IBRO Neuroscience Reports最新文献

{"title":"Understanding the influence of digital technology on human cognitive functions: A narrative review","authors":"Eugénia Correia de Barros","doi":"10.1016/j.ibneur.2024.11.006","DOIUrl":"10.1016/j.ibneur.2024.11.006","url":null,"abstract":"<div><div>In the era of rapid digitalization, the widespread integration of digital technology into various aspects of daily life has sparked significant interest in understanding its impact on cognitive mental processes. While the emerging data suggests that its influence may be positive or negative, the depth of evidence regarding neurobiological mechanisms remains limited. This review aims to synthesize previously published studies and develop a comprehensive framework that systematically categorizes digital technologies, the cognitive functions they impact, and developmental stages around the concept of neuroplasticity, while clearly illustrating their interconnections. Despite acknowledged limitations, through an exhaustive approach, this paper intends to offer a dynamic perspective on the effects of digital media on the human brain, before the onset of addiction.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 415-422"},"PeriodicalIF":2.0,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142662841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neonatal maternal separation impairs cognitive function and synaptic plasticity in adult male CD-1 mice","authors":"Zhen-Yu Hu ,&nbsp;Ru-Meng Wei ,&nbsp;Fei-Hu ,&nbsp;Ke Yu ,&nbsp;Shi-Kun Fang ,&nbsp;Xue-Yan Li ,&nbsp;Yue-Ming Zhang ,&nbsp;Gui-Hai Chen","doi":"10.1016/j.ibneur.2024.11.001","DOIUrl":"10.1016/j.ibneur.2024.11.001","url":null,"abstract":"<div><div>Maternal separation (MS) increases the risk of occurrence of anxiety, depression, and learning and memory impairment in offspring. However, the underlying molecular biological mechanisms remain unclear. In the current study, offspring CD-1 mice were separated from their mothers from postnatal day 4 to postnatal day 21. At 3 months of age, the male offspring were selected for the evaluation of anxiety- and depression-like behaviors and learning and memory function. Western blotting and RT-PCR were used to examine the expression levels of brain-derived neurotrophic factor, tyrosine kinase receptor B, postsynaptic density-95, and synaptophysin. Long-term potentiation (LTP) and long-term depression (LTD) were recorded at Schaffer collateral/CA1 synapses. Furthermore, basal synaptic transmission was evaluated via the recording of the frequency and amplitude of miniature excitatory postsynaptic currents (mEPSCs). The results showed that adult offspring CD-1 mice displayed anxiety- and depressive-like behaviors as well as impaired spatial learning and memory abilities. Electrophysiological analysis indicated that MS impaired LTP, enhanced LTD, and reduced the frequency of mEPSCs in pyramidal neurons in the CA1 region. Our findings suggested that MS can lead to anxiety, depression, and cognitive deficits, and these effects are associated with alterations in the levels of synaptic plasticity-associated proteins, consequently, also synaptic plasticity.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 431-440"},"PeriodicalIF":2.0,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700755","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valproic acid attenuates the severity of astrogliosis in the hippocampus of animal models of temporal lobe epilepsy","authors":"Hu Feng,&nbsp;Jiamin Luo,&nbsp;Zhiwei Li,&nbsp;Yuxiao Zhao,&nbsp;Yamei Liu,&nbsp;Hongyan Zhu","doi":"10.1016/j.ibneur.2024.11.003","DOIUrl":"10.1016/j.ibneur.2024.11.003","url":null,"abstract":"<div><div>Reactive astrogliosis is one of the most frequency neuropathological alterations in the hippocampus of animal models and patients with temporal lobe epilepsy (TLE). Valproic acid (VPA), a widely used antiepileptic drug (AED), acts by blocking ion channels and enhancing GABAergic activity. This study investigated the effects of VPA on hippocampal astrogliosis in a rat model of TLE. The results demonstrated that chronic administration of VPA at a dose of 200 mg/kg significantly reduced the severity of astrogliosis and ameliorated neuronal loss in the hippocampus at the early and middle stages post-status epilepticus (SE), while also improving cognitive impairments at the middle and late stages in KA-SE rats. Long-term administration of VPA at 400 mg/kg attenuated astrogliosis in the hippocampus at the middle stage post-SE, but lacked neuroprotective effects and exacerbated cognitive impairments at the late stage. These findings suggest that VPA at an appropriate dose could mitigate hippocampal astrogliosis, potentially offering a new antiepileptic mechanism for its long-term use.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 471-479"},"PeriodicalIF":2.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142721417","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the potential of probiotics in Alzheimer's disease and gut dysbiosis","authors":"Sowmiya S ,&nbsp;Dhivya L.S. ,&nbsp;Praveen Rajendran ,&nbsp;Harikrishnan N ,&nbsp;Ankul Singh S","doi":"10.1016/j.ibneur.2024.11.004","DOIUrl":"10.1016/j.ibneur.2024.11.004","url":null,"abstract":"<div><div>Alzheimer's disease is a fatal neurodegenerative disorder that causes memory loss and cognitive decline in older people. There is increasing evidence suggesting that gut microbiota alteration is a cause of Alzheimer’s disease pathogenesis. This review explores the link between gut dysbiosis and the development of Alzheimer's disease contributing to neuroinflammation, amyloid β accumulation, and cognitive decline. We examine the recent studies that illustrate the gut-brain axis (GBA) as a bidirectional communication between the gut and brain and how its alteration can influence neurological health. Furthermore, we discuss the potential of probiotic supplementation as a management approach to restore gut microbiota balance, and ultimately improve cognitive function in AD patients. Based on current research findings, this review aims to provide insights into the promising role of probiotics in Alzheimer's disease management and the need for further investigation into microbiota-targeted interventions.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 441-455"},"PeriodicalIF":2.0,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142700756","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperphosphorylated tau targeting human serum albumin Fusion protein as therapeutics for Alzheimer’s diseases","authors":"Sookhee Bang,&nbsp;Jeong Kuen Song,&nbsp;Kwan Hee Lee","doi":"10.1016/j.ibneur.2024.11.005","DOIUrl":"10.1016/j.ibneur.2024.11.005","url":null,"abstract":"<div><h3>Introduction</h3><div>Neurofibrillary tangles (NFTs) are composed of hyperphosphorylated forms of microtubule-associated protein tau (Tau), which is responsible for neurodegeneration in Alzheimer’s disease (AD). The hippocampal region has been a major focus of AD research because the deposits of phosphorylated tau protein in these regions are correlated with early memory deficits. Despite extensive studies, therapeutic strategies to reduce tau hyperphosphorylation and NFTs deposition remain unclear. AL04, a recently developed recombinant fusion protein comprising Cystatin C, human serum albumin, and a novel blood brain barrier (BBB) penetrating peptide, is currently under investigation. Previous studies have demonstrated its effectiveness in reducing amyloid beta plaques in AD mouse model.</div></div><div><h3>Methods</h3><div>In this study, we investigated the effects of AL04 on lowering hyperphosphorylated tau and NFTs in JNPL3 mouse model harboring human tau-P301L mutation. 3-month-old female mice intraperitoneally received AL04 (5 mg/kg) or PBS treatment every other week for 24 weeks. We used confocal microscopy and western blot to visualize and analyze changes in hyperphosphorylated tau Ser202/Thr205 labeled with AT8 antibody in the brain.</div></div><div><h3>Results</h3><div>We found that the AL04 treatment decreases hyperphosphorylated tau at PP2A-sensitive epitope Ser202/Thr205 in the hippocampus of the brain. In the brain lysates of AL04 treated mice, we observed the reduction of I2PP2A, inhibitor of PP2A, and the induction of autophagy receptor proteins such as SQSTM-1/p62 and OPTN.</div></div><div><h3>Conclusion</h3><div>Our data suggests that AL04 can be used as an AD prophylactic/therapeutic agent as it lowers the hyperphosphorylated tau by downregulating I2PP2A. We also propose that AL04 can induce the degradation of hyperphosphorylated tau aggregates through the upregulation of the autophagy pathway.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 423-430"},"PeriodicalIF":2.0,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142662835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repetitive transcranial magnetic stimulation as add-on the rapyin persistent postural-perceptual dizziness","authors":"Yao Jia ,&nbsp;Hongbin Wang ,&nbsp;Dan Li ,&nbsp;Xingli Wu ,&nbsp;Jiawen Yang ,&nbsp;Weifei Min ,&nbsp;Ting Ma ,&nbsp;He Huang ,&nbsp;Rui Li","doi":"10.1016/j.ibneur.2024.10.005","DOIUrl":"10.1016/j.ibneur.2024.10.005","url":null,"abstract":"<div><h3>Background</h3><div>This study aims to evaluate the clinical effectiveness of repetitive transcranial magnetic stimulation (rTMS) when used as an add-on therapy for individuals with persistent postural-perceptual dizziness (PPPD).</div></div><div><h3>Methods</h3><div>In this randomized controlled, double-blind trial conducted at Shangluo Central Hospital, patients with PPPD diagnosed in the neurology departments were included. Participants were randomized into a rTMS treatment group and a control group in a 1:1 ratio by the randomized grouping method. Patients in both groups received conventional treatment, with the rTMS treatment group underwent daily rTMS sessions, whereas the control group received sham rTMS treatments following the same schedule. The effectiveness of the treatments was primarily assessed using the Dizziness Handicap Inventory (DHI), Hamilton Anxiety Rating Scale (HAMA), and Hamilton Depression Rating Scale (HAMD), which measured symptoms of vertigo, anxiety, and depression at baseline, after two weeks, and at the end of four weeks.</div></div><div><h3>Findings</h3><div>Of the 46 participants recruited, 2 were excluded due to contraindications, 22 were randomly assigned to the rTMS treatment group, and 22 were assigned to the control group. Ultimately, 2 withdrew for personal reasons, and data from 42 participants were included in the outcome analysis. HAMA, HAMD and DHI scores were significantly lower in the rTMS treatment group than in the control group after 4 weeks of treatment (p&lt;0.05). A positive correlation was also observed between DHI scores and HAMA or HAMD scores.</div></div><div><h3>Conclusions</h3><div>This pilot study demonstrated that rTMS is a beneficial add-on therapy for patients with PPPD.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 382-388"},"PeriodicalIF":2.0,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142578533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transgenerational of Oxidative Damage Induced by Prenatal Ethanol Exposure on Spatial Learning/Memory and BDNF in the of Male Rats","authors":"Mousa Shaabani Ghahremanlo,&nbsp;Vida Hojati ,&nbsp;Gholamhassan Vaezi,&nbsp;Shahram Sharafi","doi":"10.1016/j.ibneur.2024.09.001","DOIUrl":"10.1016/j.ibneur.2024.09.001","url":null,"abstract":"<div><div>Alcohol consumption during pregnancy harms fetal development, leading to various physical and behavioral issues. This study investigates how prenatal ethanol exposure triggers oxidative stress (OS) and affects neurotrophic factors (NTFs), particularly brain-derived growth factor (BDNF) gene expression in the hippocampus, influencing learning and memory decline across two generations of male offspring from ethanol-exposed female rats. A rat model of fetal alcohol spectrum disorder (FASD) was initially generated to reflect on the deficits in the first generation, and then those transmitted via the male germline to the unexposed male ones. The pregnant rats were thus divided into four groups, namely, the control group (CTRL) receiving only distilled water (DW), and three groups being exposed to ethanol (20 %, 4.5 g/kg) by oral gavage, during the first 10-day gestation (FG), the second 10-day gestation (SG), and the entire gestation (EG) periods. Subsequent Morris water maze (MWM) tests on male offspring revealed spatial learning deficits during the second and entire gestational periods in both generations. Analysis of antioxidant enzyme activity including glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA), and BDNF gene expression in the hippocampus further highlighted the impacts of prenatal ethanol exposure. The study results demonstrated that prenatal ethanol exposure caused spatial learning/memory deficits during the SG and EG, altered antioxidant enzyme activity, and reduced BDNF gene expression in both generations. The findings underscore the role of OS in developmental and behavioral issues in FASD rat models and suggest that lasting transgenerational effects in the second generation may stem from alcohol-induced changes.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 398-406"},"PeriodicalIF":2.0,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142662839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preclinical evidence for the anxiolytic- and antidepressant-like effects of citicoline and imipramine in the sciatic nerve-ligated mice","authors":"Mohammad-Reza Zarrindast ,&nbsp;Bardia Hajikarimloo ,&nbsp;Nastaran Raissi-Dehkordi ,&nbsp;Negar Raissi-Dehkordi ,&nbsp;Fatemeh Khakpai","doi":"10.1016/j.ibneur.2024.10.007","DOIUrl":"10.1016/j.ibneur.2024.10.007","url":null,"abstract":"<div><h3>Background</h3><div>Neuropathic pain is a usual condition followed by nerve injury. Experimental neuropathy is linked with delayed behavioral variations correlated to anxiety and depression behaviors. Imipramine is a tricyclic antidepressant that can diminish anxiety- and depressive-like behaviors. Also, citicoline as a dietary supplement has antidepressant and anxiolytic effects.</div></div><div><h3>Methods</h3><div>We sought to investigate citicoline's effect on anxiety-like (by elevated plus-maze (EPM)) and depression-like (by tail suspension test (TST)) responses as well as its potential to increase imipramine antidepressant properties in nerve-ligated mice.</div></div><div><h3>Results</h3><div>The results showed that induction of neuropathic pain through sciatic nerve ligation caused anxious- and depressant-like behaviors in male mice. On the other hand, intraperitoneal (i.p.) injections of moderate (50 mg/kg) and high (100 mg/kg) doses of citicoline and high dose of imipramine (5 mg/kg) significantly reduced anxiety- and depression-like behaviors induced by sciatic nerve ligation in male mice. Additionally, a low (25 mg/kg) dose of citicoline potentiated the anxiolytic- and antidepressant-like effects of different doses of imipramine when they co-injected in nerve-ligated mice. Isobolographic analysis indicated an additive effect of imipramine and citicoline on the occurrence of anxiolytic- and antidepressant-like behaviors in nerve-ligated mice. Our results showed that citicoline alone reduces anxiety- and depression-like behaviors. Furthermore, when co-administered with imipramine, citicoline potentiates imipramine effects.</div></div><div><h3>Conclusions</h3><div>Injection of citicoline (as a dietary supplement) along with imipramine improved the effectiveness of imipramine for the management of anxiety- and depressive-like responses in nerve-ligated mice.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 364-371"},"PeriodicalIF":2.0,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142538188","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture alleviates paradoxical sleep deprivation-induced postoperative hyperalgesia via a7nAChR mediated BDNF/TrkB-KCC2 signaling pathway in the spinal cord","authors":"Yi-yang Cui (MMed) ,&nbsp;Zi-qing Xu (MMed) ,&nbsp;Xiao-yu Qin (MMed) ,&nbsp;Huai-jing Hou (MMed) ,&nbsp;Jie Zhang (MMed) ,&nbsp;Jian-jun Xue (MD)","doi":"10.1016/j.ibneur.2024.10.002","DOIUrl":"10.1016/j.ibneur.2024.10.002","url":null,"abstract":"<div><div>Perioperative Paradoxical sleep deprivation (PSD) is associated with postoperative hyperalgesia. However, the clinical therapeutic strategies for PSD-induced postoperative hyperalgesia are limited. Electroacupuncture (EA) has been used for attenuating many types of pain, including neuropathic pain and inflammatory pain, but its effect on PSD-induced postoperative hyperalgesia is still unclear, and its analgesia mechanism should be further explored. In this study, we designed to investigate the possible mechanism of PSD-induced postoperative hyperalgesia and the effect of EA on PSD-induced postoperative hyperalgesia, and whether the mechanism is related to the BDNF/TrkB signaling pathway mediated by α7nAChR in the spinal cord. The paw withdrawal thermal latency (PWTL) and paw withdrawal mechanical threshold (PWMT) of rats were used to detect PSD-induced hyperalgesia. The expression of α7nAChR, BDNF, TrkB and KCC2 in the spinal cord were evaluated by Western blot and immunofluorescence. The results showed that preoperative 24 h PSD significantly decreased the PWTL and PWMT. The expression of α7nAChR and KCC2 significantly downregulated in the spinal cord of PSD-induced postoperative hyperalgesia rats, the opposite was observed for BDNF and TrkB expression. Moreover, intrathecal injection of alpha-bungarotoxin (α-BGT), a selective antagonist for α7nAChR, not only aggravated the pain hypersensitivity, but also demonstrated a further decrease of α7nAChR and KCC2 expression and a further increase of BDNF and TrkB expression. EA stimulation increased the PWTL and PWMT values of PSD-induced postoperative hyperalgesia rats, significantly upregulated α7nAChR and KCC2 expression, and significantly downregulated BDNF and TrkB expression. Moreover, intrathecal injection of α-BGT suppressed the analgesic effect of EA, inhibited the enhancement of α7nAChR and KCC2 expression and the reduction of BDNF and TrkB expression induced by EA. In conclusion, our study indicated that 24 h PSD can cause postoperative hyperalgesia, and the mechanism may be related to the disorder of α7nAChR mediated BDNF/TrkB-KCC2 signaling pathway. EA can alleviate postoperative hyperalgesia induced by PSD, which may be related to its effect in activating α7nAChR, inhibiting the expression of BDNF/TrkB, and up-regulating the expression of KCC2 in the spinal cord.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 389-397"},"PeriodicalIF":2.0,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142578537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fasudil attenuates lipopolysaccharide-induced cognitive impairment in C57BL/6 mice through anti-oxidative and anti-inflammatory effects: Possible role of aquaporin-4","authors":"Sahra Jalalkamali ,&nbsp;Mohsen Ghahremani ,&nbsp;Vida Jashn ,&nbsp;Negin Sadat Lajevardi ,&nbsp;Sevda Mahdipoor Koloor ,&nbsp;Seyede Zohreh Jazaeri ,&nbsp;Javad Fahanik-babaei","doi":"10.1016/j.ibneur.2024.10.004","DOIUrl":"10.1016/j.ibneur.2024.10.004","url":null,"abstract":"<div><h3>Introduction</h3><div>Processes that generate systemic inflammation are strongly associated with neurodegenerative diseases. This study aimed to explore the potential anti-oxidative and anti-inflammatory effects of fasudil and its role in modulating aquaporin-4 (AQP-4) to improve cognitive impairment in a systemic inflammation model induced by lipopolysaccharide (LPS).</div></div><div><h3>Method</h3><div>fourty C57BL/6 mice were assigned to four groups, including sham, LPS, sham+fasudil, and LPS+fasudil). Intraperitoneal LPS was given (500 μg/kg/day) at hours 0, 24, 48, and 72, and fasudil (30 mg/kg) administered intraperitoneal injections 2 hours after LPS injection. The open field, Y-maze, and Novel object tasks was used to assess learning and memory. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α) in the hippocampus also measured as markers of oxidative stress and inflammation. Furthermore, the expression of AQP-4 measured in the intact and experimental groups.</div></div><div><h3>Results</h3><div>The results showed that Fasudil significantly improved memory and anxiety behavior induced by LPS in the open field maze, spatial recognition memory in the Y-maze, and performance in the novel object recognition task. It also mitigates hippocampal MDA and SOD levels. Additionally, fasudil ameliorated LPS-induced hippocampal levels of TNFα and IL-10 and increased hippocampal levels of AQP-4 expression in mice.</div></div><div><h3>Conclusion</h3><div>Our results suggest that fasudil in the LPS model of systemic inflammation could improve cognition by suppressing oxidative stress and inflammation and increasing AQP-4 protein expression. These findings highlighted the potential of fasudil as a neuroprotective agent. However, further research is required to fully understand its neuroprotective properties in the treatment of neurodegenerative disorders.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"17 ","pages":"Pages 372-381"},"PeriodicalIF":2.0,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142554544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}