Brain Research最新文献

{"title":"From Tim4 to ischemic stroke: a mitochondrial pathway driving microglial M1 polarization","authors":"Zhinan Ye ,&nbsp;Yingying Jin ,&nbsp;Hao Xu ,&nbsp;Xianwei Wang ,&nbsp;Andong Lin ,&nbsp;Qianqian Miao ,&nbsp;Weili Luo ,&nbsp;Yong Jin","doi":"10.1016/j.brainres.2025.150140","DOIUrl":"10.1016/j.brainres.2025.150140","url":null,"abstract":"<div><div>Microglia dysfunction is a critical contributor in ischemic stroke, where T-cell immunoglobulin and mucin domain 4 (Tim4) may play a significant role. After ischemic stroke modeling with the middle cerebral artery occlusion (MCAO) method, the changes in infarct volume, neurological deficits, cell apoptosis, microglial polarization, Tim4, mitochondrial fission proteins, mitochondrial membrane potential (MMP), and regulation of reactive oxygen species (ROS) were detected. In oxygen-glucose deprivation (OGD) model, the effects of Tim4 on microglial phenotypes, mitochondrial fission proteins, inflammatory factors, and MMP were evaluated. MCAO increased brain infarct volume, neurological deficits, apoptosis, and the proportion of M1-type microglia. In the OGD model, there was a drop in M2 microglia and a rise in M1 microglia, as well as upregulated tumor necrosis factor-alp (TNF-α) and Interleukin-1 beta (IL-1β). Upregulation of Tim4 was associated with increased levels of ROS in microglia, enhanced expressions of mitochondrial fission factor (MFF) and dynamin-related protein 1 (Drp1), and reduced MMP, which can be reversed by knocking down Tim4 expression. This implied that Tim4 could promote M1 microglial polarization and mitochondrial dynamics. However, Drp1 overexpression offset the effects of Tim4 knockdown on microglial polarization. In conclusion, Tim4 regulates the M1 microglial polarization via mitochondria, serving as a potential therapeutic target for ischemic stroke.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150140"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145896264","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":"K-means++ guided multi-view CNN with channel attention for EEG emotion recognition","authors":"Yi Zhou,&nbsp;Ruiwen Jiang,&nbsp;Jingxiang Zhang","doi":"10.1016/j.brainres.2026.150160","DOIUrl":"10.1016/j.brainres.2026.150160","url":null,"abstract":"<div><div>The use of artificial intelligence for emotion recognition is the focus of improving human–computer interaction. Recently, deep learning has been widely used in the study of emotion recognition. However, how to correctly identify emotions still faces a huge challenge. We propose a multi-view deep CNN based on channel attention (MVACNN) for EEG emotion recognition. MVACNN first clustered the channels and divided the channels with high similarity into the same view. Channels within the same view have highly similar patterns of neural activity, which can extract the synergistic features of specific brain regions more intensively and reduce the interference of irrelevant noise. To extract more discriminative features, MVACNN integrates channel attention into each view. Channel attention gives different channel weights to effectively learn the importance of different channels. In addition, MVACNN uses residual blocks to learn the residual variation to better represent the relationship between input and output. The residual structure preserves the original information, improving feature utilization and thus maintaining performance. Experimental results show that MVACNN achieves good results on different datasets.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150160"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951512","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":"Cortical parvalbumin-positive neurons: Functional and ontogenetic characteristics and their relationship to brain pathologies","authors":"Lina V. Becerra-Hernández ,&nbsp;Daniela Ortiz-Muñoz ,&nbsp;Adolfo Sánchez-Escobar ,&nbsp;Carlos A. González-Acosta ,&nbsp;Efraín Buriticá-Ramírez ,&nbsp;Verónica Martínez-Cerdeño","doi":"10.1016/j.brainres.2025.150141","DOIUrl":"10.1016/j.brainres.2025.150141","url":null,"abstract":"<div><div>Cortical GABAergic interneurons can be classified based on electrophysiological, biochemical, and morphological criteria. Among them, parvalbumin-positive interneurons primarily exhibit chandelier and basket cell morphologies and are characterized by a fast-spiking firing pattern. These cells originate from the medial ganglionic eminence during human brain development and are widely distributed across neocortical layers I–VI, with a predominance in layers II and III. Their distinct morphology, extensive axonal arborization, and specific synaptic contacts position them as key regulators of pyramidal neuron activity through axo-axonal and perisomatic inhibition. Parvalbumin-positive interneurons have been extensively studied in the context of neurological and psychiatric disorders associated with excitation/inhibition imbalances, including traumatic brain injury, epilepsy, autism spectrum disorder, and schizophrenia. Given the growing body of evidence, this review provides an in-depth examination of the pathophysiological roles of parvalbumin-positive interneurons, highlighting their selective vulnerability to various types of neural insults.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150141"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145899520","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":"Identification of hub genes and signaling pathways as possible therapeutic targets in human glioblastoma: evidenced by bioinformatics analysis","authors":"Haniyeh Soheil Beygi ,&nbsp;Ali Shahraki ,&nbsp;Roghayeh Sheervalilou","doi":"10.1016/j.brainres.2025.150137","DOIUrl":"10.1016/j.brainres.2025.150137","url":null,"abstract":"<div><h3>Background and aim</h3><div>Glioblastoma (GBM) is a lethal brain cancer demanding novel therapeutic targets. This study integrated bioinformatics to identify hub genes and dysregulated pathways in GBM.</div></div><div><h3>Methods</h3><div>Gene expression profiles (GSE108474: 221 GBM, 28 normal samples) were analyzed using R (Limma, clusterProfiler, BioBase). Differentially expressed genes (DEGs) were defined by |logFC| &gt; 1 and adjusted p &lt; 0.01. Gene Ontology (GO) and KEGG pathway enrichment (p &lt; 0.05), protein–protein interaction network construction (STRING/Cytoscape), and hub gene validation using TCGA-GBM/GTEx data (GEPIA2; 163 tumor, 207 normal) were performed. Immune infiltration (xCell algorithm; 64 cell types) and prognostic significance (Kaplan-Meier/log-rank tests) were assessed.</div></div><div><h3>Results</h3><div>We identified 5,710 DEGs, significantly enriched in actin cytoskeleton regulation. Eleven hub genes were validated: upregulated (PECAM1, PXDN, RPL27, RPL12, EIF3B, ENG, TGFB2, THBS1) and downregulated (CAMK2B, FGF22, RASGRF1). Hub genes correlated strongly with immunosuppressive cells: FGF22 and CAMK2B negatively correlated with M2 macrophages, while PECAM1, PXDN, RPL27, and ENG positively correlated. Consistent correlations were observed with B cells and regulatory T cells. Survival analysis revealed high THBS1 expression associated with poorer overall survival (HR = 1.4, p &lt; 0.05) and disease-free survival (HR = 1.9, p &lt; 0.05). Elevated ENG also reduced disease-free survival (HR = 1.7, p &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>THBS1 and ENG are significant prognostic biomarkers and potential therapeutic targets in GBM. Their strong correlation with immunosuppressive M2 macrophage infiltration implicates actin cytoskeleton remodeling pathways in GBM-mediated immune evasion. Targeting these hub genes may disrupt critical tumor microenvironment interactions, offering new avenues for therapy.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150137"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888615","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":"Multi-biofluid metabolomics coupled with gene network reveals stage-specific alterations in mild cognitive impairment and Alzheimer’s disease in an ethnically mixed cohort","authors":"André Simões Cadaxo ,&nbsp;Juliana Cordovil Cotrin ,&nbsp;Ana Paula Valente ,&nbsp;Flávia Gomes Lopes ,&nbsp;Renato Peixoto Veras ,&nbsp;Daniel Simplício Torres ,&nbsp;Raquel Quimas Molina da Costa ,&nbsp;Gilson Costa dos Santos Junior ,&nbsp;Cíntia Barros Santos-Rebouças","doi":"10.1016/j.brainres.2026.150167","DOIUrl":"10.1016/j.brainres.2026.150167","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most prevalent age-related neurodegenerative disorder worldwide. A prodromal stage, often manifested as Mild Cognitive Impairment (MCI), can precede dementia onset. Metabolomics provides a powerful approach to detect metabolic alterations capturing combined genetic, epigenetic, dietary, gut microbiota, and environmental influences on AD pathogenesis and progression from MCI to AD. In this study, we analysed plasma, urine, and saliva metabolomes of 94 ethnically diverse Brazilian individuals (30 AD, 16 MCI and 48 healthy controls), all comorbidity-free, using Nuclear Magnetic Resonance (NMR)-based metabolomics. Cross-sectional analysis employed multivariate modelling (PLS-DA) and univariate Mann-Whitney U tests. We identified distinct group-specific metabolic signatures involving amino acids (phenylalanine, glutamine, asparagine, valine, alanine), energy-related metabolites (pyruvate, citrate, glucose), compounds linked to lipid/redox pathways (acetate, glutamate, aspartate), epigenetic regulation (betaine), neuroinflammation, immune fitness, and gut microbiome-influenced metabolites (scyllo-inositol). Valine increased progressively (controls &lt; MCI &lt; AD), while alanine showed a biphasic pattern (reduced in MCI, elevated in AD). These consistent, biofluid-spanning alterations highlight their potential as minimally invasive biomarkers for diagnosis and monitoring. Integration of metabolite data with AD-associated genes from genome-wide association studies (GWAS) revealed six genes (<em>CYCS</em>, <em>NFAT5</em>, <em>GRIN2B</em>, <em>SLC43A2</em>, <em>MAPT</em>, and <em>SLC38A1</em>) common to all biofluids, reinforcing convergent systemic pathways. Collectively, these findings underscore the importance of integrating metabolomics with genetic networks to enhance understanding of AD pathophysiology, identify potential therapeutic targets, and guide future clinical validation and precision medicine strategies for dementia in ethnically mixed populations.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150167"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145974055","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":"Key optogenetic advances in retinal prostheses: A comparative narrative review","authors":"Laila Zahran,&nbsp;Reham H. Elnabawy","doi":"10.1016/j.brainres.2026.150166","DOIUrl":"10.1016/j.brainres.2026.150166","url":null,"abstract":"<div><div>This narrative review examines optogenetic strategies for retinal prostheses, which represent an advanced step in vision restoration, particularly for patients with retinitis pigmentosa and age-related macular degeneration. This review highlights the use of optogenetic stimulation to target high-density retinal ganglion cells (RGCs), focusing on developments like the FlexLED device. Opsins such as ChR2, ReaChR, and ChrimsonR, engineered for light sensitivity and faster responses, are critical for enhancing vision restoration. Combining optogenetic and electrical stimulation improves the reproducibility and specificity of RGC responses. Neuroimaging techniques like adaptive optics scanning laser ophthalmoscopy (AOSLO) help monitor cell activity, aiding in the development of visual repair methods. However, challenges remain in improving opsin sensitivity, gene delivery techniques, and ensuring long-term efficacy of retinal responses in patients. This review emphasizes the potential of optogenetic retinal prostheses to offer lasting, effective vision rehabilitation, significantly improving the quality of life for patients. This narrative review emphasizes that further research is needed to overcome current obstacles, such as improving opsin sensitivity and gene delivery techniques, to ensure long-term, effective vision restoration in patients.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150166"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145974421","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":"Identification of the disulfidptosis-related gene IQGAP1 as a potential diagnostic biomarker in Parkinson’s disease","authors":"Jianlin Li ,&nbsp;Jianhang You ,&nbsp;Zaipu Li ,&nbsp;Jing Zang ,&nbsp;Lin Wu ,&nbsp;Tao Zhao","doi":"10.1016/j.brainres.2026.150153","DOIUrl":"10.1016/j.brainres.2026.150153","url":null,"abstract":"<div><h3>Background</h3><div>Parkinson’s disease is the second most common and fastest-growing neurodegenerative disorder worldwide. However, its complex pathogenic mechanisms remain incompletely understood, and effective therapeutic strategies are still lacking. Disulfidptosis is a newly identified form of regulated cell death that has been shown to be closely associated with multiple diseases; nevertheless, its role in Parkinson’s disease has not yet been elucidated. In this study, we systematically investigated the expression patterns and potential functions of disulfidptosis-related differentially expressed genes that are significantly associated with Parkinson’s disease risk, using bulk transcriptomic data and single-cell RNA sequencing analyses.</div></div><div><h3>Methods</h3><div>We integrated single-cell RNA sequencing data with large-scale transcriptomic datasets to construct a disulfidptosis-related diagnostic model for Parkinson’s disease. First, twenty-five known disulfidptosis-related genes were collected from published literature and public databases. Differential expression analysis of GEO datasets was then performed to identify significantly differentially expressed genes between Parkinson’s disease and healthy control samples, which were subsequently used to build an initial diagnostic model. The expression profiles of key genes were further validated in external cohorts to enhance the robustness and reliability of the model. Next, single-cell RNA sequencing data from patients with Parkinson’s disease were incorporated to refine the identification of DRGs that were significantly associated with disease risk. Finally, quantitative real-time reverse transcription PCR was employed to experimentally validate the expression of the critical genes.</div></div><div><h3>Results</h3><div>We identified four DRGs in total. Using least absolute shrinkage and selection operator regression and random forest algorithms, three hub genes with diagnostic potential were further screened. After validation in external datasets and at the single-cell level, <em>IQGAP1</em> was ultimately confirmed as the key gene by quantitative real-time reverse transcription PCR, showing significantly upregulated expression in Parkinson’s disease samples.</div></div><div><h3>Conclusion</h3><div>This study provides the first evidence suggesting that disulfidptosis-related genes may be involved in the pathogenesis of Parkinson’s disease and highlights <em>IQGAP1</em> as a key molecule with potential value in Parkinson’s disease risk assessment and diagnosis. These findings not only offer a new perspective for elucidating the molecular mechanisms underlying Parkinson’s disease, but also provide a theoretical basis for identifying potential biomarkers and optimizing individualized therapeutic strategies, thereby further promoting the application of precision medicine in the field of Parkinson’s disease.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150153"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932082","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":"Diffusion spectrum imaging-based machine learning for temporal lobe epilepsy lateralization","authors":"Zhen-Ming Wang ,&nbsp;Yaqin Hou ,&nbsp;Chunxue Wu ,&nbsp;Miao Zhang ,&nbsp;Jie Lu","doi":"10.1016/j.brainres.2026.150154","DOIUrl":"10.1016/j.brainres.2026.150154","url":null,"abstract":"<div><h3>Objective</h3><div>Accurate preoperative lateralization of temporal lobe epilepsy (TLE) remains challenging, particularly in cases with subtle or MRI-negative lesions. This study aimed to overcome limitations of conventional MRI by developing a diffusion spectrum imaging (DSI)-based machine learning approach for noninvasive TLE lateralization.</div></div><div><h3>Methods</h3><div>We retrospectively analyzed DSI scans from 49 unilateral TLE patients (29 left, 20 right) and 25 healthy controls (HC). Local connectome fingerprints and quantitative anisotropy (QA) features were extracted. A support vector machine (SVM) was trained to classify patients from controls and to identify the epileptogenic hemisphere. Model performance was evaluated using 10-fold stratified cross-validation, with feature selection and dimensionality reduction performed within each training fold.</div></div><div><h3>Results</h3><div>The DSI-based SVM achieved high accuracy in distinguishing TLE from HC. With fingerprint features, accuracy was 97.3% (sensitivity 0.959, specificity 1.000); QA features yielded the same accuracy 97.3% (sensitivity 0.980, specificity 0.960). For lateralization among patients, the fingerprint model reached 100% accuracy versus 91.8% for QA. In the three-class classification task (left TLE, right TLE and HC), the models achieved accuracies of 78.4% (fingerprint) and 73.0% (QA). The fingerprint-based classifier yielded F1-scores of 0.943 for HC, 0.727 for LTLE, and 0.650 for RTLE; QA achieved F1-scores of 0.875, 0.677, and 0.632, respectively. DeLong’s test found no significant AUC differences.</div></div><div><h3>Conclusion</h3><div>DSI-derived metrics combined with machine learning enable accurate, noninvasive lateralization of TLE. This approach addresses clinical necessities by reliably detecting epileptogenic zones, including cases with subtle structural abnormalities, offering significant potential to enhance presurgical decision-making and patient outcomes.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150154"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932088","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":"The mechanism of Calhm2 regulating the expression of CaMKIIα in spinal dorsal horn involved in the pathogenesis of bone cancer pain","authors":"Mengyuan Xiong ,&nbsp;Xiaohui Li ,&nbsp;Shanchun Su ,&nbsp;Xueqin Xu ,&nbsp;Jiaqi Yu ,&nbsp;Wei Tian ,&nbsp;Linhan Wang ,&nbsp;Changbin Ke","doi":"10.1016/j.brainres.2026.150158","DOIUrl":"10.1016/j.brainres.2026.150158","url":null,"abstract":"<div><div>Bone cancer pain (BCP) is one of the most common and debilitating types of pain in cancer patients, severely impairing the quality of life in advanced stages of the disease. However, its underlying mechanisms remain poorly understood, highlighting the urgent need to clarify its pathogenesis and identify novel therapeutic targets. Increasing evidence suggests that altered excitability of spinal dorsal horn neurons is a prerequisite for pain generation. The dynamic balance of intracellular and extracellular calcium ion concentrations is critical for maintaining normal neuronal excitability. In this study, we investigated the role of calcium homeostasis modulator 2 (Calhm2) in BCP. In BCP mice, the expression of Calhm2 in the spinal dorsal horn was significantly upregulated, accompanied by a concomitant increase in calcium/calmodulin-dependent protein kinase II α (CaMKIIα). Lentiviral-mediated knockdown of Calhm2 in the spinal dorsal horn reduced CaMKIIα expression, alleviated mechanical allodynia, and decreased c-fos expression. These findings suggest that Calhm2 regulates CaMKIIα to promote neuronal activation in the spinal dorsal horn, thereby contributing to the development of bone cancer pain. Calhm2 may represent a promising target for therapeutic intervention in BCP.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150158"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951440","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":"Measurement of respiration in ex vivo mitochondria isolated from fresh human brain","authors":"Patrick J. McCarty ,&nbsp;Brianna A. Werner ,&nbsp;Adrienne C. Scheck ,&nbsp;Eric Wang ,&nbsp;Indrapal N. Singh ,&nbsp;John Gaitanis ,&nbsp;P. David Adelson ,&nbsp;Richard E. Frye","doi":"10.1016/j.brainres.2026.150156","DOIUrl":"10.1016/j.brainres.2026.150156","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1874 ","pages":"Article 150156"},"PeriodicalIF":2.6,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145932091","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}