Brain Research Bulletin最新文献

{"title":"Neuroimmune and neuroinflammation response for traumatic brain injury","authors":"","doi":"10.1016/j.brainresbull.2024.111066","DOIUrl":"10.1016/j.brainresbull.2024.111066","url":null,"abstract":"<div><p>Traumatic brain injury (TBI) is one of the major diseases leading to mortality and disability, causing a serious disease burden on individuals' ordinary lives as well as socioeconomics. In primary injury, neuroimmune and neuroinflammation are both responsible for the TBI. Besides, extensive and sustained injury induced by neuroimmune and neuroinflammation also prolongs the course and worsens prognosis of TBI. Therefore, this review aims to explore the role of neuroimmune, neuroinflammation and factors associated them in TBI as well as the therapies for TBI. Thus, we conducted by searching PubMed, Scopus, and Web of Science databases for articles published between 2010 and 2023. Keywords included “traumatic brain injury,” “neuroimmune response,” “neuroinflammation,” “astrocytes,” “microglia,” and “NLRP3.” Articles were selected based on relevance and quality of evidence. On this basis, we provide the cellular and molecular mechanisms of TBI-induced both neuroimmune and neuroinflammation response, as well as the different factors affecting them, are introduced based on physiology of TBI, which supply a clear overview in TBI-induced chain-reacting, for a better understanding of TBI and to offer more thoughts on the future therapies for TBI.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024002004/pdfft?md5=6d5111292395616611cec04b934b5fae&pid=1-s2.0-S0361923024002004-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142145254","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional role of lncRNA MEG3 on pyroptosis through interacting with EZH2 and YTHDC1 in postoperative cognitive dysfunction","authors":"","doi":"10.1016/j.brainresbull.2024.111060","DOIUrl":"10.1016/j.brainresbull.2024.111060","url":null,"abstract":"<div><h3>Background</h3><p>The molecular biology mechanisms underlying postoperative cognitive dysfunction (POCD) remain unclear, resulting in a lack of specific therapeutic targets and limited clinical treatment options. The NLRP3 pyroptotic pathway, induced by neuroinflammation, is known to promote the development of POCD. Research has shown that lncRNA MEG3 exacerbates cell pyroptosis in various neurological injuries, though the precise mechanism remains to be investigated.</p></div><div><h3>Methods</h3><p>In vitro and in vivo models of POCD were established through treatment with sevoflurane. Gene and protein expression were investigated using qRT-PCR, Western blot analysis, ELISA, and histological staining. Additionally, cell viability and injury were assessed through CCK-8 and LDH assays. Hippocampal-dependent memory and cognitive abilities were evaluated using the Morris Water Maze (MWM) test. Furthermore, the interactions between MEG3 and EZH2/YTHDC1 were validated through RNA immunoprecipitation (RIP) and chromatin immunoprecipitation (ChIP).</p></div><div><h3>Results</h3><p>Our findings reveal that sevoflurane significantly reduced MEG3 and pyroptosis-related proteins in mice. The overexpression of MEG3 protected mice against sevoflurane-induced cognitive dysfunction and reversed sevoflurane-induced pyroptosis in hippocampal neurons. MEG3 induced the downregulation of NLRP3 expression and reduced mRNA stability through its interaction with EZH2/YTHDC1.</p></div><div><h3>Conclusion</h3><p>In conclusion, our study elucidates that MEG3 inhibits the NLRP3 inflammasome and hippocampal neuron pyroptosis through the recruitment of EZH2/YTHDC1. These findings shed light on the underlying mechanism of MEG3 in the regulation of POCD and suggest that MEG3 could serve as a potential therapeutic target for the treatment of POCD.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001941/pdfft?md5=00893d330a46302d84dbf9086f3cbcd5&pid=1-s2.0-S0361923024001941-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142139370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transforming of scalp EEGs with different channel locations by REST for comparative study","authors":"","doi":"10.1016/j.brainresbull.2024.111064","DOIUrl":"10.1016/j.brainresbull.2024.111064","url":null,"abstract":"<div><h3>Objective</h3><p>The diversity of electrode placement systems brought the problem of channel location harmonization in large-scale electroencephalography (EEG) applications to the forefront. Therefore, our goal was to resolve this problem by introducing and assessing the reference electrode standardization technique (REST) to transform EEGs into a common electrode distribution with computational zero reference at infinity offline.</p></div><div><h3>Methods</h3><p>Simulation and eye-closed resting-state EEG datasets were used to investigate the performance of REST for EEG signals and power configurations.</p></div><div><h3>Results</h3><p>REST produced small errors (the root mean square error (RMSE): 0.2936–0.4583; absolute errors: 0.2343–0.3657) and high correlations (&gt;0.9) between the estimated signals and true ones. The comparison of configuration similarities in power among various electrode distributions revealed that REST induced infinity reference could maintain a perfect performance similar (&gt;0.9) to that of true one.</p></div><div><h3>Conclusion</h3><p>These results demonstrated that REST transformation could be adopted to resolve the channel location harmonization problem in large-scale EEG applications.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001989/pdfft?md5=a395fdf5306a8822a2d8f910c98c0736&pid=1-s2.0-S0361923024001989-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142131911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of Brucella abortus on glial activation and cell death in adult male rat's hippocampus","authors":"","doi":"10.1016/j.brainresbull.2024.111061","DOIUrl":"10.1016/j.brainresbull.2024.111061","url":null,"abstract":"<div><p>A zoonotic disease called brucellosis can cause flu-like symptoms and heart inflammation. The bacteria responsible for this disease can also enter the brain, causing a condition called neurobrucellosis that can result in long-term neurological problems. In this study, researchers aimed to determine the changes in the hippocampal cells of rats infected with <em>Brucella</em>. For the study, 24 adult male albino rats were inoculated with 1 × 10⁶ CFU <em>Brucella</em> abortus 544. The rats were then deeply anesthetized, and their hippocampus samples were taken for stereological, histological, and molecular studies. The results showed that the infected rats had increased microgliosis and astrogliosis. Furthermore, a high level of caspase-3 in their hippocampal tissue indicated their susceptibility to apoptosis. Additionally, there was a decrease in expression of Ki67, which further supported this. Sholl's analysis confirmed a significant failure in glial morphology. The study demonstrated that the pathogen has the ability to destroy the hippocampus and potentially affect its normal physiology. However, more research is needed to clarify various aspects of neurobrucellosis.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001953/pdfft?md5=5987f815429efb174109934b4001534f&pid=1-s2.0-S0361923024001953-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142119034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Motion sickness and visual impairment","authors":"","doi":"10.1016/j.brainresbull.2024.111063","DOIUrl":"10.1016/j.brainresbull.2024.111063","url":null,"abstract":"<div><p>Motion sickness (MS) is caused by exposure to unfamiliar movements. The theory is that MS is due to a conflict between information perceived by the vestibular, visual, and somatosensory systems. This study examines the role of vision in MS by comparing MS susceptibility among individuals with varying degrees of visual impairments to sighted individuals. We hypothesized that subjects with no perception of light would be less susceptible to MS than less impaired subjects, who would themselves be less susceptible than sighted subjects. To address these, the Motion Sickness Susceptibility Questionnaire (MSSQ¹) was administered to 340 subjects (170 visually impaired paired with 170 sighted subjects) to assess their susceptibility to various modes of transport under real conditions. Visually impaired subjects were divided into subgroups according to the presence (partially sighted) or absence (totally blind) of light perception, as well as the period of onset of impairment (congenital or acquired). Totally blind individuals are significantly less susceptible to MS than partially sighted (<em>p</em> = 0.001), and sighted (<em>p</em> &lt; 0.001) subjects, with no difference between partially sighted and sighted subjects (<em>p</em> = 0.526). Additionally, acquired totally blind subjects are less susceptible to MS than congenitally blind subjects (<em>p</em> = 0.038). Thus, despite a lower susceptibility totally blind subjects may still be susceptible to MS. The absence of vision reduces MS susceptibility but does not completely prevent it. This suggests that vision is more a mediator, than an essential condition for MS appearance.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001977/pdfft?md5=290f06b49d6da729abaa6ad7186829c6&pid=1-s2.0-S0361923024001977-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104607","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Valproate attenuates somatic hyperalgesia induced by orofacial inflammation combined with stress through inhibiting spinal IL-6 and STAT1 phosphorylation” [Brain Res. Bull. 208 (2024) 110889]","authors":"","doi":"10.1016/j.brainresbull.2024.111062","DOIUrl":"10.1016/j.brainresbull.2024.111062","url":null,"abstract":"","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001965/pdfft?md5=a1dd55a6807c5f210edbf9a28cc84b6a&pid=1-s2.0-S0361923024001965-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104594","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of the P38 MAPK/NLRP3 pathway mitigates cognitive dysfunction and mood alterations in aged mice after abdominal surgery plus sevoflurane","authors":"","doi":"10.1016/j.brainresbull.2024.111059","DOIUrl":"10.1016/j.brainresbull.2024.111059","url":null,"abstract":"<div><h3>Background</h3><p>Cognitive dysfunction, encompassing perioperative psychological distress and cognitive impairment, is a prevalent postoperative complication within the elderly population, and in severe cases, it may lead to dementia. Building upon our prior research that unveiled a connection between postoperative mood fluctuations and cognitive dysfunction with the phosphorylation of P38, this present investigation aims to delve deeper into the involvement of the P38 MAPK/NLRP3 pathway in perioperative neurocognitive disorders (PND) in an abdominal exploratory laparotomy (AEL) aged mice model.</p></div><div><h3>Methods</h3><p>C57BL/6 mice (male, 18-month-old) underwent AEL with 3 % anesthesia. Then, inhibitors targeting P38 MAPK (SB202190, 1 mg/kg) and GSK3β (TWS119, 10 mg/kg) were administered multiple times daily for 7 days post-surgery. The NLRP3-cKO AEL and WT AEL groups only underwent the AEL procedure. Behavioral assessments, including the open field test (OFT), novel object recognition (NOR), force swimming test (FST), and fear conditioning (FC), were initiated on postoperative day 14. Additionally, mice designated for neuroelectrophysiological monitoring had electrodes implanted on day 14 before surgery and underwent novel object recognition while their local field potential (LFP) was concurrently recorded on postoperative day 14. Lastly, after they were euthanasized, pathological analysis and western blot were performed.</p></div><div><h3>Results</h3><p>SB202190, TWS119, and astrocyte-conditional knockout NLRP3 all ameliorated the cognitive impairment behaviors induced by AEL in mice and increased mean theta power during novel location exploration. However, it is worth noting that SB202190 may exacerbate postoperative depressive and anxiety-like behaviors in mice, while TWS119 may induce impulsive behaviors.</p></div><div><h3>Conclusions</h3><p>Our study suggests that anesthesia and surgical procedures induce alterations in mood and cognition, which may be intricately linked to the P38 MAPK/NLRP3 pathway.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S036192302400193X/pdfft?md5=ab9cc7e202184d62ed659d342cfca863&pid=1-s2.0-S036192302400193X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing miR-155–5p alleviates hippocampal damage in kainic acid-induced epileptic rats via the Dusp14/MAPK pathway","authors":"","doi":"10.1016/j.brainresbull.2024.111057","DOIUrl":"10.1016/j.brainresbull.2024.111057","url":null,"abstract":"<div><p>Epilepsy with recurrent seizures is characterized by neuronal damage and glial proliferation induced by brain inflammation. Recurrent seizures can lead to changes in the microRNA (miRNA) spectrum, significantly influencing the inflammatory response of microglia. MiR-155–5p, as a pro-inflammatory miRNA, is increased in the epileptic brain. However, its specific role in acute seizures remains unknown. The study aimed to develop a new strategy for treating epilepsy by investigating how silencing of miR-155–5p initiated its anticonvulsive mechanism. The level of miR-155–5p was up-regulated in the hippocampus of epileptic immature rats induced by kainic acid (KA). The use of antago-miR-155–5p exerted significant beneficial effects on the seizure scores, brain discharges and cognition in immature rats following KA-induced epilepsy. Antago-miR-155–5p also inhibited neuron damage and microglial activation. Moreover, the silencing of miR-155–5p significantly inhibited the Dual-specificity phosphatase 14 (Dusp14)/ mitogen-activated protein kinase (MAPK) axis in vivo. MiR-155–5p interacted with dusp14 to regulate MAPK signaling way expression, verified by a dual-luciferase reporter assay. The results suggested that the silencing of miR-155–5p might reduce hippocampal damage in epileptic immature rats induced by KA via Dusp14/MAPK signaling way. This implied that miR-155–5p could serve as a therapeutic tool to prevent the development of epilepsy.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001916/pdfft?md5=ebcd914bab7c75ee564126a25262dd58&pid=1-s2.0-S0361923024001916-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal separation as early-life stress: Mechanisms of neuropsychiatric disorders and inspiration for neonatal care","authors":"","doi":"10.1016/j.brainresbull.2024.111058","DOIUrl":"10.1016/j.brainresbull.2024.111058","url":null,"abstract":"<div><p>The establishment of positive early parent–infant relationships provide essential nourishment and social stimulation for newborns. During the early stages of postnatal brain development, events such as synaptogenesis, neuronal maturation and glial differentiation occur in a highly coordinated manner. Maternal separation, as an early-life stress introducer, can disrupt the formation of parent–child bonds and exert long-term adverse effects throughout life. When offspring are exposed to maternal separation, the body regulates the stress of maternal separation through multiple mechanisms, including neuroinflammatory responses, neuroendocrinology, and neuronal electrical activity. In adulthood, early maternal separation has long-term effects, such as the induction of neuropsychiatric disorders such as anxiety, depression, and cognitive dysfunction. This review summarized the application of maternal separation models and the mechanisms of stress system response in neuropsychiatric disorders, serving as both a reminder and inspiration for approaches to improve neonatal care, “from bench to bedside”.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001928/pdfft?md5=6af1b7e0edf29981974b7741e45d6bd2&pid=1-s2.0-S0361923024001928-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142092244","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Balancing the mind: Toward a complete picture of the interplay between gut microbiota, inflammation and major depressive disorder","authors":"","doi":"10.1016/j.brainresbull.2024.111056","DOIUrl":"10.1016/j.brainresbull.2024.111056","url":null,"abstract":"<div><p>The intricate interplay existing between gut microbiota and homeostasis extends to the realm of the brain, where emerging research underscores the significant impact of the microbiota on mood regulation and overall neurological well-being and vice-versa, with inflammation playing a pivotal role in mediating these complex interactions. This comprehensive review explores the complex interplay between inflammation, alterations in gut microbiota, and their impact on major depressive disorder (MDD). It provides a cohesive framework for the puzzle pieces of this triad, emphasizing recent advancements in understanding the gut microbiota and inflammatory states' contribution to the depressive features. Two directions of communication between the gut and the brain in depression are discussed, with inflammation serving as a potential modulator. Therapeutic implications were discussed as well, drawing insights from interventional studies on the effects of probiotics on gut bacterial composition and depressive symptoms. Ultimately, this review will attempt to provide a complete and valuable framework for future research and therapeutic interventions in MDD.</p></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0361923024001904/pdfft?md5=adede8bb0ae58283e17b7762e4ca2b52&pid=1-s2.0-S0361923024001904-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142054968","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}