Brain Research最新文献

{"title":"Expression of concern: \"Sulforaphane protects brains against hypoxic-ischemic injury through induction of Nrf2-dependent phase 2 enzyme\" [BRAIN RES, Volume 1343 (2010) 178-185].","authors":"Zhang Ping, Wenwu Liu, Zhimin Kang, Jianmei Cai, Qiusha Wang, Ni Cheng, Sujian Wang, Shizhong Wang, John H Zhang, Xuejun Sun","doi":"10.1016/j.brainres.2025.149686","DOIUrl":"https://doi.org/10.1016/j.brainres.2025.149686","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1861 ","pages":"149686"},"PeriodicalIF":2.7,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144233129","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":"Functional correspondences in the human and marmoset visual cortex during movie watching: Insights from correlation, redundancy, and synergy","authors":"Qiang Li ,&nbsp;Ting Xu ,&nbsp;Vince D. Calhoun","doi":"10.1016/j.brainres.2025.149864","DOIUrl":"10.1016/j.brainres.2025.149864","url":null,"abstract":"<div><div>The world of beauty is deeply connected to the visual cortex, as perception often begins with vision in both humans and marmosets. Quantifying functional correspondences in the visual cortex across species can help us understand how information is processed in the primate visual cortex, while also providing deeper insights into human visual cortex functions through the study of marmosets. In this study, to investigate their functional correspondences, we used 13 healthy human volunteers (9 males and 4 females, aged 22-56 years) and 8 common marmosets (6 males and 2 females, aged 20-42 months). We then measured pairwise and beyond-pairwise correlations, redundancy, and synergy in movie-driven fMRI data across species. First, we consistently observed a high degree of functional similarity in visual processing within and between species, suggesting that integrative processing mechanisms are preserved in both humans and marmosets, despite potential differences in their specific activity patterns. Second, we found that the strongest functional correspondences during movie watching occurred between the human peri-entorhinal and entorhinal cortex (PeEc) and the occipitotemporal high-level visual regions in the marmoset, reflecting a synergistic functional relationship. This suggests that these regions share complementary and integrated patterns of information processing across species. Third, redundancy measures maintained stable high-order hubs, indicating a steady core of shared information processing, while synergy measures revealed a dynamic shift from low- to high-level visual regions as interaction increased, reflecting adaptive integration. This highlights distinct patterns of information processing across the visual hierarchy. Ultimately, our results reveal the marmoset as a compelling model for investigating visual perception, distinguished by its remarkable functional parallels to the human visual cortex.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149864"},"PeriodicalIF":2.6,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862127","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":"Concurrent bilateral M1 anodal and right cerebellar cathodal tDCS attenuates learning of a bimanual videogame task","authors":"Davin Greenwell ,&nbsp;Quinn McCallion ,&nbsp;Brach Poston ,&nbsp;Zachary A. Riley","doi":"10.1016/j.brainres.2025.149884","DOIUrl":"10.1016/j.brainres.2025.149884","url":null,"abstract":"<div><div>Bimanual movements require complex cortical interactions when learning new motor skills. Previous work has shown that anodal transcranial direct current stimulation (a-tDCS) of one or both primary motor cortices can accelerate learning. Given the cerebellum’s role in early motor learning, the present study sought to examine the effect of bilateral primary motor cortex (M1) a-tDCS coupled with cathodal cerebellar tDCS (biM1a + CBc) on learning of a bimanual racing videogame. 40 subjects were enrolled and received either biM1a + CBc (n = 21) or SHAM (n = 19) stimulation for a single practice session. Videogame performance was assessed before and after the practice session, and a follow-up assessment was made 24 h later. Opposite of what was expected, the tDCS stimulation condition resulted in less improvement within a single day of training than the SHAM condition (<em>p =</em> 0.007). Subjects with more gaming experience showed more retention of the training effect between days, regardless of stimulation condition (<em>p</em> = 0.031). These results suggest that the bilateral anodal M1 stimulation paired with cathodal cerebellar stimulation diminishes the rate that online learning occurs for a bimanual racing videogame task. Consistent with many tDCS studies, the electrode montage and current directions are task-specific and cannot be generalized.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149884"},"PeriodicalIF":2.6,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842649","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 role of Fezolinetant in fear memory consolidation","authors":"Mariana G. Fronza ,&nbsp;Marta Torrent ,&nbsp;Raul Andero","doi":"10.1016/j.brainres.2025.149879","DOIUrl":"10.1016/j.brainres.2025.149879","url":null,"abstract":"<div><div>Modulation of fear memories has important implications for the treatment of different psychiatric disorders including fear-based disorders such as posttraumatic stress disorder (PTSD). The Tachykinin2 (Tac2)/Neurokinin B (NkB)/neurokinin 3 receptor (Nk3R) pathway is a potential candidate for treating fear-based disorders built on animal and human studies. Here we demonstrate that the Nk3R antagonist Fezolinetant presents sex-divergent effects in the processing of fear memories in mice exposed to cued-fear conditioning. Fezolinetant (1 and 10 mg/kg, intraperitoneally (i.p.)) administered 30 min after the fear acquisition impairs the fear memory consolidation in male mice, as measured by fear expression 24 h later, showing no effects in naturally cycling female mice, with no monitoring the estrous cycle. However, when the estrous cycle was monitored, Fezolinetant (1 and 10 mg/kg, i.p.) enhanced fear memory consolidation during the proestrus phase, which suggests an effect dependent on high levels of the sex hormones estradiol and/or progesterone. Considering that Fezolinetant is currently a treatment for hot flashes in menopausal women, our results could be rapidly translated into clinical trials focused on treating or preventing fear-based disorders. Thus, these findings support the role of Tac2/NkB/Nk3R in fear memory consolidation and emphasize the importance of considering sex differences in the neurobiology of memory-related processes.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149879"},"PeriodicalIF":2.6,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144842650","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":"Corrigendum to “Adenosine ameliorated Aβ25−35-induced brain injury through the inhibition of apoptosis and oxidative stress via an ERα pathway” [Brain Res. 1788 (2022) 147944]","authors":"Mengnan Zeng ,&nbsp;Aozi Feng ,&nbsp;Chenxin Zhao ,&nbsp;Beibei Zhang ,&nbsp;Pengli Guo ,&nbsp;Meng Li ,&nbsp;Qinqin Zhang ,&nbsp;Yuhan Zhang ,&nbsp;Ruyi Fan ,&nbsp;Jun Lyu ,&nbsp;Xiaoke Zheng","doi":"10.1016/j.brainres.2025.149875","DOIUrl":"10.1016/j.brainres.2025.149875","url":null,"abstract":"","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1864 ","pages":"Article 149875"},"PeriodicalIF":2.6,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833948","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":"Single-cell transcriptome analysis reveals dysregulation of microglial iron homeostasis in temporal lobe epilepsy","authors":"Zihua He ,&nbsp;Shengyi Liu ,&nbsp;Wenyan Shi,&nbsp;Yi Yang,&nbsp;Jierui Wang,&nbsp;Jiaqi Wang,&nbsp;Jianqiong Yin,&nbsp;Sisi Shen,&nbsp;Dong Zhou,&nbsp;Jinmei Li","doi":"10.1016/j.brainres.2025.149885","DOIUrl":"10.1016/j.brainres.2025.149885","url":null,"abstract":"<div><div>Temporal lobe epilepsy (TLE) is the most common and drug-resistant type of epilepsy with an unknown mechanism. Abnormal accumulation of iron and lipid peroxides in the brain of TLE patients has been demonstrated. In this study, we investigated the role of microglia in iron metabolism and neuroinflammation by systematically analyzing single-cell/single-nucleus RNA sequencing data from TLE patients. Our results showed that cells associated with TLE phenotype were significantly increased in the ferroptosis gene set score and positive expression of ACSL4 and 4-HNE was observed by immunohistochemistry in brain tissues of TLE patients. Compared to the control group, microglia in the TLE group exhibited heightened metabolic activity in iron accumulation, ferritin synthesis, and oxidative damage, manifesting an inflammation-related phenotype and secreting multiple inflammatory factors. Furthermore, we discovered a unique microglial phenotype characterized by iron accumulation and neuroinflammation, resembling microglia associated with Alzheimer’s disease. The abundance of these microglial cells showed significant differences between TLE patients with high and low seizure frequencies and correlated positively with seizure frequency. Gene regulatory network analysis further revealed an enrichment of inflammation and oxidative stress-related transcription factors in these cells. Additionally, we identified a TLE-related gene co-expression module whose transcriptional characterization highly correlate with these distinct microglia. Multiplex immunohistochemistry validated the expression of these cellular marker genes in brain tissues of TLE patients. In summary, these findings underscore the critical role of microglial dysregulation in iron metabolism and neuroinflammation in the pathogenesis of TLE. By identifying a specific microglial phenotype, our research suggests a potential target for developing new therapeutic strategies for TLE.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149885"},"PeriodicalIF":2.6,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144828524","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":"Mitochondrial health and redox imbalance in the context of learning and memory in post-subarachnoid haemorrhage: therapeutic strategies for recovery","authors":"Ahmed Shaney Rehman ,&nbsp;Ammar Tasleem ,&nbsp;Prachi Tiwari ,&nbsp;Shaheenkousar H. Hattiwale ,&nbsp;Azfar Jamal ,&nbsp;Suhel Parvez","doi":"10.1016/j.brainres.2025.149881","DOIUrl":"10.1016/j.brainres.2025.149881","url":null,"abstract":"<div><div>Subarachnoid hemorrhage constitutes 5–10% of all strokes and is a subtype of hemorrhagic stroke that imposes a significant financial burden on medical care because it often affects younger people and has a high mortality rate with few treatment choices and poor patient outcomes. Preventing rebleeding, treating SAH patients as soon as possible, and preventing delayed cerebral ischemia (DCI) are important objectives during early brain injury (EBI) or first 72 hrs. Cerebral vasospasm and DCI continue to be issues despite surgical advances, particularly in older patients. A delayed diagnosis can result in DCI, which is linked to redox imbalance or oxidative stress (O.S) that causes learning-memory deficit, inflammation, apoptosis, mitophagy, disruption to the blood–brain barrier, and other detrimental processes that exacerbate these disorders. Individuals over 50 are susceptible to SAH, and as we age, our body’s excessive oxidative stress increases our risk of hemorrhagic stroke. This review highlights innovative approaches that target mitochondria for the treatment of SAH and emphasizes their role in learning, memory, EBI and DCI post-SAH, as well as their therapeutic potential.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149881"},"PeriodicalIF":2.6,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144844393","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":"TDP-43 mediated oxidative stress induced mitochondrial dysfunction in neurons and hyperalgesia in sciatic nerve injured mice","authors":"Li Li ,&nbsp;Penghui Huang ,&nbsp;Dan Zhu ,&nbsp;Yaohua Chen ,&nbsp;Yuping Li ,&nbsp;Bangbi Weng ,&nbsp;Xue Bai ,&nbsp;Jian Cui","doi":"10.1016/j.brainres.2025.149883","DOIUrl":"10.1016/j.brainres.2025.149883","url":null,"abstract":"<div><div>Neuropathic pain (NP) is a chronic pain with a highly complex pathogenesis, in which oxidative stress and mitochondrial dysfunction play significant roles in its progression, but its underlying mechanism is still unclear. TAR DNA-binding protein 43 (TDP-43) is one of the DNA-binding protein contributing to the homeostasis of mitochondria. This study is to explore the role of TDP-43 in mitochondrial dysfunction and pain formation in a mouse model. Therefore, in the mouse sciatic nerve chronic constriction injury (CCI) model and the H₂O₂-induced oxidative stress damage model in N2a cells, we examined the expression of TDP-43, and assessed whether inhibiting TDP-43 alleviated oxidative stress induced mitochondrial dysfunction. Additionally, we examined whether knockdown of TDP-43 could alleviate nociceptive behavior in CCI mice. Our results revealed a time-dependent upregulation of TDP-43 expression in the lumbar spinal dorsal horn neurons of CCI mice. In both in vivo and in vitro experiments, inhibiting TDP-43 attenuates oxidative stress-induced alterations in mitochondrial membrane potential (ΔΨm) and optic atrophy 1 (opa1) expression—a key regulator of mitochondrial fission. Furthermore, intrathecal injection of siRNA to knock down TDP-43 alleviated hyperalgesia and allodynia in CCI mice. These data indicate that TDP-43 in spinal neurons may contribute to NP by impairing mitochondrial function induced by oxidative stress, which may provide a new potential target for the treatment of NP.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149883"},"PeriodicalIF":2.6,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826930","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":"In vivo imaging of dorsal root ganglia in the mouse: from ex vivo MR-microscopy towards quantitative in vivo MRI","authors":"F. Hessenauer ,&nbsp;A.C. Nauroth-Kreß ,&nbsp;M. Spitzel ,&nbsp;S. Kemmerzell ,&nbsp;S. Weiner ,&nbsp;M. Schindehütte ,&nbsp;C. Sommer ,&nbsp;N. Üçeyler ,&nbsp;M. Pham ,&nbsp;T. Kampf","doi":"10.1016/j.brainres.2025.149872","DOIUrl":"10.1016/j.brainres.2025.149872","url":null,"abstract":"<div><div>Dorsal root ganglia (DRG) of the peripheral nervous system (PNS) transmit information from inside and outside the body to the central nervous system (CNS). The DRG’s unique multicellular unit of neurons, endothelial cells, satellite glial and immune cells undergoes remarkable changes after nerve injury and in neuropathic pain conditions and is a target for local and systemic pain therapies. DRG-magnetic resonance imaging (DRG-MRI) visualizes structural DRG injury in various neuropathic pain syndromes and has become a promising tool for detection and monitoring of DRG-pathology in humans. Here, we provide novel insights for murine DRG-MRI by applying MR-microscopy and high field MR-sequences optimized for DRG visualization and DRG-volumetry. We characterize murine DRG-volume (DRG_vol) as level specific for the lumbar levels L2 &lt; L3 &lt; L4 (p &lt; 0.001) and positively correlated to height (p &lt; 0.001), age (p &lt; 0.001) and weight (p &lt; 0.05) but independent of sex in a cohort of 24 wildtype mice. In a proof of principle experiment we report DRG-enlargement by up to 30 % in an α-galactosidase A deficient mouse model of Fabry disease (p &lt; 0.01). Finally, we demonstrate the DRG’s high microvascular perfusion compared to muscle and spinal cord in dynamic contrast enhanced MRI in a subcohort of six wildtype mice. DRG-MRI is a promising non-invasive imaging method, applicable not only to humans but also to rodent models, which are frequently utilized in pain research. The parallel use of DRG-MRI in humans and rodents can enhance comparability and translatability in preclinical and clinical pain research thoroughly.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149872"},"PeriodicalIF":2.6,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144815706","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":"Traumatic brain injury and neurodegenerative diseases: the role of axonal injury and amyloid-β","authors":"Dexi Bi ,&nbsp;Boying Gao ,&nbsp;Yanan Shen ,&nbsp;Zhibo Dai ,&nbsp;Shichun Yang ,&nbsp;Ligang Wang","doi":"10.1016/j.brainres.2025.149873","DOIUrl":"10.1016/j.brainres.2025.149873","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) often leads to neurodegenerative diseases (NDDs) such as Alzheimer’s disease (AD), imposing a substantial global disease burden. However, the underlying mechanistic link remains elusive. Recent research highlights the critical role of traumatic axonal injury (TAI) in TBI-induced Alzheimer’s disease. TAI disrupts axonal transport, leading to the pathological accumulation of proteins such as amyloid precursor protein (APP) and its cleavage product amyloid-beta (Aβ). These disruptions contribute to neurodegenerative processes in Alzheimer’s disease, including the formation of Aβ oligomers and plaques, which produce neurotoxicity. This review summarizes recent advancements in understanding these pathophysiological processes and underscores novel insights and methodologies for post-traumatic Alzheimer’s disease. The implications of these findings for future research and clinical significance are also discussed.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1865 ","pages":"Article 149873"},"PeriodicalIF":2.6,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144815707","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}