IBRO Neuroscience Reports最新文献

{"title":"Ginsenoside C-K inhibits Aβ oligomer-induced Alzheimer's disease pathology progression by regulating microglia-neuron interactions","authors":"Chenghu Xie ,&nbsp;Cunxin Zhang ,&nbsp;Kefeng Zhang ,&nbsp;Shanshan Zhang","doi":"10.1016/j.ibneur.2025.05.007","DOIUrl":"10.1016/j.ibneur.2025.05.007","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer’s disease is a progressive neurodegenerative disorder. Current therapeutic agents primarily focus on symptom alleviation and fail to effectively halt disease progression. Therefore, there is a need to develop novel therapeutic strategies, particularly those involving natural active compounds with multi-target actions.</div></div><div><h3>Objective</h3><div>To investigate the intervention effects and multi-target regulatory mechanisms of Ginsenoside C-K (GCK) on β-amyloid (Aβ) oligomer-induced Alzheimer's disease (AD) pathological progression.</div></div><div><h3>Methods</h3><div>BV2 microglia and HT22 neurons were used as in vitro models. Cell viability was measured via CCK-8 assay, cell migration ability assessed by scratch assay, and apoptosis rate analyzed using Annexin V/PI dual staining. A conditioned medium (CM) strategy was employed to validate microglia-neuron interactions. Western blot was performed to detect key NF-κB signaling pathway proteins (p-IκBα, p-p65) and inflammatory cytokines (TNF-α, IL-1β).</div></div><div><h3>Results</h3><div>GCK pretreatment significantly ameliorated Aβ₁₋₄₂ oligomer-induced BV2 cell dysfunction (viability recovery rate &gt;80 %, p &lt; 0.01), suppressed pro-inflammatory cytokine secretion (TNF-α reduced by 62.3 %, IL-1β by 57.8 %), and inhibited NF-κB pathway activation (p-IκBα/p-p65 expression downregulated &gt;50 %). In HT22 neurons, GCK directly counteracted Aβ toxicity (apoptosis rate decreased from 38.7 % to 15.2 %) and exerted indirect neuroprotection by modulating microglia-derived conditioned medium (CM2 group showed a 2.1-fold increase in neuronal viability compared to CM1).</div></div><div><h3>Conclusion</h3><div>GCK mitigates AD pathology through dual mechanisms-direct inhibition of Aβ neurotoxicity and indirect regulation of microglial homeostasis-with NF-κB signaling suppression as a core mechanism. This study provides new experimental evidence for natural product-based multi-target AD therapies, though further animal studies are required to validate its in vivo efficacy and safety.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 783-793"},"PeriodicalIF":2.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147189","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":"A study on structural imaging changes and serum neurofilament light chain (NfL) levels in individuals with white matter hyperintensities, combining imaging techniques with biomarker analysis","authors":"Meini Wu ,&nbsp;Zihao Li ,&nbsp;Yuhang Ren ,&nbsp;Siou Li ,&nbsp;Weina Zhao ,&nbsp;Jian Xing ,&nbsp;Jiangnan Yi ,&nbsp;Fengze Zhao ,&nbsp;Changhao Yin","doi":"10.1016/j.ibneur.2025.05.008","DOIUrl":"10.1016/j.ibneur.2025.05.008","url":null,"abstract":"<div><h3>Objective</h3><div>To elucidate the association between serum neurofilament light chain (NfL) levels and structural brain alterations in individuals exhibiting white matter hyperintensities (WMHs), as well as to investigate the potential utility of serum NfL as a predictive biomarker for the progression of WMH.</div></div><div><h3>Methods</h3><div>A total of 151 subjects were included in the study, among whom 117 demonstrated the presence of white matter hyperintensities (WMHs) on magnetic resonance imaging (MRI). We assessed the relationship between changes in serum neurofilament light chain (NfL) levels and alterations in brain volume across three distinct groups. Additionally, we analyzed trends in brain structural changes and serum NfL level variations within the population exhibiting varying severities of WMHs, exploring the correlation between these two variables.</div></div><div><h3>Results</h3><div>Serum NfL levels were significantly elevated in individuals with WMHs compared to those with none-low WMHs (p &lt; 0.001). Furthermore, higher serum NfL levels were observed in individuals with severe-moderate WMHs compared to those with mild WMHs (p &lt; 0.01). Within the mild WMHs group, serum NfL levels exhibited a negative correlation with gray matter volume. In contrast, within the severe to moderate WMHs group, serum NfL levels were negatively correlated with both gray matter volume (GMV) and white matter volume (WMV). Voxel-based morphometry (VBM) analysis indicated the presence of gray matter atrophy in several brain regions when comparing the none-low WMHs group with the severe to moderate WMHs group, as well as when comparing the mild WMHs group with the severe-moderate WMHs group. However, no significant differences were observed in the comparison between the none to low WMHs group and the mild WMHs group.</div></div><div><h3>Conclusion</h3><div>Serum NfL levels have been observed to rise in conjunction with the increasing severity of WMH and show a correlation with gray matter atrophy in individuals exhibiting WMHs. These levels are anticipated to serve as a biological marker for predicting the progression of WMH.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 794-802"},"PeriodicalIF":2.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147190","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":"Governor Vessel combined with local acupoints electroacupuncture improves the therapeutic effect of nerve conduit transplantation bridging long segment defects of the median nerve","authors":"Yu Cheng ,&nbsp;Fanqi Meng ,&nbsp;Zhanmou Liang ,&nbsp;Xin Zhou ,&nbsp;Wenya Pei ,&nbsp;Jingwen Ruan ,&nbsp;Xiaozhou Lu ,&nbsp;Ying Ding ,&nbsp;Guanheng He","doi":"10.1016/j.ibneur.2025.05.003","DOIUrl":"10.1016/j.ibneur.2025.05.003","url":null,"abstract":"<div><div>Nerve defect is a relatively serious injury in peripheral nerve injury, which often leads to the neuron apoptosis of the corresponding spinal cord segment and the difficulty of long-distance regeneration of the damaged nerve fibers, collectively resulting in poor recovery of nerve function after surgery. All experimental rats were randomly assigned to the following groups: Control, Conduit, Local acupoints electroacupuncture (EA) (Local-EA), and governor vessel (GV) combined with local acupoints electroacupuncture (GV+Local-EA) groups. A 10-mm defect model was established in the left median nerve, and a chitosan nerve conduit was used to bridge the defect. After 4 weeks, nerve regeneration and functional recovery were evaluated using immunofluorescence histochemistry, behavioral assays, and electrophysiological measurements. Results showed that the GV+Local-EA group exhibited significantly elevated the number of ChAT-positive motor neurons and enhanced the GDNF expression within the C8 spinal cord anterior horn compared with other experimental groups (<em>P</em> &lt; 0.01). Furthermore, the density of NF-positive nerve fibers and S100β-positive Schwann cells in the middle and distal parts of the transplanted conduits was significantly higher in the GV+Local-EA group than in other groups (<em>P</em> &lt; 0.05). The behavioral improvements and the median nerve conduction complex action potential were significantly better in the GV+Local-EA group (<em>P</em> &lt; 0.05). These results suggest that GV combined with local acupoints electroacupuncture can prevent the loss of spinal motor neurons and upregulating the GDNF expression, and then facilitates the regeneration of damaged median nerve fibers along the Schwann cell-formed Bungner band toward the distal end, thereby accelerating functional recovery of the affected forelimb and demonstrating superior therapeutic efficacy compared with conventional local acupoint protocols.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 814-822"},"PeriodicalIF":2.0,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144168750","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":"An approach to screen susceptible rats and efficacy of an antidepressive treatment after chronic stress","authors":"Kenji B. Valencia-Flores ,&nbsp;Yahel Vidal-de-laO ,&nbsp;Diana Paz-Trejo ,&nbsp;Hugo Sánchez-Castillo","doi":"10.1016/j.ibneur.2025.05.001","DOIUrl":"10.1016/j.ibneur.2025.05.001","url":null,"abstract":"<div><div>Chronic stress during life has been considered a risk factor for the development of psychiatric illness in humans. Chronic unpredictable stress battery (CUSB) is an animal model to study depression through stress exposition in rodents. CUSB induces depression and anxiety behavioral markers that could be modulated with fluoxetine an antidepressant treatment. However, it is well known that not all subjects develop depression-like behaviors or do not respond to antidepressant treatments. The way to screen these individual differences in susceptibility to stress or the efficacy of antidepressant therapy in depression models is not well studied. Here we show that saccharine consumption, immobility and time spent in the center of the area could be useful as behavioral markers for screening susceptibility to stress and depression, also we show that fluoxetine treatment had different efficacy depending on the age when the stress occurred. First, we found that after CUSB (during adolescence, adulthood, or both) rodents show depression and anxiety profiles. Second, we found that fluoxetine (10 mg/kg) could recover depression but no anxiety profile in all the groups exposed to stress. Finally, we use the machine learning clustering method (k-means), to classify the subjects in all groups based on the individual effects modulated by stress exposure and antidepressant treatment to find the ratio of stress effects and pharmacological efficacy. Using altered behaviors as classifiers, we found three possible clusters, (1) Without alterations, (2) Moderated anxiety and depression profile (3) Serious anxiety and depression profile, suggesting two groups of susceptible animals with different intensities of altered behavior. Also, fluoxetine could change the ratio of rats previously classified in groups 2 or 3, showing the beneficial effects of antidepressant treatment. Our results demonstrate that CUSB has different consequences even in subjects that experienced the same stress protocol. Also, fluoxetine has different efficacy in recovering behavior associated with the age of exposure to stress. Finally, we suggest k-means as an easy and useful method to apply in susceptible rodent studies of depression and to study the individual efficacy of antidepressant treatment.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 803-813"},"PeriodicalIF":2.0,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144147191","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":"Environmental restraint: A hidden risk factor for stress-induced depression in rats","authors":"Hiroko Mochizuki-Kawai ,&nbsp;Seita Nakazawa ,&nbsp;Hideaki Oike ,&nbsp;Hiromi Kimoto ,&nbsp;Satoru Tomita ,&nbsp;Michimasa Toyoshima ,&nbsp;Tingbi Xiong ,&nbsp;Kazuo Yamada","doi":"10.1016/j.ibneur.2025.05.002","DOIUrl":"10.1016/j.ibneur.2025.05.002","url":null,"abstract":"<div><div>Little is known about the impact of environmental restraint, characterized by limited space and a lack of stimulating elements, on adult mental and physical health. We examined the influence of environmental restraint on depression-like behaviors and physical status in rats, and the potential mitigating effects of <em>Lactococcus cremoris</em> H61 as a beneficial bacterium. Rats subjected to environmental restraint exhibited prolonged maladaptive immobility in the forced swim test without showing changes in body weight, locomotion, or social motivation. Daily activities remained unaffected. These findings suggest that environmental restraint may be a covert risk factor for stress-induced depression, potentially alleviated by supplementation with strain H61.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 754-758"},"PeriodicalIF":2.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143948732","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":"Bridging neuro-biomarkers and MR imaging: The synergistic role of glial fibrillary acidic protein in early CNS disease diagnosis","authors":"Mohammad Ghaderian ,&nbsp;Daryoush Shahbazi-Gahrouei ,&nbsp;Safoora Nikzad ,&nbsp;Elnaz Didehban ,&nbsp;Hossein Hafezi ,&nbsp;Ismail Laher ,&nbsp;Fahime Hossein Beigi ,&nbsp;Saghar Shahbazi-Gahrouei ,&nbsp;Tahereh Boustani","doi":"10.1016/j.ibneur.2025.04.016","DOIUrl":"10.1016/j.ibneur.2025.04.016","url":null,"abstract":"<div><div>Molecular neuroimaging is a powerful and emerging tool for the early detection and monitoring of central nervous system (CNS)-related and neurodegenerative diseases. Biomarkers play a crucial role in diagnostic accuracy, prognosis, and treatment efficacy. Among these, Glial Fibrillary Acidic Protein (GFAP), a cytoskeletal intermediate filament protein, serves as a key indicator of astrocytic activation and neuroaxonal injury. Elevated levels of GFAP in cerebrospinal fluid (CSF) and blood-based samples (serum/plasma) are increasingly recognized as potential biomarkers for neurodegeneration and CNS pathology. Advanced molecular imaging techniques, including Diffusion Tensor Imaging (DTI) and Diffusion-Weighted Imaging (DWI), along with conventional magnetic resonance imaging (MRI), provide visual scoring, local morphometry, and volumetric analysis. Therefore, integrating GFAP with neuroimaging modalities offers the potential to improve disease characterization, allowing for accurate spatial mapping of neurodegeneration and monitoring of disease progression at a molecular level. The relationship between MRI and GFAP is currently under evaluation. This review explores the interplay between GFAP and molecular neuroimaging, highlighting their combined potential to enhance early diagnosis, prognosis, and treatment monitoring of CNS disorders.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 739-753"},"PeriodicalIF":2.0,"publicationDate":"2025-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143942994","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":"The reduction in locomotor activity induced by restraint stress in young male mice involves the downregulation of hippocampal serotonergic and dopaminergic markers","authors":"Megumi Furukawa ,&nbsp;Nobuo Izumo ,&nbsp;Masahiro Toho ,&nbsp;Ryoken Aoki ,&nbsp;Hiroki Nishijima ,&nbsp;Yusuke Nakamura ,&nbsp;Yumi Sakai ,&nbsp;Yukiko Ishibashi ,&nbsp;Haruna Kurono ,&nbsp;Takayuki Manabe ,&nbsp;Hideo Matsuzaki","doi":"10.1016/j.ibneur.2025.04.017","DOIUrl":"10.1016/j.ibneur.2025.04.017","url":null,"abstract":"<div><div>The novel coronavirus (COVID-19) pandemic led to widespread restrictions on human activities, including limits on physical activity and public gatherings. In particular, the physical and mental effects of restricting childhood activities such as exercise and play urgently need to be elucidated. In this study, we analyzed the effects of restraint stress on young (4-week-old) and adult (10-week-old) mice using behavioral experiments and gene expression analysis. Restraint stress did not cause a decrease in the expression of BDNF, a depression marker, in the hippocampus, suggesting that it may be a relatively mild form of stress. In young mice, restraint stress caused significant reductions in locomotor activity and sucrose preference. In contrast, in adult mice, no significant difference was observed in locomotor activity or sucrose preference. Increased expression of the <em>XBP-1</em> gene might be involved in the resistance to endoplasmic reticulum stress and resilience to restraint stress in adult mice. Moreover, serotoninergic and dopaminergic markers were significantly downregulated in young mice exposed to restraint stress. These findings strongly suggest an increased vulnerability to stress during early childhood, which may substantially impact subsequent brain development in children.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 726-731"},"PeriodicalIF":2.0,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143921792","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":"Potential Mediating Role of Polygenic Hazard Score in the Association Between Neurofilament Light Chain and Default Mode Network Connectivity Across the Alzheimer's Disease Continuum","authors":"Parsa Saberian ,&nbsp;Hamide Nasiri ,&nbsp;Fatemeh Kaffashian ,&nbsp;Parisa Nasiriansari ,&nbsp;Fatemeh Nazari Nasab ,&nbsp;Niusha Mehrvarz ,&nbsp;Fatemeh Talebizadeh ,&nbsp;Shayan Shakeri ,&nbsp;Mahsa Mayeli ,&nbsp;for the Alzheimer’s Disease Neuroimaging Initiative","doi":"10.1016/j.ibneur.2025.04.018","DOIUrl":"10.1016/j.ibneur.2025.04.018","url":null,"abstract":"<div><h3>Background</h3><div>Alzheimer’s disease (AD) is a complex neurodegenerative disorder marked by progressive cognitive decline and disrupted brain network connectivity, particularly within the default mode network (DMN). Neurofilament light chain (NfL) serves as a biomarker for axonal injury, but the role of genetic predisposition, assessed via the Polygenic Hazard Score (PHS), in mediating the association between plasma NfL and DMN connectivity remains unclear. This study investigates whether PHS mediates the association between plasma NfL levels and DMN connectivity in individuals across different cognitive stages, including cognitively normal (CN), mild cognitive impairment (MCI), and AD.</div></div><div><h3>Methods</h3><div>Data were extracted from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Plasma NfL concentrations were measured using the Simoa assay, and resting-state fMRI (rs-fMRI), assessed DMN connectivity. The cohort included 102 participants (nCN=28, nMCI=52, and nAD=22). Partial correlation analyses and mediation models were performed, adjusting for age and gender. Statistical significance was set at p &lt; 0.05, after corrections for multiple comparisons.</div></div><div><h3>Results</h3><div>Plasma NfL levels were significantly higher in AD group compared to CN and MCI groups (p = 0.030). DMN connectivity showed substantial declines in the AD group, particularly in the posterior and ventral regions. Significant negative correlations were observed between plasma NfL and ventral DMN connectivity in AD. However, mediation analysis indicated no significant indirect effect of PHS, suggesting that genetic risk does not mediate the plasma NfL-DMN association.</div></div><div><h3>Conclusion</h3><div>These findings suggest that elevated plasma NfL levels are associated with disrupted ventral DMN connectivity in AD, reflecting neurodegeneration-related network dysfunction. However, the lack of a mediating effect by PHS indicates that this relationship is likely independent of genetic risk burden.</div></div><div><h3>Clinical Trial Number</h3><div>not applicable.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 732-738"},"PeriodicalIF":2.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143927446","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":"Alterations in apoptotic pathways and expression of miR-134, miR-181, and miR-497 induced by Wharton’s jelly-derived mesenchymal stem cells in a rat model of ischemic brain injury","authors":"Tahereh Alizamir ,&nbsp;Ali Fathi Jouzdani ,&nbsp;Fatemeh Attari ,&nbsp;Leila Arab ,&nbsp;Zeinab Ashaari ,&nbsp;Alireza Komaki ,&nbsp;Gholamreza Hassanzadeh","doi":"10.1016/j.ibneur.2025.04.015","DOIUrl":"10.1016/j.ibneur.2025.04.015","url":null,"abstract":"<div><h3>Background</h3><div>MicroRNAs (miRNAs) play crucial roles in regulating cell survival and signaling pathways. Mesenchymal stem cells (MSCs), particularly those derived from Wharton’s Jelly (WJ-MSCs), have shown potential in promoting cell survival and reducing apoptosis. This study evaluates the effects of WJ-MSCs on miRNA expression and apoptosis markers in an ischemic brain injury model.</div></div><div><h3>Methods</h3><div>Male Wistar rats (n = 30) were divided into control, sham, WJ-MSCs, Middle Cerebral Artery Occlusion (MCAO), and MCAO+WJ-MSCs groups. After 60 minutes of ischemia and 24 hours of reperfusion, WJ-MSCs were administered intracerebroventricularly. Post-surgical brain samples were analyzed using immunohistochemistry, TUNEL assay, and qRT-PCR to measure Bax/Bcl-2 ratios and miRNA (miR-497, miR-134, miR-181) expression in the cortex.</div></div><div><h3>Results</h3><div>Immunohistochemistry revealed that the Bax/Bcl-2 ratio was significantly increased in the MCAO group, reflecting a pro-apoptotic state. In contrast, WJ-MSC treatment significantly reduced the Bax/Bcl-2 ratio in the ischemic cortex, suggesting a shift towards anti-apoptotic activity. Additionally, analysis of miRNA expression showed significantly elevated levels of miR-497, miR-134, and miR-181 in the brains of ischemic rats, which were associated with increased neuronal cell death. WJ-MSC treatment effectively modulated these miRNAs, resulting in a marked reduction in their expression. Furthermore, the TUNEL assay confirmed a substantial reduction in the number of apoptotic cells in the MCAO+WJ-MSCs group compared to the MCAO group. In the cortex, apoptotic cells were observed in WJ-MSC-treated rats, indicating enhanced neuronal survival.</div></div><div><h3>Conclusion</h3><div>WJ-MSCs mitigate ischemic brain injury by modulating miRNA expression and apoptotic markers, promoting neuronal survival. These findings highlight their potential as a therapeutic strategy for ischemic brain injuries.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 759-770"},"PeriodicalIF":2.0,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144115376","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":"The impact of perioperative hyperglycemia on postoperative cognitive function: A comprehensive review","authors":"Jiale Song ,&nbsp;Shuqin Li ,&nbsp;Heng Zhao ,&nbsp;Qian Hao ,&nbsp;Hongyuan Sui ,&nbsp;Hongmei Zhou ,&nbsp;Jian Lu","doi":"10.1016/j.ibneur.2025.04.010","DOIUrl":"10.1016/j.ibneur.2025.04.010","url":null,"abstract":"<div><div>Hyperglycemia, commonly triggered by the physiological stress of surgery, is exacerbated by counter-regulatory hormonal responses and can lead to significant complications including Postoperative Cognitive Dysfunction (POCD) and delirium. These conditions not only extend hospitalization and increase healthcare costs but also negatively impact long-term patient well-being. This review addresses multiple objectives by conducting a comprehensive literature review that synthesizes existing research across various surgical disciplines to assess the impact of hyperglycemia on cognitive outcomes. This involves integrating findings from both observational studies and clinical trials to offer a nuanced perspective on the current knowledge landscape. Secondly, it identifies significant gaps in research, including inconsistencies in outcomes and methodological shortcomings. Highlighting these gaps emphasizes the need for a more standardized approach to understanding hyperglycemia's cognitive effects post-surgery. Lastly, the review proposes future research directions, advocating for innovative research methodologies and clinical interventions aimed at mitigating the cognitive impairments associated with perioperative hyperglycemia. By providing an exhaustive examination of these aspects, the review seeks to enhance scholarly discourse and inform clinical practice, ultimately aiming to refine perioperative care protocols. This will protect cognitive functions and improve overall patient outcomes, bridging the gap between theoretical research and practical application, thereby setting the stage for advancements that could transform perioperative management standards.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"18 ","pages":"Pages 698-704"},"PeriodicalIF":2.0,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143886484","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}