Brain Research Bulletin最新文献

{"title":"PLB2Tau mice are impaired in novel and temporal object recognition and show corresponding traits in brain MRI","authors":"Jacques Micheau ,&nbsp;Gwenaelle Catheline ,&nbsp;Elodie Barse ,&nbsp;Bassem Hiba ,&nbsp;Anne Marcilhac ,&nbsp;Michèle Allard ,&nbsp;Bettina Platt ,&nbsp;Gernot Riedel","doi":"10.1016/j.brainresbull.2024.111161","DOIUrl":"10.1016/j.brainresbull.2024.111161","url":null,"abstract":"<div><div>Recent clinical trials targeting tau protein aggregation have heightened interest in tau-based therapies for dementia. Success of such treatments depends crucially on translation from non-clinical animal models. Here, we present the age profile of the PLB2_Tau knock-in model of fronto-temporal dementia in terms of cognition, and by utilising a directly translatable magnetic resonance imaging approach. Separate cohorts of mice aged 3, 6 and 12 months were tested in an object recognition protocol interrogating visual, spatial, and temporal discrimination in consecutive tests. Upon completion of their behavioural testing, animals were recorded in a 7 T MRI for brain structural integrity and diffusion tensor imaging (DTI) analysis. We report that PLB2_Tau mice presented with an age-dependent deficit in novel object discrimination relative to wild-type controls at 6 and 12 months. Spatial and temporal discrimination, though not significantly different from controls, appeared extremely challenging for PLB2_Tau subjects, especially at 12 months, since they explored objects less than controls and were devoid of memory. Controls readily recalled all relevant object-related information. At the same time, the T2 weighted voxel-based image analysis revealed a progressive shrinkage of total brain volumes in 6- and 12-month-old PLB2_Tau mice as well as relative striatal, but not hippocampal volumes. A regional DTI analysis yielded only reduced mean diffusivity of the fimbria, but not CA1 or dentate gyrus, amygdala, cingulate cortex, or corpus callosum. These data confirm the PLB2_Tau mouse as a translationally useful model for dementia research and suggest the importance of the hippocampal input as a determinant for novel object discrimination.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111161"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142791447","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":"Role of BDNF-TrkB signaling in the improvement of motor function and neuroplasticity after ischemic stroke in rats by transcranial direct current stimulation","authors":"Yu Chen ,&nbsp;Lin Mao ,&nbsp;Qinxiang Zhou ,&nbsp;Dingqun Bai ,&nbsp;Yuhan Kong","doi":"10.1016/j.brainresbull.2024.111164","DOIUrl":"10.1016/j.brainresbull.2024.111164","url":null,"abstract":"<div><h3>Background</h3><div>Transcranial direct current stimulation (tDCS) has an impact on improving cognitive and motor dysfunction induced by ischemia-reperfusion injury. However, to use this technology more rationally in clinical practice, a deepened understanding of the molecular mechanisms behind its therapeutic effects is needed. This study explored the role of the brain-derived neurotrophic factor(BDNF) and its associated receptor tropomyosin-receptor kinase B(TrkB) while deciphering the underlying mechanisms in transcranial direct current therapy to treat ischemic stroke.</div></div><div><h3>Methods</h3><div>A middle cerebral artery occlusion-reperfusion(MCAO/R) model was established in rats to observe tDCS effects on brain damage. Behavioral tests, the modified neurologic severity score(mNSS), and the Hoffman reflex / the M wave(H_max/M_max) ratio helped assess motor function and neurologic deficits. HE and Nissl staining helped observe the morphological changes and count of nerve cells. We tested the expression of growth-associated protein-43(Gap-43) and microtubule-associated protein-2(Map-2), K⁺-Cl^- co-transporter 2(KCC2), γ-aminobutyric acid(GABA), and key BDNF-TrkB downstream signaling, the phospholipase C gamma(PLCγ) / CaMK IV / cAMP response element binding protein(CREB), and extracellular signal-regulated protein kinase(ERK1/2) / ribosomal S6 kinase(RSK) using western blotting. Moreover, BDNF was analyzed in plasma using the enzyme-linked immunosorbent assay (ELISA) to investigate the tDCS effect on human BDNF expression levels. Finally, a BDNF receptor antagonist, ANA-12, was administered to explore the tDCS mechanism mediating BDNF-TrkB signaling.</div></div><div><h3>Results</h3><div>After tDCS treatment, the mNSS was improved, and the motor function was restored. Moreover, tDCS decreased cell swelling after MCAO/R and enhanced the number of neurons. tDCS treatment increased: (1) BDNF, Gap-43, Map-2 expression, (2) KCC2, GABA, and (3) PLCγ, CaMK IV, CREB and ERK1/2, RSK. Furthermore, ELISA results indicate that tDCS elevated human plasma BDNF protein expression. However, the therapeutic effect of tDCS was suppressed to a certain extent by adding ANA-12.</div></div><div><h3>Conclusion</h3><div>Our findings indicate that tDCS may exert a neuroprotective effect by activating the downstream key molecules of BDNF-TrkB expression, for instance, PLCγ/ CaMK IV/ CREB and ERK/ RSK pathway. Moreover, tDCS can control neuronal excitability, promote axonal regeneration, and accelerate motor function recovery in ischemia reperfusion-injured rats.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111164"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142812192","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":"Knowledge mapping and emerging trends in cognitive impairment associated with chronic pain: A 2000–2024 bibliometric study","authors":"Li-yuan Zhao ,&nbsp;Guang-fen Zhang ,&nbsp;Jian-jun Yang ,&nbsp;Yu-gang Diao ,&nbsp;Kenji Hashimoto","doi":"10.1016/j.brainresbull.2024.111175","DOIUrl":"10.1016/j.brainresbull.2024.111175","url":null,"abstract":"<div><div>Chronic pain is commonly recognized as a distressing symptom or a standalone disease, with over half of those affected experiencing cognitive impairment, which significantly impacts their quality of life. Despite a recent surge in literature on cognitive impairment associated with chronic pain, a comprehensive bibliometric analysis in this field has yet to be conducted. In this study, we performed a bibliometric analysis on this topic. We retrieved English-language publications on chronic pain and cognitive impairment from 2000 to 2024 using the Web of Science Core Collection database. These publications were visually analyzed using tools such as VOSviewer, CiteSpace, and the R package “bibliometrix.” We identified 1656 publications from 72 countries/regions across 722 journals on the topic of chronic pain and cognitive impairment. Publication numbers showed a steady increase, peaking in 2022. The United States led in contributions, with Harvard Medical School emerging as the most prominent institution involved. The journal <em>Pain</em> was the most prolific and frequently co-cited in this area. Among the authors, Stefan Duschek was the most productive, while Frederick Wolfe was the most frequently co-cited. Key research areas include investigating the bidirectional long-term effects between chronic pain and cognitive impairment and exploring the mechanisms underlying cognitive changes associated with chronic pain. In conclusion, this study highlights a global surge in research on cognitive impairment related to chronic pain. Emerging hotspots and future research trends point towards brain imaging mechanisms and neuronal circuit-mediated processes.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111175"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871400","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":"Lipoxin A4 suppresses neutrophil extracellular traps formation through the FPR2-dependent regulation of METTL3 in ischemic stroke","authors":"Na Wei ,&nbsp;Tan Lu ,&nbsp;JianBang Gu ,&nbsp;Huan Cai","doi":"10.1016/j.brainresbull.2024.111178","DOIUrl":"10.1016/j.brainresbull.2024.111178","url":null,"abstract":"<div><h3>Background</h3><div>This study aimed to clarify whether the neuroprotective effect of LXA4 is associated with the targeting of neutrophil extracellular traps (NETs) in ischemic stroke (IS).</div></div><div><h3>Methods</h3><div>The MCAO rat model was established to assess cerebral infarction, brain water content and neurological deficits. ELISA was employed to examine the activities of MPO, NE, MMP-9. RT-qPCR and western blot was performed to analyze molecular expressions. A luciferase reporter assay was performed to measure the effect of EGR1 on the METTL3 promoter. The formation of NETs and cell viability were evaluated using immunofluorescence staining and CCK8 assay, respectively.</div></div><div><h3>Results</h3><div>LXA4 decreased cerebral infarction and brain water content, improved neurological deficits, and reduced the release of NETs-associated indicators (MPO, NE) in MCAO rats. LXA4 reduced NETs formation, MPO and NE levels <em>in vitro</em>. In addition, LXA4 reduced Fe^2 + levels while increasing GPX4, SLC7A11 protein expressions, as well as enhancing cell viability <em>in vitro</em>, suggesting the inhibitory effect of LXA4 on ferroptosis. Notably, METTL3 overexpression produced the opposite effects. Furthermore, the effects of METTL3 overexpression on NETs formation and ferroptosis were partially reversed by LXA4 treatment. The inhibition of METTL3 by LXA4 was found to be dependent on FPR2. <em>In vivo</em> experiments verified that LXA4 inhibited NETs formation through inhibition of METTL3 to alleviate brain injury.</div></div><div><h3>Conclusion</h3><div>This study demonstrates that LXA4 suppresses NETs formation through the FPR2-dependent regulation of METTL3, thereby alleviating brain injury in IS.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111178"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871401","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 \"Single high-frequency repetitive transcranial magnetic stimulation and intermittent theta pulse stimulation promote working memory behavior in participants: An event-related potential study\" [Brain Res. Bull. 220 (2025) 111147]","authors":"Longting Hu ,&nbsp;Jinyan He ,&nbsp;Menglin Han ,&nbsp;Zhiqiang Wang ,&nbsp;Yulan Gao ,&nbsp;Boyu Zhang ,&nbsp;Shuyan Zhou ,&nbsp;Shuning Li ,&nbsp;Xuan Wu ,&nbsp;Kangling Wang","doi":"10.1016/j.brainresbull.2024.111179","DOIUrl":"10.1016/j.brainresbull.2024.111179","url":null,"abstract":"","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111179"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892265","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":"USP22 inhibits microglial M1 polarization by regulating the PU.1/NLRP3 inflammasome pathway","authors":"Ming-chen Yu ,&nbsp;Xiao-lin Li ,&nbsp;Ming-liang Ning ,&nbsp;Zhen-zhong Yan ,&nbsp;Wan-tao Yu","doi":"10.1016/j.brainresbull.2024.111157","DOIUrl":"10.1016/j.brainresbull.2024.111157","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to investigate the effect of Ubiquitin-Specific Peptidase 22 (USP22) on the inflammatory response mediated by BV-2 mouse microglia and explore the role of the PU box binding protein 1 (PU.1)/NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome in the USP22-induced polarization of BV-2 cells.</div></div><div><h3>Methods</h3><div>The BV-2 mouse microglia line was cultured in vitro, and plasmid and siRNA transfection was performed to overexpress or knockdown USP22. Subsequently, BV-2 cells were treated with lipopolysaccharide (LPS) and interferon-gamma (IFN-γ) and interleukin (IL)-4 to induce M1 and M2 polarization, respectively. Western blot was used to detect the expression levels of USP22, PU.1, M1 polarization markers [inducible nitric oxide synthase (iNOS), and cluster of differentiation (CD) 86], M2 polarization markers [arginase 1 (Arg1), and CD206], in BV-2 cells from different treatment groups. Additionally, measurement was performed on the inflammasome NLRP3, and its activation-related proteins [NIMA-related kinase7 (NEK7), cleaved-caspase 1, apoptosis-associated speck-like protein containing a CARD (ASC)]. Enzyme-linked immunosorbent (ELISA) assay was employed to determine the levels of inflammatory cytokines tumor necrosis factor-alpha (TNF-α), IL-1 β, and IL-10 in the cells. Furthermore, immunofluorescence was utilized to analyze the levels of iNOS and Arg1-positive BV-2 cells in different treatment groups. Moreover, the ubiquitination level of PU.1 was detected using immunoprecipitation.</div></div><div><h3>Results</h3><div>The protein expression level of USP22 was significantly down-regulated in BV-2 cells treated with M1 polarization. Overexpression of USP22 remarkably reduced the protein levels of iNOS and CD86, but markedly increased the protein levels of Arg1 and CD206 in cells. Besides, there was a notable reduction in the levels of TNF-α and IL-1 β in the cell culture medium, while a remarkable increase was observed in the level of IL-10. Additionally, the level of iNOS-positive cells was significantly decreased, while the level of Arg1-positive cells was considerably increased. However, up-regulation of PU.1 expression could reverse the above results and promoted the expression of NLRP3 and its activation-related proteins. Notably, overexpression of USP22 significantly down-regulated the protein expression and ubiquitination level of PU.1.</div></div><div><h3>Conclusion</h3><div>USP22 inhibits the M1 polarization of BV-2 mouse microglia. The PU.1/NLRP3 inflammasome pathway may be a critical regulatory pathway of USP22 in BV-2 cell polarization.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111157"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142778983","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":"Voluntary running exercise promotes maturation differentiation and myelination of oligodendrocytes around Aβ plaques in the medial prefrontal cortex of APP/PS1 mice","authors":"Qing Pan ,&nbsp;Lin Jiang ,&nbsp;Yao Xiong ,&nbsp;Feng-lei Chao ,&nbsp;Shan Liu ,&nbsp;Shan-shan Zhang ,&nbsp;Lin Zhu ,&nbsp;Yan-min Luo ,&nbsp;Qian Xiao ,&nbsp;Jing Tang ,&nbsp;Xin Liang ,&nbsp;Yong Tang ,&nbsp;Chun-ni Zhou ,&nbsp;Lei Zhang","doi":"10.1016/j.brainresbull.2024.111170","DOIUrl":"10.1016/j.brainresbull.2024.111170","url":null,"abstract":"<div><h3>Background</h3><div>Previous studies have reported that running exercise could improves myelinization in hippocampus. However, the effects of running exercise on the differentiation and maturation of oligodendrocytes, and myelination surrounding Aβ plaques in the medial prefrontal cortex (mPFC) of the Alzheimer's disease (AD) brain have not been reported.</div></div><div><h3>Methods</h3><div>Forty 10-month-old male APP/PS1 AD mice were randomly divided into the AD group and the AD running (AD+RUN) group, while 20 age-matched wild-type littermate mice were included in the WT group. The running group received three-month voluntary running exercise in a running cage, while the AD and WT groups were untreated. After the exercise intervention, all mice were given behavioral tests. The total number of mature oligodendrocytes (CC1⁺) in the mPFC of mice was precisely quantified using unbiased stereology. Myelin basic protein (MBP) and Aβ plaque, as well as the fluorescence area of MBP surrounding Aβ plaques, and the density and morphology of PDGFα⁺ cells in the mPFC were analyzed using immunofluorescence.</div></div><div><h3>Results</h3><div>The levels of working memory, cognitive memory, spatial learning and memory ability were decreased significantly in the AD group compared to the WT group, while these functions were significantly improved in the AD+RUN group compared to the AD group. The Aβ plaques in the mPFC were significantly reduced in the AD+RUN group compared to the AD group. The total number of CC1⁺ cells and the percentage of MBP fluorescence area surrounding Aβ plaques in the mPFC were significantly lower in the AD group compared to the WT group, but they were significantly higher in the AD+RUN group compared to the AD group. The density and branching complexity of PDGFα⁺ cells surrounding Aβ plaques in the mPFC were significantly higher in the AD group than in the WT group, while the AD+RUN group showed significantly lower density and branching complexity than the AD group. Changes in MBP expression around Aβ plaques, cell density and cell branching complexity of PDGFα⁺ cells around Aβ plaques were closely related to the number of Aβ plaques in mPFC, and they were also closely related to behavioral changes in mice.</div></div><div><h3>Conclusions</h3><div>Voluntary running exercise could reduce Aβ plaque deposition and promote the maturation and myelination capacity of oligodendrocytes surrounding Aβ plaques in the mPFC of AD mice, thereby improving the learning and memory abilities of APP/PS1 transgenic AD mice.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111170"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827512","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":"Structure and dynamics analysis of brain functional hypernetworks based on the null models","authors":"Chen Cheng ,&nbsp;Yao Li ,&nbsp;Chunyan Wang ,&nbsp;Yanli Yang ,&nbsp;Hao Guo","doi":"10.1016/j.brainresbull.2024.111177","DOIUrl":"10.1016/j.brainresbull.2024.111177","url":null,"abstract":"<div><div>Brain functional hypernetworks that can characterize the complex and multivariate interactions among multiple brain regions have been widely used in the diagnosis and prediction of brain diseases. However, there are few studies on the structure and dynamics of brain functional hypernetworks. Such studies can help to explore how the important functional features of brain functional hypernetworks characterize the working and pathological mechanisms of the human brain. Therefore, this article introduces the hypernetwork null model to analyze the dependencies between the features of interest. Specifically, first, based on the original brain functional hypernetwork, this article proposed the optimized hyper dK-series algorithm with hyperedges to construct null models that preserved the different node attributes and hyperedge attributes of the original brain functional hypernetwork, respectively. Next, based on the original hypernetwork model and the null model, multiple node attributes and hyperedge attributes were respectively introduced. Then, the level of similarity and correlation between the topological attributes of the original brain functional hypernetwork and the topological attributes of the brain functional hypernetwork null model were calculated to analyze the dependencies between the features of interest. The results showed that there were differences in the level of dependence between the features of interest. Node degree is the main dependency attribute for multiple metrics. Hyperedge degree, node degree-dependent redundancy coefficient, and hyperedge degree-dependent redundancy coefficient are partial dependency attributes for some metrics. The dependency attributes and level of dependency are the same for the hypernetwork clustering coefficients—HCC² and HCC³. This indicates that the node degree is redundant with respect to other attributes, while the hyperedge degree, node degree-dependent redundancy coefficient, and hyperedge degree-dependent redundancy coefficient perhaps contain other topology information. In addition, there is redundancy between HCC² and HCC³. Therefore, the effects of these redundant attributes need to be considered when performing network analysis.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111177"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876266","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":"Preclinical evaluation on human platelet lysate for the treatment of secondary injury following intracerebral hemorrhage","authors":"Dachang Qiu ,&nbsp;Guangwei Li ,&nbsp;Xianchao Hu ,&nbsp;Lanlan Wang ,&nbsp;Yongfei Dong","doi":"10.1016/j.brainresbull.2024.111153","DOIUrl":"10.1016/j.brainresbull.2024.111153","url":null,"abstract":"<div><div>Intracerebral hemorrhage (ICH) is a condition with high mortality and disability. Secondary injury processes following ICH include neuroinflammation, oxidative stress, and neuronal apoptosis. Human platelet lysate (HPL), derived from crushed platelets, is rich in cytokines and has demonstrated therapeutic potential in neurological disorders in several studies. However, studies on HPL for ICH remain limited. In this study, we prepared HPL for intranasal administration in ICH treatment. We determined the concentration of growth factors in HPL, validated the targeting of HPL, and established a mouse model of ICH. We observed that HPL improved neuromotor deficits in ICH mice. Barnes maze training showed that HPL enhanced spatial memory and learning ability in mice. Furthermore, HPL reduced neuroinflammation, brain edema, oxidative stress, neuronal apoptosis, and neural axonal damage. Additionally, 5 % HPL demonstrated potent functional activity with no cytotoxicity in SH-5YSY cell cultures. These findings indicate that HPL is a promising therapeutic approach for mitigating secondary brain injury following ICH.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111153"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142766386","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":"Cognitive disorders: Potential astrocyte-based mechanism","authors":"Shiyu Li,&nbsp;Yeru Chen,&nbsp;Gang Chen","doi":"10.1016/j.brainresbull.2024.111181","DOIUrl":"10.1016/j.brainresbull.2024.111181","url":null,"abstract":"<div><div>Cognitive disorders are a common clinical manifestation, including a deterioration in the patient's memory ability, attention, executive power, language, and other functions. The contributing factors of cognitive disorders are numerous and diverse in nature, including organic diseases and other mental disorders. Neurodegenerative diseases are a common type of organic disease related to the pathology of neuronal death and disruption of glial cell balance, ultimately accompanied with cognitive impairment. Thus, cognitive disorder frequently serves as an extremely critical indicator of neurodegenerative disorders. Cognitive impairments negatively affect patients' daily lives. However, our understanding of the precise pathogenic pathways of cognitive defects remains incomplete. The most prevalent kind of glial cells in the central nervous system are called astrocytes. They have a unique significance in cerebral function because of their wide range of functions in maintaining homeostasis in the central nervous system, regulating synaptic plasticity, and so on. Dysfunction of astrocytes is intimately linked to cognitive disorders, and we are attempting to understand this phenomenon predominantly from those perspectives: neuroinflammation, astrocytic senescence, connexin, Ca2 + signaling, mitochondrial dysfunction, and the glymphatic system.</div></div>","PeriodicalId":9302,"journal":{"name":"Brain Research Bulletin","volume":"220 ","pages":"Article 111181"},"PeriodicalIF":3.5,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892263","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}