Neuroreport最新文献

{"title":"Kaempferol ameliorated central nervous injury induced by alcohol uptake through improving intestinal barrier function.","authors":"Shinan Zhou, Lu Liang, Wenyan Zhong, Jingjing Chen, Li Xiao","doi":"10.1097/WNR.0000000000002170","DOIUrl":"10.1097/WNR.0000000000002170","url":null,"abstract":"<p><strong>Introduction: </strong>Excessive neuroinflammation resulting from chronic alcohol intake is an important risk factor for central nervous system injury. The aim of this study was to investigate the effect of kaempferol (KAE) on alcohol-induced neural injury and its underlying mechanism.</p><p><strong>Methods: </strong>C57BL/6 N mice were employed to develop a binge-on-chronic alcohol exposure model, with different doses of KAE as an interventional drug for 6 weeks. Neuronal damage and microglial activation in the brain, as well as colonic tissue damage and serum lipopolysaccharide (LPS) concentrations, were systematically assessed. Additionally, Caco-2 cells were exposed to alcohol to induce intestinal epithelial injury in vitro.</p><p><strong>Results: </strong>Chronic alcohol exposure let to significant neuronal damage in the cortex and hippocampus of mice. KAE treatment effectively attenuated microglial activation and reduced neuronal damage in the brains of alcohol-exposed mice. Analysis of colonic tissues revealed that KAE administration inhibited miRNA-122a expression, alleviated pathological damage, and enhanced occludin expression, thereby significantly lowing serum LPS concentrations in alcohol-fed mice. In vitro, KAE markedly decreased miRNA-122a expression and enhanced occludin levels in Caco-2 cells treated with alcohol. Furthermore, overexpression of miRNA-122a was found to diminish occludin protein production in Caco-2 cells, which was significantly counteracted by KAE treatment.</p><p><strong>Conclusion: </strong>KAE treatment enhanced intestinal barrier function to alleviate neuronal damage caused by microglial activation mediated by gut-derived LPS under alcohol expose. This effect of KAE was involved in the enhance of intestinal occludin expression by inhibiting the expression of miRNA-122a. This suggested that KAE had the potential to prevent alcohol-induced neurological damage.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"524-531"},"PeriodicalIF":1.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144004440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of peripheral adiponectin on perioperative neurocognitive disorder via regulation of glucose metabolism in aged rats.","authors":"Zhijing Zhang, Chengyuan Hu, Yuqing Chi, Baiqin Su, Huiqun Chen, Haihui Xie","doi":"10.1097/WNR.0000000000002169","DOIUrl":"10.1097/WNR.0000000000002169","url":null,"abstract":"<p><strong>Objective: </strong>Perioperative neurocognitive disorder (PND) is a significant complication affecting elderly patients after surgery, with limited effective interventions to improve its prognosis yet. We have found that decreased serum adiponectin (APN) and increased cerebrospinal fluid (CSF) lactate are involved in the pathophysiological process of PND in elderly patients. APN is known for its anti-insulin resistance property. In this study, we further explored the regulatory effects of APN on cerebral glucose metabolism in PND rats.</p><p><strong>Methods: </strong>Twelve-month-old male Sprague-Dawley rats were divided into 3 groups: the sham, PND (splenectomy) and PND+APN (50 mg/kg/day intragastrically) groups. ELISA, quantitative PCR and colorimetric analysis were conducted to analyze tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), pyruvate and lactate in serum, CSF and hippocampus. Open field and Morris water maze (MWM) tests were used to detect hippocampus-dependent cognitive function. Western blot and flow cytometry were conducted to detect neuronal apoptosis in primary hippocampal neurons.</p><p><strong>Results: </strong>In vivo, peripheral APN administration reversed surgery-induced reductions in serum APN expression and elevated levels of cerebral lactate, the ratio of lactate/pyruvate, TNF-α and IL-1β, thereby improving cognitive performance in MWM and Open Field tests. In vitro, APN at concentrations of 2 and 10 ng/ml dose-dependently reduced lipopolysaccharide-induced caspase 3 expression and p38 phosphorylation in neurons, inhibiting apoptosis.</p><p><strong>Conclusions: </strong>Cerebral hypometabolism is one of the pathogenic mechanisms of PND. APN shows its effects on regulating glucose metabolism to inhibit neuroinflammation and neuronal apoptosis in PND. And the underlying mechanism of APN should be investigated further.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"505-513"},"PeriodicalIF":1.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tetrandrine mediates autophagy via sirtuin 3/adenosine 5-monophosphate-activated protein kinase/mammalian target of rapamycin signal pathway to attenuate early brain injury after subarachnoid hemorrhage.","authors":"Wenliang Wang, Yang Li, Yuan Li, Yan-Meng Zhao, Jia-Bei Ye, Tao Qian","doi":"10.1097/WNR.0000000000002171","DOIUrl":"10.1097/WNR.0000000000002171","url":null,"abstract":"<p><strong>Objective: </strong>Early brain injury (EBI) is the main cause of poor outcomes in patients with subarachnoid hemorrhage (SAH). Tetrandrine (Tet) is the root of Stephania tetrandra S Moore extract that has been shown to promote neuronal survival and regulate a variety of signaling pathways; however, the mechanism through which it exerts neuroprotective effects in patients with SAH is unknown. This investigation was to examine Tet's effect on EBI in SAH rats.</p><p><strong>Basic methods: </strong>We divided the rats into four groups. The effects of Tet treatment on the pathological changes of neurons in rat brains were evaluated, as well as autophagy-related and signaling pathway proteins.</p><p><strong>Main results: </strong>We found that Tet had a neuroprotective effect on EBI after SAH, as evidenced by the fact that Tet ameliorated SAH-mediated neurologic impairment and neuronal morphological damage and reduced brain water content, neuronal apoptosis rate, and neuronal cell loss. Tet decreased the LC3II/LC3I ratio, elevated P62 protein expression, and inhibited autophagosome production after SAH. Tet may have increased sirtuin 3 (SIRT3) expression, decreased adenosine 5-monophosphate-activated protein kinase (AMPK) phosphorylation, and increased phosphor-mammalian target of rapamycin (mTOR) levels, all of which may have occurred particularly via SIRT3/AMPK/mTOR signaling pathway activation; However, this trend can be reversed by 3-(1H-1,2,3-triazol-4-yl) pyridine (SIRT3 inhibitors).</p><p><strong>Conclusions: </strong>Tet exerts neuroprotective effects by inhibiting autophagy, this may be associated with SIRT3's inhibitory effect on the AMPK/mTOR signaling pathway. This inhibition could function as a potential mechanism for the neuroprotective effects observed in patients suffering from SAH.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"514-523"},"PeriodicalIF":1.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12133048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporal integration and stream segregation because of differences in base tones.","authors":"Ken Suzutani, Tetsuya Shiga, Hiroshi Hoshino, Ayaka Arakawa, Yuhei Mori, Kazuko Kanno, Yuichi Takahashi, Tomohiro Wada, Aya Sato, Shuntaro Itagaki, Itaru Miura, Hirooki Yabe","doi":"10.1097/WNR.0000000000002173","DOIUrl":"10.1097/WNR.0000000000002173","url":null,"abstract":"<p><strong>Background: </strong>Humans live surrounded by many sounds and have the ability to filter out various background sounds. It involves stream segregation and temporal integration. When the reference frequency is set to 3000 Hz, stream segregation will precede temporal integration when the frequency difference is 1000 Hz or larger; however, there is no report that examines whether the threshold of frequency difference at which stream segregation occurs before temporal integration is similar to different base tones.</p><p><strong>Methods: </strong>We created 10 blocks of tone sequences in which high tones and low tones were alternated with a constant stimulus onset asynchrony of 120 ms. In the first group (group A), the frequency of base tones was fixed at 3000 Hz. In the second group (group B), the frequency of base tones was fixed at 2000 Hz. The frequency of pair tones was set at 3000, 2750, 2500, 2250, and 2000 Hz in each block, respectively presented with six blocks of alternating high tones and low tones.</p><p><strong>Results: </strong>In group A, the mean voltage in response to omission was significantly lower than the mean voltage in response to opposite tones except in the fifth block. On the other hand, in group B, the mean voltage in response to omission was significantly lower than the mean voltage in response to opposite tones in all blocks.</p><p><strong>Conclusions: </strong>Our results indicated that whether a temporal window of integration or stream segregation is preferred depends on the base tone's Hz.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"532-539"},"PeriodicalIF":1.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The regulatory role of cell cycle exit and neuronal differentiation 1 in the pathogenesis of Parkinson's disease by regulating the nuclear factor kappa B pathway.","authors":"Zewei Cong, Chan Li","doi":"10.1097/WNR.0000000000002193","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002193","url":null,"abstract":"<p><strong>Objective: </strong>This study seeks to investigate the roles and underlying mechanisms of cell cycle exit and neuronal differentiation 1 (CEND1) on Parkinson's disease.</p><p><strong>Methods: </strong>Real-time quantitative PCR (RT-qPCR) was employed to assess the expression levels of CEND1 in peripheral blood samples of Parkinson's patients. A cell model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPP+)-induced Parkinson's disease was established in-vitro. 3-[4,5-Dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide assays were used to evaluate the impact of CEND1 on the viability of SH-SY5Y cells induced by MPP+, while flow cytometry was used to assess apoptosis of these cells. The expression of oxidative stress and inflammatory factors in MPP+-treated cells was detected by ELISA. In addition, the effect of CEND1 on Parkinson's disease was interfered by an activator of the nuclear factor kappa B (NF-κB) pathway to clarify the relationship between CEND1 and the NF-κB pathway in a cell model of Parkinson's disease.</p><p><strong>Results: </strong>CEND1 expression is markedly downregulated in patients with Parkinson's disease and cells of the Parkinson's disease model. Downregulation of CEND1-induced apoptosis, inhibited cell proliferation, and promoted expression of inflammatory factors in MPP+-treated cells; however, high expression of CEND1 inhibited MPP+-induced apoptosis, inflammatory factor release, and oxidative stress. In addition, CEND1 inhibited the activation of the NF-κB pathway induced by MPP+, and phorbol 12-myristate 13-acetate reversed the effect of CEND1 on Parkinson's disease.</p><p><strong>Conclusion: </strong>CEND1 plays a protective role in the Parkinson's disease cell model by suppressing NF-κB signaling pathway activation, offering a potential target and foundation for the diagnosis and therapy of Parkinson's disease.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144591850","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture improves ischemic stroke by intervening in neurovascular remodeling via miR-210-mediated regulation of the Wnt/HIF1A/netrin-1 signaling axis.","authors":"Chao Liang, Kebing Zheng, Jiao Liu, Shaoping Chen, Mengrui Zhang, Chong Sun, Qinghua Wu","doi":"10.1097/WNR.0000000000002181","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002181","url":null,"abstract":"<p><strong>Objective: </strong>Cerebral infarction (stroke) is a major global public health issue. This study explores the mechanisms by which electroacupuncture affects motor function after cerebral infarction by combining complementary experimental approaches in middle cerebral artery occlusion mice. The work focuses particularly on the Wnt/hypoxia-inducible factor-1 alpha (HIF1A)/netrin-1 signaling axis and downstream targets, including netrin-1 and vascular endothelial growth factor (VEGF), to provide a comprehensive understanding of the mechanisms that underpin electroacupuncture stimulation after stroke.</p><p><strong>Methods: </strong>The middle cerebral artery occlusion model was established with electroacupuncture intervention. The cerebral cortex of mice was collected for detections, including RNA sequencing, western blot, immunofluorescence, quantitative PCR, and so forth. HIF1A-overexpressing and knockdown cell lines in SH-SY5Y cells were used for further verification.</p><p><strong>Results: </strong>Exosome and RNA sequencing identified the key microRNA mir-210 and the Wnt/HIF1A/netrin-1 signaling axis after electroacupuncture treatment at head acupoints in the murine model. In addition, the HIF1A transcription factor was upregulated and bound to promoters of genes for netrin-1 and VEGF thereby activating transcription of these loci. Dual luciferase reporter assays revealed that mir-210 targets the gene for the tumor suppressor adenomatous polyposis coli, thereby stimulating the Wnt-signaling pathway. Furthermore, behavioral experiments demonstrated that electroacupuncture intervention in the Wnt/HIF1A/netrin-1 signaling axis improved motor function in middle cerebral artery occlusion mice.</p><p><strong>Conclusion: </strong>The study reveals that electroacupuncture stimulation promotes angiogenesis and neural reconstruction after cerebral infarction by regulating the Wnt/HIF1A/netrin-1 signaling axis through mir-210, and suggests novel therapeutic targets for the treatment of cerebral infarction with electroacupuncture.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian disruption exacerbates cognitive impairment via an intense neuroinflammatory reaction and alpha-synuclein deposition in a Parkinson's disease mouse model.","authors":"Rong Deng, Chang Liu, Hong Jin, Yulan Cao, Lanxiang Wang, Yuting Zhang, Fen Wang, Jing Chen","doi":"10.1097/WNR.0000000000002182","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002182","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease (PD) is a chronic neurodegenerative disorder marked by motor symptoms and nonmotor complications, notably cognitive impairment, which severely impairs patients' quality of life. While circadian disruption (CD) correlates with cognitive decline in PD, it remains unclear whether CD is merely secondary to motor symptoms or directly contributes to cognitive dysfunction. The objective of this study was to investigate whether chronic CD exacerbates cognitive decline in PD.</p><p><strong>Basic methods: </strong>Male mice were subjected to the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD and divided into groups with or without chronic exposure to CD. Observational assessments of cognitive deficits were performed alongside analytical measurements of tyrosine hydroxylase (TH) content in the striatum, α-synuclein deposition levels, and neuroinflammatory responses in the hippocampus.</p><p><strong>Main results: </strong>MPTP-treated mice exposed to CD exhibited significantly more severe cognitive deficits compared to MPTP-treated controls without CD. These deficits correlated with pronounced reductions in striatal TH content, elevated α-synuclein accumulation, and intensified neuroinflammatory activity in the hippocampal region. The observed changes demonstrated CD-induced exacerbation of pathological hallmarks.</p><p><strong>Conclusions: </strong>Chronic CD directly aggravates MPTP-driven neuroinflammatory processes and α-synuclein pathology in the hippocampus, leading to accelerated cognitive deterioration. These findings substantiate CD as an environmental risk factor for cognitive decline in PD progression, independent of motor symptom sequelae. The study provides mechanistic insights into CD's contributory role in PD-related cognitive impairment.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-06-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disrupted functional topology of the white matter connectome in rhegmatogenous retinal detachment: insights from graph theory and machine learning.","authors":"Yu Ji, Zhuo-Er Dong, Yi-Chong Duan, Li-Li Yao, Xiao-Rong Wu","doi":"10.1097/WNR.0000000000002190","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002190","url":null,"abstract":"<p><strong>Background: </strong>Rhegmatogenous retinal detachment (RRD) is known to induce functional alterations in the gray matter regions associated with vision. However, the impact of RRD on the white matter (WM) connectome remains largely unexplored.</p><p><strong>Methods: </strong>We applied graph theory to evaluate the functional network topology of the WM connectome in RRD patients. A support vector machine (SVM) classifier, combined with SHapley Additive exPlanations (SHAP), was then employed to distinguish RRD patients from healthy controls (HCs) and to identify key brain regions driving model predictions.</p><p><strong>Results: </strong>Compared to HCs, RRD patients exhibited significant disruptions in both global and nodal network topology. Network-based statistics identified 23 subnetworks with altered connectivity. Notably, the integration of SVM and SHAP analyses revealed that betweenness centrality (Bc) was the most discriminative topological feature, achieving an area under the curve of 0.9211.</p><p><strong>Conclusion: </strong>These findings suggest that RRD disrupts critical hubs within the central visual and higher-order cognitive networks, leading to characteristic network reorganization. Moreover, Bc shows promise as an early neuroimaging biomarker for RRD. Overall, our results advance the understanding of neuroadaptive changes in RRD and support the clinical application of network topological metrics in early diagnosis.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Menthol preferentially inhibits persistent Na+ current mediated by NaV1.8 in small-sized dural afferent neurons of rats.","authors":"Michiko Nakamura, Il-Sung Jang","doi":"10.1097/WNR.0000000000002189","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002189","url":null,"abstract":"<p><strong>Objective: </strong>Menthol is widely used as a cooling agent and an adjunctive analgesic to relieve various painful conditions, such as migraine. As menthol acts as an agonist for the thermosensitive ion channel transient receptor potential melastatin 8 (TRPM8), other ion channels, such as voltage-gated Na+ channels, are also involved in the antinociceptive effect of menthol. In this study, we explored the effect of menthol on tetrodotoxin-resistant (TTX-R) Na+ channels in nociceptive sensory neurons.</p><p><strong>Methods: </strong>TTX-R Na+ current (INa) was recorded from acutely isolated rat dural afferent neurons identified with the fluorescent dye DiI using a whole-cell patch-clamp technique.</p><p><strong>Results: </strong>Under a voltage-clamp condition, menthol potently decreased the amplitude of the persistent TTX-R Na+ current (INa) in a concentration-dependent manner, with a minor effect on the transient current. The inhibition of persistent TTX-R INa by menthol was not affected by the TRPM8 antagonist. Menthol (300 μM) (1) shifted the steady-state fast inactivation relationship to hyperpolarizing ranges without affecting the voltage-activation relationship, (2) accelerated the onset of inactivation, and (3) retarded the recovery from the inactivation of TTX-R Na+ channels. Under the current clamp condition, menthol (300 μM) decreased the threshold for action potential generation but reduced the number of action potentials elicited by strong depolarizing current stimuli.</p><p><strong>Conclusion: </strong>The results of this study suggest that menthol exerts an analgesic effect by preferentially inhibiting persistent TTX-R INa and modulating the inactivation and recovery kinetics of TTX-R Na+ channels.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alterations in dynamic effective connectivity of brain functional networks in patients with high myopia: a Granger causality analysis.","authors":"Lin Zhou, Hao-Yu Yuan, Hua Chai, Zhuo-Er Dong, Li-Li Yao, Yi-Chong Duan, Xiao-Rong Wu","doi":"10.1097/WNR.0000000000002191","DOIUrl":"https://doi.org/10.1097/WNR.0000000000002191","url":null,"abstract":"<p><strong>Background: </strong>Although previous neuroimaging studies have revealed alterations in the static brain networks of patients with high myopia, little is known about changes in their dynamic brain networks, particularly regarding directional connectivity within these networks, warranting further investigation.</p><p><strong>Methods: </strong>In this study, resting-state functional MRI was conducted on 82 confirmed patients with high myopia and 59 healthy controls. Employing dynamic Granger causality analysis, sliding time windows, and K-means clustering, we assessed dynamic alterations in effective connectivity within the brain's functional networks in patients with high myopia.</p><p><strong>Results: </strong>Patients with high myopia show significantly enhanced dynamic effective connectivity (dEC) between the visual network and the default mode network (DMN) compared with healthy controls. Furthermore, aberrant connectivity is detected between the visual network and the limbic network. In addition, intravisual network dEC is markedly increased. In state 1, the frequency differed significantly between the two groups, with high myopia patients showing a markedly higher frequency than healthy controls.</p><p><strong>Conclusion: </strong>This study found that patients with high myopia exhibit significantly altered patterns of dEC, especially increased connectivity between the visual network, the DMN, and the limbic network. Furthermore, significantly increased intranetwork dEC within the visual network indicates enhanced internal visual information processing. These findings offer new insights into the neural mechanisms of high myopia and suggest that long-term visual impairment may trigger functional reorganization in both visual and nonvisual brain networks.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":""},"PeriodicalIF":1.6,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144507085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}