Experimental Neurobiology最新文献

{"title":"Domain-generalized Deep Learning for Improved Subject-independent Emotion Recognition Based on Electroencephalography.","authors":"Jung-Hwan Kim, Hyerin Nam, Doyeon Won, Chang-Hwan Im","doi":"10.5607/en25011","DOIUrl":"https://doi.org/10.5607/en25011","url":null,"abstract":"<p><p>Electroencephalography (EEG) provides high temporal resolution and noninvasiveness for a range of practical applications, including emotion recognition. However, inherent variability across subjects poses significant challenges to model generalizability. In this study, we systematically evaluated twelve approaches by combining four domain generalization (DG) techniques, Deep CORAL, GroupDRO, VREx, and DANN, with three representative deep learning architectures (ShallowFBCSPNet, EEGNet, and TSception) to enable improved subject-independent EEG-based emotion recognition. The performances of the DG-integrated deep learning models were quantitatively evaluated using two emotional EEG datasets collected by the authors. Data from each subject were treated as distinct domains in each model. Binary classification tasks were conducted to identify the valence or arousal state of each participant based on a ten-fold cross-validation strategy. The results indicated that the application of DG methods consistently enhanced classification accuracy across datasets. In one dataset, TSception combined with VREx achieved the highest performance for both valence and arousal classifications. In the other dataset, TSception with VREx still yielded the highest valence classification accuracy, while TSception combined with GroupDRO showed the best arousal classification performance among the twelve models, slightly outperforming TSception with VREx. These findings underscore the potential of DG approaches to mitigate distributional shifts caused by intersubject and intersession variabilities to implement robust subject-independent EEG-based emotion recognition systems.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":" ","pages":""},"PeriodicalIF":1.8,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971614","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":"Celiac Disease Increases the Risk of Multiple Sclerosis: Evidence from Mendelian Randomization and the Role of CCL19.","authors":"Seongjin Lim, Junhua Wu, Yeon Woo Kim, Sun Woo Lim, Juhee Shin, Hyo Jung Shin, Sang Ryong Kim, Dong Woon Kim","doi":"10.5607/en25009","DOIUrl":"10.5607/en25009","url":null,"abstract":"<p><p>Celiac disease (CeD) is an autoimmune disorder triggered by gluten, primarily affecting the small intestine but potentially impacting other systems, including the nervous system through the gut-brain axis. This study employed Mendelian randomization (MR) to explore the causal relationships between CeD and several neurological disorders, with a particular focus on multiple sclerosis (MS). Utilizing genetic data from the OpenGWAS and Finngen databases, we applied various MR methods, including Inverse Variance Weighted (IVW), IVW-multiplicative random effects (MRE), weighted median (WM), MR-Egger, and robust adjusted profile score (RAPS), to investigate these associations. The analysis revealed no significant causal relationship between CeD and several other neurological disorders, but a significant positive association with MS was found (IVW OR=1.1919, 95% CI: 1.0851~1.3092, p=0.0002). Further analysis indicated that the mediator CCL19 plays a significant role in the pathway from CeD to MS, suggesting that CCL19 may be a key factor in the immune response linking these conditions. This mediation effect highlights the potential mechanism through which CeD increases the risk of developing MS. These findings emphasize the complexity of the relationship between CeD and MS, indicating the need for further research to understand these connections better and their clinical implications.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 2","pages":"63-76"},"PeriodicalIF":1.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069928/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144062690","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":"Magnesium-L-threonate Ameliorates Cognitive Deficit by Attenuating Adult Hippocampal Neurogenesis Impairment in a Mouse Model of Alzheimer's Disease.","authors":"Ying Xiong, Yuwen Yang, Yuting Ruan, Wencai Ou, Zhiwen Hu, Wei Li, Nina Xiao, Wang Liao, Jianhua Liu, Zhenlu Liu, Qiong Luo, Feifei Liu, Jun Liu","doi":"10.5607/en24030","DOIUrl":"10.5607/en24030","url":null,"abstract":"<p><p>Impaired adult hippocampal neurogenesis is a key pathological mechanism contributing to memory deficits in Alzheimer's disease (AD). Recent studies have shown that elevating magnesium levels promotes neurogenesis by enhancing the neuronal differentiation of adult neural progenitor cells in vitro. Therefore, this in vivo study aims to determine if magnesium-L-threonate (MgT) can ameliorate cognitive deficit of AD mice by attenuating adult hippocampal neurogenesis impairment and to reveal the underlying mechanisms. APPswe/PS1dE9 mice were treated with different doses of MgT and ERK inhibitor PD0325901. The memory ability of each mouse was recorded by Morris Water Maze test. After cognitive test, hippocampus tissues were collected to measure the proportion of BrdU/doublecortin double-labeled cells using the flow cytometry test and assess the expression of doublecortin using PCR and Western blot. Furthermore, the activations of CREB, ERK, P38 and JNK were measured by Western blot to identify the involved mechanisms. The cognitive test confirmed that MgT treatment attenuated the memory impairment of APPswe/PS1dE9 mice. Flow cytometry test showed that Brdu/doublecortin labeled newborn neurons gradually increased following MgT administration. In line with the flow cytometry results, Western blot and PCR confirmed that MgT administration significantly increased doublecortin expression levels. Furthermore, the ratios of p-ERK/ERK and p-CREB/CREB increased with MgT elevation. In addition, these effects of MgT treatment were markedly reversed by PD0325901 supplementation. In conclusion, MgT treatment improved cognitive decline by ameliorating adult hippocampal neurogenesis impairment in this AD model, possibly via ERK/CREB activation.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 2","pages":"53-62"},"PeriodicalIF":1.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989861","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":"Astrocytic Ornithine Decarboxylase 1 in Alzheimer's Disease.","authors":"Mridula Bhalla, C Justin Lee","doi":"10.5607/en25006","DOIUrl":"10.5607/en25006","url":null,"abstract":"<p><p>Recent research has shed light on the metabolic changes in reactive astrocytes associated with Alzheimer's disease, contributing to disease pathology. In this article, we summarize key findings related to reactive astrogliosis and how the discovery of the role of the enzyme ornithine decarboxylase 1 can set us on the path to finding more effective therapeutic strategies against neurodegenerative diseases.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 2","pages":"49-52"},"PeriodicalIF":1.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069927/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143975993","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":"Modeling Temporal Dependencies in Brain Functional Connectivity to Identify Autism Spectrum Disorders Based on Heterogeneous rs-fMRI Data.","authors":"Yaya Liu, Qiang Zhao, Lishuang Zhao, Yanchun Liu, Xiaoli Li","doi":"10.5607/en24028","DOIUrl":"10.5607/en24028","url":null,"abstract":"<p><p>Brain functional connectivity has shown promise for developing objective biomarkers for autism spectrum disorder (ASD). Although many imaging studies have demonstrated its potential, most have focused on static measurements. In this study, we explored the dynamic changes in functional connectivity over time to uncover potential temporal dependencies. These dynamic patterns were abstracted into high-level representations and used as predictors to identify individuals at risk of ASD. To achieve this, we employed a deep learning framework that combines attention mechanism with long short-term memory (LSTM) neural network. Experiments were conducted using heterogeneous resting-state functional magnetic resonance imaging (rs-fMRI) data from the Autism Brain Imaging Data Exchange (ABIDE) database. The resulting classification achieved an accuracy of 74.9% and precision of 75.5% under intra-site cross-validation, outperforming traditional classifiers such as support vector machines (SVM), random forests (RF), and single LSTM network. Further analyses demonstrated the robustness and generalizability of our model, with classification performance less affected by subjects' gender or age. The optimal model's weights revealed atypical temporal dependencies in the brain functional connectivity of individuals with ASD, highlighting the potential for these patterns to serve as biomarkers. Our findings underscore the importance of dynamic functional connectivity in understanding ASD and suggest that our deep learning framework could aid in the development of more accurate and reliable diagnostic tools for this disorder.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 2","pages":"77-86"},"PeriodicalIF":1.8,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12069925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990508","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":"Neuroinflammation in Adaptive Immunodeficient Mice with Colitis-like Symptoms.","authors":"Sung Hee Park, Junghwa Kang, Ji-Young Lee, Jeong Seon Yoon, Sung Hwan Hwang, Ji Young Lee, Deepak Prasad Gupta, Il Hyun Baek, Ki Jun Han, Gyun Jee Song","doi":"10.5607/en24016","DOIUrl":"10.5607/en24016","url":null,"abstract":"<p><p>Emerging evidence suggests that systemic inflammation may play a critical role in neurological disorders. Recent studies have shown the connection between inflammatory bowel diseases (IBD) and neurological disorders, revealing a bidirectional relationship through the gut-brain axis. Immunotherapies, such as Treg cells infusion, have been proposed for IBD. However, the role of adaptive immune cells in IBD-induced neuroinflammation remains unclear. In this study, we established an animal model for IBD in mice with severe combined immune-deficient (SCID), an adaptive immune deficiency, to investigate the role of adaptive immune cells in IBD-induced neuroinflammation. Mice were fed 1%, 3%, or 5% dextran sulfate sodium (DSS) for 5 days. We measured body weight, colon length, disease activity index (DAI), and crypt damage. Pro-inflammatory cytokines were measured in the colon, while microglial morphology, neuronal count, and inflammatory cytokines were analyzed in the brain. In the 3% DSS group, colitis symptoms appeared at day 7, with reduced colon length and increased crypt damage showing colitis-like symptoms. By day 21, colon length and crypt damage persisted, while DAI showed recovery. Although colonic inflammation peaked at day 7, no significant increase in inflammatory cytokines or microglial hyperactivation was observed in the brain. By day 21, neuroinflammation was detected, albeit with a slight delay, in the absence of adaptive immune cells. The colitis-induced neuroinflammation model provides insights into the fundamental immune mechanisms of the gut-brain axis and may contribute to developing immune cell therapies for IBD-induced neuroinflammation.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 1","pages":"34-47"},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919638/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647857","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":"Transcriptomic Alteration in the Brain and Gut of Offspring Following Prenatal Exposure to Corticosterone.","authors":"Eun-A Ko, Tong Zhou, Jae-Hong Ko, Sung-Cherl Jung","doi":"10.5607/en24029","DOIUrl":"10.5607/en24029","url":null,"abstract":"<p><p>Maternal stress during pregnancy can profoundly affect offspring health, increasing the risk of psychiatric disorders, metabolic diseases, and gastrointestinal problems. In this study, the effects of high prenatal corticosterone exposure on gene expression in the brain and small intestine of rat offspring were investigated via RNA-sequencing analysis. Pregnant rats were divided into two groups: Corti.Moms were injected with corticosterone daily, while Nor.Moms were given saline injections. Their offspring were labeled as Corti.Pups and Nor.Pups, respectively. The brain tissue analysis of Corti.Pups showed that the expression levels of the genes linked to neurodegenerative conditions increased and enhanced mitochondrial biogenesis, possibly due to higher ATP demands. The genes associated with calcium signaling pathways, neuroactive ligand-receptor interactions, and IgA production were also upregulated in the small intestine of Corti.pups. Conversely, the genes related to protein digestion, absorption, and serotonergic and dopaminergic synaptic activities were downregulated. These findings revealed that gene expression patterns in both the brain and intestinal smooth muscle of offspring prenatally exposed to corticosterone were substantially altered. Thus, this study provided valuable insights into the effects of prenatal stress on neurodevelopment and gut function.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 1","pages":"9-19"},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919639/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647858","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":"<i>Sphingomonas Paucimobilis</i>-derived Extracellular Vesicles Reverse Aβ-induced Dysregulation of Neurotrophic Factors, Mitochondrial Function, and Inflammatory Factors through MeCP2-mediated Mechanism.","authors":"Eun-Hwa Lee, Hyejin Kwon, So-Young Park, Jin-Young Park, Jin-Hwan Hong, Jae-Won Paeng, Yoon-Keun Kim, Pyung-Lim Han","doi":"10.5607/en25001","DOIUrl":"10.5607/en25001","url":null,"abstract":"<p><p>Recent studies have shown an increased abundance of <i>Sphingomonas paucimobilis</i>, an aerobic, Gram-negative bacterium with a distinctive cell envelope rich in glycosphingolipids, within the gut microbiome of individuals with Alzheimer Disease (AD). However, the fact that <i>S. paucimobilis</i> is a well-known pathogen associated with nosocomial infections presents a significant challenge in investigating whether its presence in the gut microbiome is detrimental or beneficial, particularly in the context of AD. This study examines the impact of <i>S. paucimobilis</i>-derived extracellular vesicles (Spa-EV) on Aβ-induced pathology in cellular and animal models of AD. Microarray analysis reveals that <i>Spa</i>-EV treatment modulates Aβ42-induced alterations in gene expression in both HT22 neuronal cells and BV2 microglia cells. Among the genes significantly affected by Spa-EV, notable examples include Bdnf, Nt3/4, and Trkb, which are key players of neurotrophic signaling; Pgc1α, an upstream regulator of mitochondrial biogenesis; Mecp2 and Sirt1, epigenetic factors that regulate numerous gene expressions; and Il1β, Tnfα, and Nfκb-p65, which are associated with neuroinflammation. Remarkably, <i>Spa</i>-EV effectively reverses Aβ42-induced alteration in the expression of these genes through the upregulation of Mecp2. Furthermore, administration of <i>Spa</i>-EV in Tg-APP/PS1 mice restores the reduced expression of neurotrophic factors, Pgc1α, MeCP2, and Sirt1, while suppressing the increased expression of proinflammatory genes in the brain. Our results indicate that <i>Spa</i>-EV has the potential to reverse Aβ-induced dysregulation of gene expression in neuronal and microglial cells. These alterations encompass those essential for neurotrophic signaling and neuronal plasticity, mitochondrial function, and the regulation of inflammatory processes.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 1","pages":"20-33"},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919641/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647855","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":"Combination of Aβ40, Aβ42, and Tau Plasma Levels to Distinguish Amyloid-PET Positive Alzheimer Patients from Normal Controls.","authors":"Seungyeop Baek, Jinny Claire Lee, Byung Hyun Byun, Su Yeon Park, Jeong Ho Ha, Kyo Chul Lee, Seung-Hoon Yang, Jun-Seok Lee, Seungpyo Hong, Gyoonhee Han, Sang Moo Lim, YoungSoo Kim, Hye Yun Kim","doi":"10.5607/en25008","DOIUrl":"10.5607/en25008","url":null,"abstract":"<p><p>Alzheimer disease (AD) diagnosis is confirmed using a medley of modalities, such as the detection of amyloid-β (Aβ) neuritic plaques and neurofibrillary tangles with positron electron tomography (PET) or the appraisal of irregularities in cognitive function with examinations. Although these methods have been efficient in confirming AD pathology, the rising demand for earlier intervention during pathogenesis has led researchers to explore the diagnostic potential of fluid biomarkers in cerebrospinal fluid (CSF) and plasma. Since CSF sample collection is invasive and limited in quantity, biomarker detection in plasma has become more attractive and modern advancements in technology has permitted more efficient and accurate analysis of plasma biomolecules. In this study, we found that a composite of standard factors, Aβ40 and total tau levels in plasma, divided by the variation factor, plasma Aβ42 level, provide better correlation with amyloid neuroimaging and neuropsychological test results than a level comparison between total tau and Aβ42 in plasma. We collected EDTA-treated blood plasma samples of 53 subjects, of randomly selected 27 AD patients and 26 normal cognition (NC) individuals, who received amyloid-PET scans for plaque quantification, and measured plasma levels of Aβ40, Aβ42, and total tau with digital enzyme-linked immunosorbent assay (ELISA) in a blinded manner. There was difficulty distinguishing AD patients from controls when analyzing biomarkers independently. However, significant differentiation was observed between the two groups when comparing individual ratios of total-tau×Aβ40/Aβ42. Our results indicate that collectively comparing fluctuations of these fluid biomarkers could aid in monitoring AD pathogenesis.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"34 1","pages":"1-8"},"PeriodicalIF":1.8,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11919640/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647856","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":"Current Status and Future Perspective of Seoul National University Hospital-Dementia Brain Bank with Concordance of Clinical and Neuropathological Diagnosis.","authors":"Kwanghoon Lee, Seong-Ik Kim, Yu-Mi Shim, Eric Eunshik Kim, Sooyeon Yoo, Jae-Kyung Won, Sung-Hye Park","doi":"10.5607/en24027","DOIUrl":"10.5607/en24027","url":null,"abstract":"<p><p>This paper introduces the current status of Seoul National University Hospital Dementia Brain Bank (SNUH-DBB), focusing on the concordance rate between clinical diagnoses and postmortem neuropathological diagnoses. We detail SNUH-DBB operations, including protocols for specimen handling, induced pluripotent stem cells (iPSC) and cerebral organoids establishment from postmortem dural fibroblasts, and adult neural progenitor cell cultures. We assessed clinical-neuropathological diagnostic concordance rate. Between 2015 and September 2024, 162 brain specimens were collected via brain donation and autopsy. The median donor age was 73 years (1-94) with a male-to -female ratio of 2:1. The median postmortem interval was 9.5 hours (range: 2.5-65). Common neuropathological diagnoses included pure Lewy body disease (10.6%), Lewy body disease (LBD) with other brain diseases (10.6%), pure Alzheimer's disease-neuropathological change (ADNC) (6.0%), ADNC with other brain diseases (10.7%), vascular brain injury (15.2%), and primary age-related tauopathy (7.3%). APOE genotype distribution was following: ε3/ε3: 62.3%, ε2/ε3: 9.6%, ε2/ε4: 3.4%, ε3/ε4: 24.0%, and ε4/ε4: 0.7%. Concordance rates between pathological and clinical diagnoses were: ADNC/AD at 42.4%; LBD at 59.0%; PSP at 100%; ALS at 85.7%; Huntington's disease 100%. The varying concordance rates across different diseases emphasize the need for improved diagnostic criteria and biomarkers, particularly for AD and LBD. Tissues have been distributed to over 40 national studies. SNUH-DBB provides high-quality brain tissues and cell models for neuroscience research, operating under standardized procedures and international guidelines. It supports translational research in dementia and neurodegenerative diseases, potentially advancing diagnostic and therapeutic strategies.</p>","PeriodicalId":12263,"journal":{"name":"Experimental Neurobiology","volume":"33 6","pages":"295-311"},"PeriodicalIF":1.8,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11738475/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142978105","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}