IBRO Neuroscience Reports最新文献

{"title":"Brain functional reorganization in pediatric patients with spinal cord injury and the impact of motor imagery training on it: a preliminary study","authors":"Ling Wang ,&nbsp;Beining Yang ,&nbsp;Qunya Qi ,&nbsp;Haotian Xin ,&nbsp;Yu Wang ,&nbsp;Yulong Jia ,&nbsp;Qian Chen ,&nbsp;Weimin Zheng ,&nbsp;Xin Chen ,&nbsp;Tengfei Liang ,&nbsp;Chuchu Sun ,&nbsp;Jubao Du ,&nbsp;Baowei Li ,&nbsp;Jie Lu ,&nbsp;Nan Chen","doi":"10.1016/j.ibneur.2025.08.003","DOIUrl":"10.1016/j.ibneur.2025.08.003","url":null,"abstract":"<div><div>To study the brain functional alterations of children after spinal cord injury (SCI) and explore their changes after motor imagery training (MIT), revealing brain functional reorganizations in pediatric SCI and finding possible neural mechanisms of MIT. Thirty pediatric SCI patients and 30 age- and gender-matched healthy controls (HCs) were recruited. Brain resting-state functional MRI images of all subjects were obtained using a 3.0 Tesla MRI system. Subsequently, eight of the patients completed a 4-week MIT, and then functional MRI scans were conducted once again. Then two-sample t-tests were used to compare amplitude of low frequency (ALFF), fractional ALFF (fALFF), regional homogeneity (ReHo) between groups at baseline, and paired t-tests were used to investigate the changes in ALFF, fALFF and ReHo of patients before and after the treatment. Compared with HCs, the patients showed decreased ALFF and/or ReHo in bilateral postcentral gyrus (S1) and right orbitofrontal cortex, while increased ALFF and/or ReHo in the bilateral cerebellar lobules IV-VI, thalamus, left middle cingulate cortex (MCC), cerebellar Crus II, and right parahippocampal gyrus, caudate nucleus, middle temporal gyrus (MTG). Compared with those before MIT, the patients showed significantly increased ALFF in the right S1 after the treatment. These findings demonstrated brain functional reorganization in sensoriomotor, cognitive-emotional and auditory/language related regions, and MIT may promote the rehabilitation by reversing the functionally reorganized sensoriomotor areas, which may provide a possible mechanism for MIT.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 391-399"},"PeriodicalIF":2.9,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144826454","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Systemic administration of gold nanoparticles attenuates anxiety-related behaviors and enhances spatial learning performance in rats","authors":"Farideh Bahrami ,&nbsp;Sajjad Rahimzadeh ,&nbsp;Mahdi Mashhadi Akbar Boojar ,&nbsp;Ahad Baqeri ,&nbsp;Maryam Ghorbani ,&nbsp;Mehdi Saberi","doi":"10.1016/j.ibneur.2025.08.004","DOIUrl":"10.1016/j.ibneur.2025.08.004","url":null,"abstract":"<div><h3>Background</h3><div>Due to the unique characteristics of gold nanoparticles, including low toxicity, tissue compatibility, high surface-to-volume ratio, excellent stability, lack of immunogenicity, and the ability to cross the blood-brain barrier, gold nanoparticles can affect brain cells and impact neuronal functions. This study aimed to investigate the effect of gold nanoparticles (AuNPs) on rats' anxiety, memory, and learning ability.</div></div><div><h3>Method</h3><div>This study was conducted on 35 male Wistar rats that were obtained from the Animal Center of Baqiyatallah University. In order to measure the anxiety level of rats, an open field test and elevated maze were used. To measure the spatial learning of rats, the Barnes maze test was used. Also, to measure active avoidance behavior, the shuttle box was used. Data analysis was done using one-way ANOVA and P &lt; 0.05 was considered significant.</div></div><div><h3>Results</h3><div>The results of the study showed that gold nanoparticles with doses of 200 and 300 μg/ml had a significant effect on memory and learning, which was observed both in the Barnes maze and the shuttle box test. Also, gold nanoparticles with a dose of 100 μg/ml reduced the induced anxiety of the animal, which had a significant difference with the control group (P &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>The study revealed that gold nanoparticles can impact rats' anxiety, memory, and learning. This suggests gold nanoparticles could be a new therapy to help with anxiety and cognitive issues in rodents, with potential benefits for humans.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 409-416"},"PeriodicalIF":2.9,"publicationDate":"2025-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144841427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antidepressant effect of Crossopteryx febrifuga trunk bark aqueous extract on chronic stress-induced depression-related behaviors in male and female rats","authors":"Daniel Ndavoumta,&nbsp;Harquin Simplice Foyet,&nbsp;Guillaume Woumitna Camdi,&nbsp;Serge Hermann Defo Tchinda,&nbsp;Hervé Hervé Abaïssou Ngatanko,&nbsp;Roland Nhouma Rebe,&nbsp;Kalib Kodji,&nbsp;Dieudonné Abengue Weinkai,&nbsp;Elisabeth Ngo Bum","doi":"10.1016/j.ibneur.2025.07.014","DOIUrl":"10.1016/j.ibneur.2025.07.014","url":null,"abstract":"<div><div>Depression is a highly prevalent neuropsychiatric disorder globally, and its increasing incidence is thought to be mediated by the growing exposure to stressful life events and conditions. <em>Crossopteryx febrifuga</em> is widely used in traditional medicine to treat fever, pain, epilepsy, and depression. This study aimed at evaluating the antidepressant effect of <em>C. febrifuga</em> aqueous extract (CF) using the chronic physical restriction stress (CRS) model on male and female rats. Sixty Wistar rats were randomly divided into six groups of 10 rats each (5 males and 5 females per group) were used. CRS was used to induce depressive-like behavior in rats for a period of 21 days. Novelty-suppressed feeding test (NSFT) and the forced swimming test (FST) were used to delineate depressive behavior. Corticosterone, serotonin, dopamine, noradrenalin, MAO, BDNF, and cytokines (IL-1, IL-6, IL-10, TNF-α), as well as oxidative and nitrosative stress markers such as NO, MDA, SOD, GSH, and CAT expressions, were evaluated. Histological sections of hippocampi were achieved to verify structural changes in neural architecture. From the results, in the negative control group both in female and male, CRS induced an increment in the time taken to consume food associated with a decrement in the quantity of food consumed in NSFT, an increase in immobility time, and a decrease in climbing and swimming times in the FST. CF reversed these different parameters in both male and female rats compared to the negative control group. All CF doses also led to a decrease in corticosterone and MAO concentrations and an increase in serotonin, dopamine, and noradrenaline concentrations. CF decreased the concentration of MDA and NO, increased GSH concentration (only in females, with all extract doses), and SOD and CAT activity (only in females at 25 mg/kg). All CF doses also affected cytokine expression by decreasing IL-1, IL-6, and TNF-α concentrations, associated with an increase of IL-10 in female subjects only. CF protected hippocampal structures and amygdala in both males and females. After 21 days, CRS induced a depressed state in rats of the negative control group. However, CF shown and antidepressant effect both in female and male by reversed all these trends on corticosolaemia, thus modulating monoamine concentrations, oxidative status, and through anti-inflammatory and anti-acetylcholinesterase actions. These effects could be attributed to their polyphenols, flavonoids, saponins, and tannins-rich content.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 471-490"},"PeriodicalIF":2.9,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144864394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Watching live performances enhances subjective and physiological emotional responses compared to viewing the same performance on screen","authors":"Damien Gabriel ,&nbsp;Julie Devos ,&nbsp;Sandrine Chapuis ,&nbsp;Alexandre Comte ,&nbsp;Pierre-Edouard Billot","doi":"10.1016/j.ibneur.2025.08.002","DOIUrl":"10.1016/j.ibneur.2025.08.002","url":null,"abstract":"<div><div>Live performances are known to evoke stronger emotional and physiological responses compared to recorded versions. However, isolating the effect of the physical presence of performers from other environmental factors remains a challenge. This study investigates the specific emotional and physiological responses elicited by a live performance compared to its identical recorded version, projected in the same theater under controlled conditions. Twenty-seven participants (19 females, 8 males, aged 21–67) attended a 5-minute 30-second performance combining dance, singing, and guitar, presented either live or as a video projection. Both formats were viewed under identical spatial conditions, with the screen positioned where the live performance took place. The viewing order was counterbalanced. Participants all completed self-report questionnaires on emotional states before and after each version of the show. A subset of participants was equipped with EEG headsets, electrodermal activity sensors, and photoplethysmography devices. Self-reported data indicated significantly higher pleasure and wakefulness after the live performance compared to the recorded version, while both formats equally reduced anxiety levels. A significant correlation was found between participants' screen viewing habits and their emotional engagement, suggesting that frequent exposure to digital performances might dampen emotional sensitivity to live experiences. Physiological measures revealed distinct patterns: skin conductance response frequency increased significantly in the final segment of the live performance but not in the video condition, indicating higher emotional arousal. Heart rate increased with musical intensity in both conditions, while EEG data showed reduced arousal levels during the live performance, possibly reflecting deeper cognitive absorption. This study provides evidence that live performances elicit stronger emotional and physiological engagement compared to their recorded counterparts, even under identical viewing conditions. The findings highlight the unique impact of performer-audience interaction and suggest that digital media cannot fully replicate the emotional richness of live experiences. Future research should further explore the mechanisms underlying emotional transmission in virtual environments.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 381-390"},"PeriodicalIF":2.9,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144810055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of calcitriol in cerebral ischemia/reperfusion injury: In vivo and in silico insights into TLR4 and FGFR2 pathways","authors":"Fahimeh Ramshini ,&nbsp;Javad Amini Mahabadi ,&nbsp;Reza Bayat ,&nbsp;Sayyed Alireza Talaei ,&nbsp;Zeinab Vahidinia ,&nbsp;Hassan Hassani Bafrani","doi":"10.1016/j.ibneur.2025.06.018","DOIUrl":"10.1016/j.ibneur.2025.06.018","url":null,"abstract":"<div><h3>Background</h3><div>Cerebral ischemic injury remains a major cause of high mortality, with limited effective treatments available. Inflammatory responses play a critical role in the pathophysiology of cerebral ischemia/reperfusion (I/R) injury. Suppressing inflammation is a key strategy for mitigating cerebral I/R injury, making it a promising therapeutic target for stroke. Vitamin D supplementation has been revealed to exhibit anti-inflammatory and neuroprotective properties during I/R injury; however, the underlying protective mechanisms are not yet fully understood. This study aimed to investigate the effects of post-ischemic calcitriol treatment on ischemic stroke, focusing specifically on the TLR4/MyD88/NF-κB and FGFR2 signaling pathways</div></div><div><h3>Methods</h3><div>Male Wistar rats were divided into three main groups: sham, I/R+ Vehicle, and I/R+ Calcitriol. An experimental I/R model was created by occluding the middle cerebral artery (MCA) for 1 h, followed by a 72-h reperfusion period. Calcitriol (1 μg/kg) was administered intraperitoneally for three consecutive days post-stroke. Neurological deficit scores and infarct size were evaluated 72 h after MCAO. Gene expression levels of TLR4, MyD88, NF-κB, and FGFR2 in the brain cortex were measured using RT-PCR. Additionally, histopathological changes in the cortex were examined with Nissl staining. A molecular docking analysis was performed to investigate the interactions of calcitriol with TLR4 and FGFR2, providing insights into their binding affinities and potential functional implications.</div></div><div><h3>Results</h3><div>Our findings indicated that calcitriol treatment significantly enhanced neurological function (P &lt; 0.05) and reduced infarct volume (P &lt; 0.001) in cerebral I/R injury. Furthermore, calcitriol decreased the number of damaged neurons while markedly increasing the count of neurons with normal morphology (P &lt; 0.001). Consistent with the results from molecular docking showing that calcitriol antagonizes TLR4 and FGFR2, RT-PCR analysis also revealed that calcitriol significantly suppressed the upregulation of TLR4 (P &lt; 0.05), MyD88 (P &lt; 0.01), NF-κB (P &lt; 0.01), and FGFR2 (P &lt; 0.001) mRNA expression levels.</div></div><div><h3>Conclusion</h3><div>The results demonstrate that calcitriol treatment offers significant neuroprotective benefits following cerebral I/R injury. These protective effects may be mediated, at least in part, by the inhibition of inflammation through the TLR4/MyD88/NF-κB and FGFR2 signaling pathways. This study enhances our understanding of the molecular mechanisms involved in calcitriol's neuroprotective actions.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 345-353"},"PeriodicalIF":2.9,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144750471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"View-invariant object representation in anterior and posterior inferotemporal cortex: A machine learning approach","authors":"Jun-ya Okamura,&nbsp;Daisuke Fukano,&nbsp;Keisuke Murakami,&nbsp;Gang Wang","doi":"10.1016/j.ibneur.2025.07.010","DOIUrl":"10.1016/j.ibneur.2025.07.010","url":null,"abstract":"<div><div>Inferotemporal (IT) cortex is the final visual area in the ventral stream where object information is processed. Previous electrophysiological studies showed viewing angle tolerance of 30–60° of single IT cells to the objects experienced in discrimination at each of several viewing angles, and to the objects experienced in learning association of different views. IT is divided into anterior (cytoarchitectonic area TE) and posterior (TEO) parts. It was reported that single cells in area TE showed the viewing angle tolerance while those in area TEO did not. In the present study population activities were compared between cell populations in area TE and those in area TEO using machine learning algorithm. An object set consisted of four similar objects created by deforming a prototype object, and four views each separated by 30°. A population vector was created by aligning responses of the cells to each object image. A classifier was trained by support vector machine (SVM) to create a hyperplane that separated one object from the other three objects at the same viewing angles, and then tested by response vectors to the object images at different viewing angles. In area TE, dynamics of the performance evaluated by d’ showed viewing angle tolerance of 30–90° to the objects with prior experience in learning association of different views. In area TEO, populations of the cells showed the viewing angle tolerance of 30°. Significant increase of the d’ values in area TE in the late time period for the objects with prior experience in learning association of different views may suggest view-invariance is more represented in late time period than early time period. These results suggest that viewpoint invariance is expressed more strongly in the TE region, and expressed in part in the population of the TEO cells.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 323-331"},"PeriodicalIF":2.9,"publicationDate":"2025-07-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144721711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OPTN deficiency through CRISPR/Cas9 downregulates autophagy and mitophagy in a SOD1-G93A-expressing transgenic cell line","authors":"Di Wen ,&nbsp;Qiusheng Li ,&nbsp;Yuanyuan Li ,&nbsp;Wenyu Yan ,&nbsp;Yanyan Wang ,&nbsp;Yakun Liu","doi":"10.1016/j.ibneur.2025.07.011","DOIUrl":"10.1016/j.ibneur.2025.07.011","url":null,"abstract":"<div><div>Amyotrophic lateral sclerosis (ALS) is characterized by the loss of upper and lower motor neurons (MNs) and is the most common adult paralysis neurodegenerative disease. Dysregulated autophagy, which has been reported in the pathogenesis of familial ALS, has been found in superoxide dismutase 1 (SOD1) transgenic mice and cell lines. Optineurin (OPTN) is a signal regulator that coordinates many crucial cellular processes, including autophagy, mitophagy and aggrephagy. Recent studies have shown that <em>OPTN</em> gene mutations are correlated with ALS, glaucoma and Paget’s disease of the bone. Indeed, defects in autophagosome–lysosome fusion have been reported in patients with ALS-associated <em>OPTN</em> mutations. However, the exact function of <em>OPTN</em> in the pathology of ALS remains unknown. To determine the function of OPTN, we generated <em>OPTN</em>-knockdown cell lines from SOD1-G93A-expressing NSC34 cells with the clustered regularly interspaced short palindromic repeats/associated system 9 (CRISPR/Cas9) approach. In our research, we observed that the loss of OPTN resulted in the impairment of autophagy and mitophagy pathways. Moreover, the mitochondrial transmembrane potential was depolarized by LV-sgRNA-OPTN. On the basis of observations of live cells, the production of reactive oxygen species (ROS) was increased, the autophagic flux decreased, and the autophagic flux merged with that of mitochondria according to confocal live-cell imaging. A decreased LC3-II and an increased p62 levels indicated that autophagy pathway activation was decreased. The protein levels of VDAC1 and TBK1 decreased after OPTN knockdown, suggesting that mitophagy was blocked. Our results suggest that OPTN plays a pivotal role in regulating autophagy and mitophagy.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 307-316"},"PeriodicalIF":2.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144721709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beclin1-mediated vascular autophagy negatively regulates angiogenesis and secondary neural damage in the thalamus following cerebral cortical infarction","authors":"Mengzhi Liu ,&nbsp;Yuqian Chen ,&nbsp;Xinyan Fan ,&nbsp;Jinmin Gu ,&nbsp;Shihui Xing","doi":"10.1016/j.ibneur.2025.07.008","DOIUrl":"10.1016/j.ibneur.2025.07.008","url":null,"abstract":"<div><div>Focal cerebral infarction induces angiogenesis in the thalamus, which influences cognitive recovery. However, the mechanisms of angiogenesis in the thalamus remain unclear. This study was designed to investigate the potential role of Beclin1-mediated vascular autophagy in angiogenesis occurring in the thalamus after cerebral infarction. Cerebral infarction was induced by middle cerebral artery occlusion (MCAO). Cognitive function was evaluated using the Morris Water Maze. We assessed secondary neuronal damage, angiogenesis, Beclin1 expression and vascular autophagy in blood vessels of the ipsilateral thalamus. The functional effects of Beclin1 on vascular autophagy, angiogenesis and angiogenesis-related factors were determined using lentiviral-delivered siRNA. The results revealed significant angiogenesis in the ipsilateral thalamus at 7 days after MCAO, concurrent with elevated LC3-I to LC3-II conversion and increased Beclin1 expression in the ipsilateral thalamic vessels. Knockdown of Beclin1 markedly suppressed vascular autophagic activation and potentiated thalamic angiogenesis at the above time point. This enhanced angiogenesis correlated with significant reductions of neuronal loss and astrogliosis in the ipsilateral thalamus, alongside improved cognitive function. Furthermore, Beclin1 knockdown significantly increased the levels of angiopoietin-2 (ANG-2) and vascular endothelial growth factor (VEGF) in the ipsilateral thalamus after cerebral infarction. Collectively, these findings implicate that inhibition of Beclin1-mediated vascular autophagy enhances angiogenesis and mitigates secondary thalamic neuronal damage following cerebral infarction. This neuroprotective effect likely related to the restoration of ANG-2 and VEGF levels mediated by vascular autophagy in the thalamus.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 290-299"},"PeriodicalIF":2.0,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144680317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Reactive astrocyte-derived neurotoxicity is mitigated by vitronectin in traumatic brain injury mouse model","authors":"Minori Yamashita ,&nbsp;Nito Nakahira ,&nbsp;Kei Hashimoto ,&nbsp;Hirono Kobayashi ,&nbsp;Mari Nakashima ,&nbsp;Hiroko Ikeshima-Kataoka ,&nbsp;Yasunori Miyamoto","doi":"10.1016/j.ibneur.2025.07.009","DOIUrl":"10.1016/j.ibneur.2025.07.009","url":null,"abstract":"<div><div>Vitronectin (VN) is an extracellular matrix protein that contributes to brain injury repair by regulating the fibrinolytic system. VN interacts with glial cells to regulate cytokine production. However, it is unclear how VN affects glial dynamics to promote repair of brain injury in a mouse model of traumatic brain injury (TBI). Here, we examined the effect of VN on astrocyte dynamics and neuronal cell death in mouse cerebral cortices after stab wounds. First, we verified that <em>Vn</em>^<em>-/-</em> cortices with stab wound surgery showed severe neuronal cell death and astrocyte activation around the lesion. In addition, the concentration of complement C3 was increased in <em>Vn</em>^<em>-/-</em> cortices after the stab wound, which was co-localized with astrocytes, suggesting that VN regulates astrocyte-derived C3 secretion and attenuates neurodegeneration after TBI. To further examine this, we collected secretions from VN-treated primary astrocytes and added them to primary cortical neurons, and found that secretions from VN-treated astrocytes have low neurotoxicity. Because the secretion from VN-treated astrocytes contained high levels of C3, we treated primary cortical neurons with the secretion from astrocytes and an inhibitor of the complement pathway, CD59, and analyzed neuronal cell death; results showed that inhibition of the complement pathway attenuates astrocyte secretion-induced neuronal apoptosis. Our results indicate that VN exerts a neuroprotective function through the suppression of C3 secretion from astrocytes. Therefore, VN plays a role in mitigating neurodegeneration after TBI by suppressing complement C3 secretion from reactive astrocytes.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 300-306"},"PeriodicalIF":2.0,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144702577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tat-NR2B9c prevent cognitive dysfunction in mice modeling Alzheimer's Disease induced by Aβ1–42 via perturbing PSD-95 interactions with NR2B-subtype receptors","authors":"Yaqin Huang,&nbsp;Weiping Lei,&nbsp;Jiahong Shen,&nbsp;Jianliang Sun","doi":"10.1016/j.ibneur.2025.07.006","DOIUrl":"10.1016/j.ibneur.2025.07.006","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer’s Disease (AD) is one of common progressive and fatal neurodegenerative disorders,and its main clinical symptoms are progressive memory impairment and cognitive dysfunction. The Tat-NR2B9c, a peptide was known as postsynaptic density protein-95(PSD-95) inhibitors, has shown clinical efficacy as a neuroprotective effects in some diseases such as acute stroke and neuropathic pain.</div><div>The aim of the study is to clarify whether Tat-NR2B9c has the same neuroprotective effects in AD.</div></div><div><h3>Methods</h3><div>Studies were performed in mice modeling AD induced by Aβ_1–42. Animals were treated with drugs after modeling AD for 14 days,and the spatial learning and memory ability were assessed after drug treatment. Then, mice were euthanized for biochemical tests.</div></div><div><h3>Results</h3><div>The levels of PSD-95 and NR2B decreased,and the levels of N-methyl-d-aspartate receptor–postsynaptic density protein-95 interaction increased in hippocampus in AD mice. Tat-NR2B9c can improve spatial learning and memory ability in AD mice by perturbing PSD-95 interactions with NR2B-subtype but not inhibiting PSD-95 levels.</div></div><div><h3>Conclusion</h3><div>Tat-NR2B9c can prevent cognitive dysfunction in mice modeling AD induced by Aβ1–42 via perturbing PSD-95 interactions with NR2B-subtype receptors.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 317-322"},"PeriodicalIF":2.9,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144721710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}