Ellen McCabe, Lasse D Jensen, Bernadette S Creaven, Derek A Costello","doi":"10.1007/s12031-025-02371-2","DOIUrl":"10.1007/s12031-025-02371-2","url":null,"abstract":"Metal dyshomeostasis in the brain is a key feature of many neuropathologies, including hypoxic and traumatic injury and chronic conditions such as Alzheimer's and Parkinson's disease. Ferroptosis is a form of cell death driven by the intracellular accumulation of iron. This is primarily characterised by a loss in endogenous antioxidant capacity and uncontrolled lipid peroxidation. Ferroptosis has been reported to underlie the pathology associated with several neurological and neurodegenerative conditions and has, therefore, become an attractive target for therapeutic intervention. Salicylaldehyde benzoylhydrazone (SBH) is a specialised hydrazone agent, known for its antibacterial and anticancer properties. It has robust metal-chelating capacity, with a particular affinity for complexing with iron and copper. The current study sought to investigate the potential of SBH to act as an anti-ferroptotic agent and to alleviate the neurotoxic and dysfunctional consequences of iron overload. We demonstrate that SBH can alleviate the death of HT22 hippocampal neurons, induced by exposure to the iron donor, ferric ammonium citrate (FAC). This was accompanied by a reduction in intracellular iron and lipid peroxidation, and alleviation of hallmark changes in gene expression indicative of ferroptosis. Using FAC-incubated zebrafish larvae as an in vivo model of iron overload, we reveal that SBH can reduce the mortality and toxicity associated with FAC exposure. Moreover, we report a FAC-mediated dysfunction in intrinsic sensorimotor reflex behaviour, which is restored by SBH. Taken together, our findings highlight SBH as an anti-ferroptotic agent and support its further investigation as a potential neurotherapeutic for conditions associated with iron dysregulation.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":"77"},"PeriodicalIF":2.8,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12167254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293082","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}

引用次数: 0

Drp1-Mediated Mitochondrial Fission Is Essential for Chemical-Induced Neuronal Transdifferentiation from Human Primary Fibroblasts. drp1介导的线粒体分裂对化学诱导的人原代成纤维细胞的神经元转分化至关重要。

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-13 DOI: 10.1007/s12031-025-02367-y

Jijuan Yang, Chun Li, Chunhua Wang, Xuemei Wang, Jiaqi Liu, Nan Yu, Wenqing Du, Shuhong Chi

{"title":"Drp1-Mediated Mitochondrial Fission Is Essential for Chemical-Induced Neuronal Transdifferentiation from Human Primary Fibroblasts.","authors":"Jijuan Yang, Chun Li, Chunhua Wang, Xuemei Wang, Jiaqi Liu, Nan Yu, Wenqing Du, Shuhong Chi","doi":"10.1007/s12031-025-02367-y","DOIUrl":"https://doi.org/10.1007/s12031-025-02367-y","url":null,"abstract":"Neuronal replacement therapy recently holds promise for neurodegenerative disease treatment. Somatic cell-derived neurons are the main cell source for this therapy; however, the induction mechanisms remain to be fully elucidated. Emerging evidence indicates that mitochondrial architecture undergoes substantial remodeling throughout cellular reprogramming processes. To explore the implications of mitochondrial dynamics in chemical-induced neuronal transdifferentiation, human foreskin fibroblasts (HFFs) were directly reprogrammed into functional neurons with our previously developed small molecule compound. The results showed that the mitochondrial morphology of HFFs shifted from tubular and reticular to fragmented shapes at an early stage of induced neurulation. Concurrently, gene and protein expression levels of the mitochondrial fission protein Drp1 was significantly increased in HFFs after induction. Both Drp1-specific siRNA and Drp1-GTPase inhibitor mdivi-1 treatment significantly attenuated the neuronal transdifferentiation of HFFs to neurons respectively, which can be attributed to the modulation of mitochondrial dynamics toward a fusion-dominant state through Drp1 suppression. Collectively, our experimental findings establish Drp1-dependent mitochondrial fission as a critical early requirement in the chemical reprogramming cascade that facilitates HFF transdifferentiation into neuronal lineages. Targeting Drp1 may enhance the efficiency of neuronal transdifferentiation, thereby providing sufficient therapeutically relevant neurons for neurodegenerative disease treatment.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":"75"},"PeriodicalIF":2.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144281903","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}

引用次数: 0

Altered Expression of MeCP2 and PTEN Genes in the Molecular Basis of Specific Learning Disorder. MeCP2和PTEN基因在特异性学习障碍分子基础中的表达改变。

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-06 DOI: 10.1007/s12031-025-02370-3

Fatma Atasever, Nil Özbilüm Şahin, Cansu Mercan Işık

{"title":"Altered Expression of MeCP2 and PTEN Genes in the Molecular Basis of Specific Learning Disorder.","authors":"Fatma Atasever, Nil Özbilüm Şahin, Cansu Mercan Işık","doi":"10.1007/s12031-025-02370-3","DOIUrl":"10.1007/s12031-025-02370-3","url":null,"abstract":"Specific learning disorders (SLD) are neurodevelopmental disorders that affect cognitive abilities such as reading, writing, and mathematics. The molecular mechanisms underlying SLD remain unclear, though genetic and epigenetic factors are thought to play a significant role. MeCP2 is an epigenetic regulator that binds to methylated DNA, playing a crucial role in the regulation of gene expression and SP in neuronal cells. PTEN, a tumor suppressor gene, regulates cell growth, survival, and apoptosis, and is critical for maintaining synaptic integrity. In this study, we aimed to examine the expression of MeCP2 and PTEN in individuals with SLD. RNA was isolated from blood samples, and gene expression was assessed using quantitative PCR (qPCR). A total of 38 participants with SLD and 35 healthy controls were included in the study. Our results revealed a 15.44-fold upregulation of MeCP2 and a 13.66-fold downregulation of PTEN in the SLD group compared to controls, suggesting a disrupted balance of gene expression. There was no significant difference in gene expression between severe and non-severe SLD groups. These findings suggest that the dysregulation of MeCP2 and PTEN may be involved in the pathophysiology of SLD, influencing SP and neuronal function. In conclusion, the altered expression of these genes in individuals with SLD highlights potential biomarkers for early diagnosis and therapeutic targets, opening avenues for future research and intervention strategies.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":"74"},"PeriodicalIF":2.8,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12144048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144232906","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}

引用次数: 0

Neuroinflammation Markers in Tear Fluid of Mild Alzheimer's Disease. 轻度阿尔茨海默病泪液中的神经炎症标志物

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-06-05 DOI: 10.1007/s12031-025-02368-x

Virve Kärkkäinen, Toni Saari, Minna Rusanen, Hannu Uusitalo, Ville Leinonen, Bernd Thiede, Kai Kaarniranta, Anne M Koivisto, Tor P Utheim

{"title":"Neuroinflammation Markers in Tear Fluid of Mild Alzheimer's Disease.","authors":"Virve Kärkkäinen, Toni Saari, Minna Rusanen, Hannu Uusitalo, Ville Leinonen, Bernd Thiede, Kai Kaarniranta, Anne M Koivisto, Tor P Utheim","doi":"10.1007/s12031-025-02368-x","DOIUrl":"10.1007/s12031-025-02368-x","url":null,"abstract":"The protein composition of tear fluid (TF) reflects the severity and progression of many age-related diseases. Here, we evaluated TF proteins from patients with mild Alzheimer's disease (AD) and cognitively healthy controls (CO) to explore potential new biomarker molecules. The aim of this study was to explore potential new biomarker molecules by examining the expression of TF proteins whose function is related to neuroinflammation. We examined 53 participants (34 COs, mean age 71 years, Mini-Mental State Examination (MMSE) score 28.9 ± 1.4; 19 with AD, Clinical Dementia Rating 0.5-1, mean age 72 years, MMSE 23.8 ± 2.8). All participants underwent neurological status examination, cognitive testing, and ophthalmological examination. TF was collected using Schirmer strips, and TF protein content was evaluated using mass spectrometry-based proteomics and label-free quantification. We report 14 TF proteins that showed altered protein expression in the AD group compared to the CO group. Twelve proteins were significantly upregulated (SERPINA3, FGA, SIAS, ORM1, ANXA3, G6PI/NLK, CH3L2, MSLN, CPPED1, JCHAIN, IGHV5-51, SPARCL1) and two were downregulated (PIP, SCGB2A1) (p ≤ 0.05). Observed altered expression of TF proteins in the AD group may have potential in AD pathology. Since inflammation is one of the earliest signs of neurodegeneration in AD, these proteins are putative new biomarker candidates of early AD.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":"73"},"PeriodicalIF":2.8,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12141408/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223896","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}

引用次数: 0

Genetics and Epigenetics of Alzheimer's Disease: Understanding Pathogenesis and Exploring Therapeutic Potential. 阿尔茨海默病的遗传学和表观遗传学：了解发病机制和探索治疗潜力。

IF 2.8 4区医学

Journal of Molecular Neuroscience Pub Date : 2025-05-30 DOI: 10.1007/s12031-025-02363-2

Prabhakar Tiwari, Rekha Dwivedi, Meenakshi Kaushik, Manjari Tripathi, Rima Dada

{"title":"Genetics and Epigenetics of Alzheimer's Disease: Understanding Pathogenesis and Exploring Therapeutic Potential.","authors":"Prabhakar Tiwari, Rekha Dwivedi, Meenakshi Kaushik, Manjari Tripathi, Rima Dada","doi":"10.1007/s12031-025-02363-2","DOIUrl":"https://doi.org/10.1007/s12031-025-02363-2","url":null,"abstract":"Alzheimer's disease (AD) is a complex, multifactorial neurodegenerative disorder that affects millions of individuals globally. Despite extensive research efforts, effective treatments for AD remain elusive. AD pathogenesis is driven by a combination of genetic, epigenetic, and environmental factors. However, challenges persist in AD genetic and epigenetic research, including the need for larger and more diverse cohorts, the integration of multi-omic data, and the development of advanced computational and experimental tools. A comprehensive understanding of these factors is crucial for the development of effective treatments and ultimately a cure for this debilitating condition. In this review, we summarize key regulatory pathways involved in AD pathogenesis, emphasizing genetic factors such as the apolipoprotein E (APOE) gene and high-impact genetic mutations in amyloid precursor protein (APP) and presenilin 1 (PSEN1). We also explore significant epigenetic regulators, including DNA methylation, histone deacetylases (HDACs), and microRNAs (miRNAs), which modulate gene expression and contribute to disease progression. Furthermore, we discuss the interplay between genetic and epigenetic factors, highlighting their combined impact on β-amyloid deposition, tau pathology, neuroinflammation, and synaptic dysfunction. Finally, we examine the potential of epigenetic modifications as promising therapeutic targets for AD, due to their reversible nature, and propose future research directions to address current knowledge gaps. This review offers an updated perspective on AD genetics and epigenetics, providing insights into novel avenues for therapeutic intervention.","PeriodicalId":652,"journal":{"name":"Journal of Molecular Neuroscience","volume":"75 2","pages":"72"},"PeriodicalIF":2.8,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144186196","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}

引用次数: 0