BMC Neuroscience最新文献

{"title":"Identification of the IL-1β/miRNA-326 axis as a key regulator of ferroptosis in spinal cord injury.","authors":"Senming Xu, Yangyang Jiang, Yuchang Gui, Jianmin Chen, Qinhe Pan, Minli Jiang, Jianwen Xu","doi":"10.1186/s12868-026-01001-w","DOIUrl":"10.1186/s12868-026-01001-w","url":null,"abstract":"<p><p>INTRODUCTION: Spinal cord injury (SCI) is a devastating condition with high rates of disability and mortality, and secondary injury mechanisms such as ferroptosis have emerged as crucial contributors to its pathophysiology. However, the regulatory mechanisms underlying ferroptosis in SCI remain largely unclear. METHODS: We analyzed peripheral blood transcriptome data (GSE151371) from 10 healthy controls, 10 non-CNS trauma patients, and 38 SCI patients to identify differentially expressed mRNAs (DE-mRNAs) and miRNAs (DE-miRNAs). Ferroptosis-related genes (FRGs) were screened by intersecting DE-mRNAs with a curated list of FRGs. Functional enrichment analyses, regulatory network construction (lncRNA–miRNA–mRNA, TF-miRNA-mRNA), and drug target predictions were conducted. Key findings were validated using the GSE166009 dataset from a rat SCI model and through experimental verification in a TSCI rat model. RESULTS: We identified 38 differentially expressed FRGs (DE-FRGs) in SCI, enriched in lipid metabolism and inflammatory pathways, including IL-17 and TNF signaling. Protein–protein interaction network analysis identified IL-1β as a central hub gene. A miRNA–mRNA network revealed miR-326 as a key regulator of IL-1β. The IL-1β/miR-326 axis was also closely associated with lncRNA-miRNA-mRNA networks, transcription factor regulation, and drug target predictions. Validation in the GSE166009 dataset and a rat SCI model confirmed progressive downregulation of miR-326 and upregulation of IL-1β post-SCI. Dual-luciferase reporter assays demonstrated that miR-326 directly binds the 3′UTR of IL-1β, suppressing its expression. DISCUSSION: Our study highlights the IL-1β/miR-326 axis as a critical regulator of ferroptosis in SCI and a potential therapeutic target for intervention. </p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13059498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343560","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":"Involvement of CB1 cannabinoid receptors in methamphetamine-related decision-making and social behavior deficits.","authors":"Tahoora Mousavi, Nadia Hatami, Saba Niknamfar, Mahshid Naseri, Raheleh Rafaiee, Seyedeh Masoumeh Seyedhosseini Tamijani, Mohammad Saleh Ranaiy, Hamed Ghazvini","doi":"10.1186/s12868-026-01000-x","DOIUrl":"10.1186/s12868-026-01000-x","url":null,"abstract":"<p><p>BACKGROUND: Methamphetamine (METH) abuse is associated with profound cognitive and behavioral impairments, notably in decision-making and social interaction. Emerging evidence suggests the endocannabinoid system, particularly CB1 receptors (CB1Rs), plays a modulatory role in these processes. This study investigated whether pharmacological modulation of CB1Rs can alter METH-induced deficits in decision-making, social behavior, and anxiety in a rodent model. METHODS: Adult male Wistar rats were administered METH and treated with either a CB1R agonist WIN55,212-2 (WIN; 3 mg/kg; i.p) or antagonist (Rimonabant;1 mg/kg; i.p.). Behavioral assessments included effort-based decision-making via the Y-maze barrier task, social behavior tests, and anxiety evaluation using the elevated plus maze. RESULTS: METH exposure significantly reduced high-reward choices in effort-based tasks and impaired multiple domains of social behavior. It also induced anxiety-like behaviors. Rimonabant treatment partially reversed these effects, improving decision-making performance, enhancing social interactions, and reducing anxiety-related responses. In contrast, WIN did not significantly alleviate METH-induced behavioral impairments. CONCLUSION: CB1R antagonism via Rimonabant may mitigate METH-induced cognitive and social deficits, underscoring the therapeutic potential of targeting the endocannabinoid system in stimulant-related neuropsychiatric disorders. These findings highlight CB1R antagonists as promising agents for future interventions in METH addiction and its associated behavioral disruptions. CLINICAL TRIAL NUMBER: Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13037093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147275716","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":"Slc6a9 is distributed in glial cells and neurons across several nervous system regions, whereas Slc6a5 is more restricted to neurons in the caudal brain.","authors":"Mikaela M Ceder, Malin C Lagerström","doi":"10.1186/s12868-026-00999-3","DOIUrl":"10.1186/s12868-026-00999-3","url":null,"abstract":"<p><p>BACKGROUND: The glycinergic system constitutes a main source of inhibitory regulation in the central nervous system. Glycine transporters (GLYT1 and GLYT2), encoded by Slc6a9 and Slc6a5, respectively, are responsible for glycine reuptake and clearance from the synaptic cleft, thereby maintaining neurotransmitter homeostasis. Emerging evidence from pharmacological and mechanistic studies has highlighted GLYTs as promising therapeutic targets for psychiatric disorders and persistent pain. Nevertheless, data on anatomical and cellular distribution of GLYTs and sex-dependent differences in GLYT expression remain limited. METHODS: To address this gap, the aim of this study was to examine the Slc6a9 and Slc6a5 mRNA expression across mouse brain regions and peripheral organs using three complementary approaches focusing on mRNA expression: re-analysis of single-cell RNA sequencing data, quantitative RT-PCR, and RNAscope. RESULTS: Both genes were detected in multiple brain regions, with Slc6a9 exhibiting a broader distribution in both glial cells and neurons, while Slc6a5 was more restricted to neurons. Sex-dependent differences were detected for Slc6a9 in the amygdala and thalamus, liver, intestine, spleen, kidney and genitalia using quantitative RT-PCR, and for Slc6a5 in the cortex, striatum, hippocampus, and spinal cord using quantitative RT-PCR. Spatial analysis of the glycine transporters showed that Slc6a9 can be found in several brain regions spanning the rostral to the caudal axis, in both glial cells and neurons, while Slc6a5 was more restricted to the caudal brain regions. CONCLUSIONS: In general, in regions where differences were detected using quantitative RT-PCR, higher expression levels were observed in male mice. Moreover, Slc6a9 expression was found to occur in both glial cells, such as astrocytes, oligodendrocytes and ependymal cells, as well as both excitatory and inhibitory neurons, while Slc6a5 mainly occurred in inhibitory neurons. These findings provide novel insights into the spatial and sex-dependent expression of glycine transporters.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12931055/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212005","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":"Acetyl-11-keto-β-boswellic acid attenuates tau oligomer-induced neurotoxicity in neuroblastoma cell model.","authors":"Shahnaz Pourhossein, Ibrahim Bahrami Mianrood, Seyyed Hossein Khatami, Sajad Ehtiati, Majid Ghasemian, Farzad Mokhtari, Reyhane Ahmadzade, Marziyeh Goudarzi, Nastaran Hamed, Fatemeh Namvarjah, Saeed Karima","doi":"10.1186/s12868-026-00996-6","DOIUrl":"10.1186/s12868-026-00996-6","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by microtubule destabilization, neuroinflammation, and tau pathology. Among the proposed therapeutic approaches, acetyl-11-keto-β-boswellic acid (AKBA), a bioactive triterpene from Boswellia serrata, has gained attention due to its multiple neuroprotective mechanisms, including microtubule stabilization, anti-inflammatory activity, antioxidant effects, and promotion of neurogenesis. In this study, we aimed to investigate the neuroprotective effect of AKBA against tau oligomer-induced cytotoxicity in SH-SY5Y neuroblastoma cells.</p><p><strong>Results: </strong>Recombinant human tau protein was expressed, purified, and oligomerized, and the formation of oligomers was confirmed by thioflavin T fluorescence and dynamic light scattering (DLS). SH-SY5Y cells were then treated with AKBA and exposed to tau oligomers. Cell viability was assessed via MTT assay, and apoptosis was evaluated by flow cytometry. The morphology of tau aggregates was visualized using transmission electron microscopy.</p><p><strong>Conclusions: </strong>Our findings demonstrated that AKBA significantly reduced tau oligomer-induced cytotoxicity and enhanced cell viability. These results suggest that AKBA, through its multifaceted protective mechanisms, holds promise as a potential therapeutic agent for the treatment of tauopathies such as Alzheimer's disease.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146177962","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":"MEF2A-mediated inhibition of ischemic stroke injury via the PI3K/AKT pathway: a comprehensive bioinformatics and in vitro study.","authors":"Tingyu Zhang, Jiaqi Cheng, Yushi Tian, Ying Hai","doi":"10.1186/s12868-026-00997-5","DOIUrl":"10.1186/s12868-026-00997-5","url":null,"abstract":"<p><p>BACKGROUND: Thrombosis or embolism causes blood flow stoppage, resulting in ischemic stroke (IS), the most frequent clinical cerebrovascular disorder. It accounts for more than 80% of all strokes and has a significant disability and mortality rate. Regulating critical targets to stop the ischemia pathophysiological cascade and preserve brain cells is essential for treating IS. METHODS: We included a deCODE analysis encompassing data on cis-acting variations for 4719 blood proteins. The IS summary statistics consist of 11,929 cases and 472,192 controls. We identified blood proteins associated with IS susceptibility using the Mendelian randomization (MR) method. We comprehensively analyzed the GSE58294 dataset, including differential expression gene identification, functional enrichment analysis, weighted gene co-expression network analysis, least absolute shrinkage and selection operator analysis, and transcription factor identification. The expression patterns of key genes were identified using single-cell sequencing data. The oxygen-glucose deprivation/reperfusion (OGD/R) model was established, and myocyte enhancer factor 2 A (MEF2A) was overexpressed in Neuro-2a/PC12 cells using an overexpression vector. We used CCK-8 and western blotting to observe the cell viability, oxidative stress level, and p-PI3K and p-Akt protein expression. RESULTS: We discovered 73 blood proteins related to IS, and the sensitivity analysis findings supported the causal associations. The MR results and bioinformatics underwent a thorough examination, revealing MEF2A as a transcription factor involved in the development of IS. Single-cell sequencing results revealed that MEF2A was mostly expressed in microglia and endothelial cells. Additional in vitro experiments showed that overexpression of MEF2A could significantly mitigate OGD/R-induced Neuro-2a/PC12 cell injury and oxidative stress, potentially associated with increased PI3K/Akt protein production. CONCLUSION: This study, using MR analysis, transcriptomics, and in vitro experiments, identified the transcription factor MEF2A as a potential target for treatment. This gives preclinical evidence for drug development. CLINICAL TRIAL NUMBER: Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12954911/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146099752","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":"Modulation of stress and neuroplasticity biomarkers via rhythmic vocalization: a controlled study on NDNF, cortisol, and monoamines.","authors":"Süheyb Okur, Bülent Bayraktar","doi":"10.1186/s12868-026-00998-4","DOIUrl":"10.1186/s12868-026-00998-4","url":null,"abstract":"<p><p>BACKGROUND: The aim of this study is to investigate the effect of reciting the Quran (from Mushaf) on serotonin, dopamine, NDNF, and cortisol levels in relation to mental well-being. METHODS: This study was conducted on a sample of university students who know how to read the Quran in Türkiye, selected by a non-probability method, with a pre-test-post-test control group and a longitudinal design; the assignment to the groups was also done randomly. The research was carried out with 72 university students (36 female, 36 male), aged 19–30, who know how to read the Quran and do not have any health problems. Two groups were formed: a 36-person experimental group and a 36-person passive resting control group. The Mental Well-Being Scale and a personal information form were used to evaluate the participants’ well-being status. Salivary serotonin, dopamine, NDNF, and cortisol levels were examined using the ELISA technique in samples taken before and after the experimental group recited verses 195–200 of Surah Al-i Imran aloud. Number, percentage, mean, Pearson correlation, and ANOVA tests were used to evaluate the data. Statistical significance was accepted as p < .05 for all analyses. RESULTS: A significant group-time interaction was found (p < .05). Compared to the passive resting control group, the experimental group showed statistically significant increases in salivary serotonin, dopamine, and NDNF levels, and a significant decrease in cortisol levels. However, a critical dissociation was observed: despite this neuroprotective biomarker profile, the control group reported statistically significantly higher post-intervention mental well-being scores than the experimental group (p < .05). This suggests that the acute cognitive load and performance anxiety associated with the recitation task may temporarily mask physiological benefits in self-reports. CONCLUSIONS: A brief (5-minute) ‘Tartil’ recitation of the Quran demonstrates immediate, positive neurobiological effects by reducing stress hormones (cortisol) and increasing reward- and neuroplasticity-related biomarkers (dopamine, serotonin, NDNF). However, this did not immediately translate to higher self-reported well-being, suggesting the relationship between the neurobiology of recitation and its perceived psychological effects is complex and potentially confounded by factors such as performance anxiety or cognitive load in an experimental setting. CLINICAL TRIAL NUMBER: Not applicable.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":""},"PeriodicalIF":3.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12924569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084179","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":"Precise Aβ clearance and antioxidant therapy in Alzheimer's disease via photoacoustic imaging-guided palladium hydride nanosheet-mediated photothermal treatment.","authors":"Lujie Yu, Mingxin Zhao, Wenjing Zhang, Zhigan Lv, Keqi Zhao, Huailiang Li, Yunjie Qi, Xin Peng, Ziliang Zheng, Weiwei Zhang","doi":"10.1186/s12868-025-00994-0","DOIUrl":"10.1186/s12868-025-00994-0","url":null,"abstract":"<p><p>Inflammation and oxidative stress are critical pathological hallmarks of Alzheimer’s disease (AD). Hydrogen therapy shows promise due to its selective hydroxyl radical (∙OH) scavenging capacity, yet conventional hydrogen delivery fails to effectively accumulate in the brain due to low solubility and rapid diffusion. Here, we report ultra-small palladium hydride (PdH) nanosheets as a dual-functional nanomedicine for AD treatment. The PdH nanosheets exhibit high hydrogen-releasing efficiency via autocatalysis, enabling in situ ∙OH scavenging in the brain. Concurrently, their near-infrared (NIR) photothermal effect, degrading amyloid-β (Aβ) aggregates and transiently enhancing blood-brain barrier (BBB) permeability for improved drug delivery. In AD mice, intravenous PdH treatment combined with NIR irradiation significantly reduced escape latency in the Morris water maze, paralleling reductions in brain Aβ plaques and ROS levels. This study establishes a synergistic strategy of nanoscale hydrogen delivery and photothermal therapy, addressing the dual challenges of BBB penetration and multi-pathology intervention in AD.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":"8"},"PeriodicalIF":3.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12874838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084103","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":"Modulating subjective and objective cognitive state fatigue in long COVID with repetitive anodal tDCS: results from a double-blinded randomized controlled trial.","authors":"Magdalena Mischke, Tino Zaehle","doi":"10.1186/s12868-025-00989-x","DOIUrl":"10.1186/s12868-025-00989-x","url":null,"abstract":"<p><strong>Background: </strong>Cognitive fatigue is a frequently reported and debilitating symptom of long COVID, yet effective therapeutic interventions remain limited. Anodal transcranial direct current stimulation (tDCS) over the dorsolateral prefrontal cortex (dlPFC) has been proposed as a promising approach to modulate fatigue-related neural networks. To comprehensively assess cognitive fatigue, the integration of subjective and objective behavioral and electrophysiological measures of induced state fatigue is essential.</p><p><strong>Methods: </strong>This double-blind, randomized, sham-controlled study investigated the effects of four consecutive daily sessions of 30-minute anodal tDCS over the left dlPFC on subjective and objective markers of cognitive state fatigue in individuals with long COVID. The present paper focuses on secondary outcomes, including subjective state fatigue ratings via visual analogue scales, behavioral performance indices, and electrophysiological markers such as temporal alterations of frontal theta and occipital alpha activity as well as p50 sensory gating.</p><p><strong>Results: </strong>Forty participants received either verum or sham tDCS while completing a gamified adaptive Go/No-Go task. Before and after the stimulation period, cognitive state fatigue was reliably induced using the AX-Continuous Performance Task (AX-CPT). Although tDCS did not significantly affect subjective state-fatigue ratings or behavioral performance, our findings indicate that verum stimulation may stabilize fatigue-related changes in occipital alpha power. No immediate stimulation-related improvements were found in the Go/No-Go task.</p><p><strong>Conclusions: </strong>These findings indicate that while tDCS may modulate neurophysiological correlates of cognitive state fatigue, its impact on subjective experience and behavioral performance remain limited under the current protocol. These results, however, underscore the importance of including neurophysiological endpoints in intervention research and highlight the need for developing more robust and individualized stimulation protocols. Future studies should consider extended stimulation regimens, alternative task paradigms, and more sensitive behavioral measures to further elucidate the neuromodulatory potential of tDCS in long COVID-related cognitive fatigue.</p><p><strong>Trial registration: </strong>drks.de Identifier: DRKS00031294, date of registration: 17.02.2023.</p>","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":" ","pages":"6"},"PeriodicalIF":2.3,"publicationDate":"2026-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12849268/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146043881","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":"Retraction Note: Diabetes mellitus and risk of incident dementia in APOE ɛ4 carriers: an updated meta-analysis.","authors":"Ava Rashtchian, Mohammad Hossein Etemadi, Elham Asadi, Sara Binaei, Mina Abbasi, Maedeh Bayani, Erfan Izadi, Sayedeh-Fatemeh Sadat-Madani, Mahdyieh Naziri, Sahar Khoshravesh, Mahsa Shirani, Mahsa Asadi Anar, Niloofar Deravi","doi":"10.1186/s12868-026-00995-7","DOIUrl":"10.1186/s12868-026-00995-7","url":null,"abstract":"","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"27 1","pages":"1"},"PeriodicalIF":2.3,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12797609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145965251","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":"Editorial expression of concern: Neuroprotective effects of bis(7)-tacrine against glutamate-induced retinal ganglion cells damage.","authors":"Jia Hua Fang, Xing Hua Wang, Zhi Rong Xu, Fa Gang Jiang","doi":"10.1186/s12868-025-00990-4","DOIUrl":"10.1186/s12868-025-00990-4","url":null,"abstract":"","PeriodicalId":9031,"journal":{"name":"BMC Neuroscience","volume":"27 1","pages":"2"},"PeriodicalIF":2.3,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12797980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145965202","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}