Neuroreport最新文献

{"title":"Reticulon 4 reflects endoplasmic reticulum stress in arginine vasopressin neurons.","authors":"Yohei Kawaguchi, Yuichi Hodai, Satoshi Naito, Yuichi Kondo, Tetsuro Tsumura, Takashi Miyata, Tomoko Kobayashi, Mariko Sugiyama, Takeshi Onoue, Shintaro Iwama, Hidetaka Suga, Ryoichi Banno, Hiroshi Arima, Daisuke Hagiwara","doi":"10.1097/WNR.0000000000002174","DOIUrl":"10.1097/WNR.0000000000002174","url":null,"abstract":"<p><strong>Objectives: </strong>Arginine vasopressin (AVP) is synthesized in the magnocellular supraoptic nucleus and paraventricular nuclei of the hypothalamus, where AVP neurons function under a consistently high demand for AVP production. AVP neurons are subject to endoplasmic reticulum (ER) stress even under basal conditions, and this ER stress is further exacerbated when AVP production increases due to dehydration. Reticulon (RTN) is essential for ER formation and stabilization and plays a critical role in membrane morphogenesis within the ER. This study aimed to investigate the expression of RTN family members in hypothalamic AVP neurons.</p><p><strong>Methods: </strong>Fluorescence immunohistochemistry and in-situ hybridization were employed to examine the expression of RTN family members in hypothalamic AVP neurons of adult male mice. Water deprivation and treatment with a chemical chaperone 4-phenylbutyric acid were used to increase and decrease the ER stress of AVP neurons, respectively.</p><p><strong>Results: </strong>Among the RTN family members, only RTN4 was found to be expressed in hypothalamic AVP neurons. RTN4 was colocalized with ER organelle markers, including immunoglobulin heavy chain binding protein and calnexin. Furthermore, RTN4 expression increased during ER stress induced by water deprivation. On the other hand, increased RTN4 expression by water deprivation was attenuated by 4-phenylbutyric acid treatment.</p><p><strong>Conclusions: </strong>Our results suggest that RTN4 expression in AVP neurons is closely associated with ER stress caused by increased protein production in neuroendocrine cells.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"540-546"},"PeriodicalIF":1.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079181","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":"Astrocytic mitochondria modulate poststroke splenic immune responses, promote interleukin 10 production, and mediate neuroprotection after intracerebral hemorrhage.","authors":"Ryosuke Tashiro, Yuki Kitamura, Jesus Bautista-Garrido, Guanghua Sun, Gab Seok Kim, Jaroslaw Aronowski, Joo Eun Jung","doi":"10.1097/WNR.0000000000002175","DOIUrl":"10.1097/WNR.0000000000002175","url":null,"abstract":"<p><strong>Background: </strong>We recently demonstrated that systemically transplanted astrocytic mitochondria enter the intracerebral hemorrhage (ICH)-affected brain, where they protect the neurons by mitigating oxidative damage via upregulation of the manganese superoxide dismutase (Mn-SOD), ultimately contributing to functional recovery after ICH in mice. Although our previous study clearly demonstrated the beneficial effects of mitochondria within the brain, the effect of transferred mitochondria on the peripheral system was not yet studied. Thus, here, we studied the impact of astrocytic mitochondria transfer on post-ICH recovery and modulation of systemic immune responses.</p><p><strong>Methods: </strong>We used the autologous blood injection model for the mouse ICH surgery. Mice subjected to ICH received astrocytic mitochondria intravenously at 1 h, 7, and 14 days post-ICH onset, and the splenic immune responses of these mice were analyzed at 21 days. An ICH-like injury was induced in vitro using primary cultured neurons treated with recombinant interleukin-10, and cell viability, reactive oxygen species levels, and gene expressions were analyzed.</p><p><strong>Results: </strong>We demonstrate that systemic transplantation of astrocytic mitochondria increases the population of splenic B cells, production of interleukin-10 by B cells, and plasma interleukin-10 levels in mice after ICH. Furthermore, in the ICH-like injury in vitro , exogenous interleukin-10 (to model spleen-mediated interleukin-10 increase) upregulated Mn-SOD expression in the cultured neurons and promoted neuronal survival and neuroplasticity-related gene expressions, suggesting interleukin-10 role in cytoprotection and repair/recovery under ICH-like condition.</p><p><strong>Conclusions: </strong>Thus, systemic transfer of astrocytic mitochondria modulates post-ICH peripheral immune responses, which may participate in functional recovery.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"547-554"},"PeriodicalIF":1.6,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079166","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":"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":"Effects of electroacupuncture on neural function and the expression of inflammation-related proteins NLRP3/caspase-1 in rats with ischemic stroke.","authors":"Zhifeng Wang, Yujiang Xi, Junfeng Lan, Jiao Yang, Ting Shi, Shuangfeng Xu, Liwei Xing, Pan Pan, Jian Wang","doi":"10.1097/WNR.0000000000002167","DOIUrl":"10.1097/WNR.0000000000002167","url":null,"abstract":"<p><p>This study aimed to investigate the neuroprotective effects of electroacupuncture (EA) at the Baihui and Dazhui acupoints in a rat model of ischemia-reperfusion injury. Ninety-six male Sprague-Dawley rats were randomly assigned to four groups ( n  = 24 per group): Sham, middle cerebral artery occlusion (MCAO), MCAO+EA, and MCAO+MCC950. The MCAO model was induced using filament embolization. Neurological function was assessed using Zea Longa scores on days 1 and 7 posttreatment, while cerebral infarction volume was measured using 2,3,5-triphenyltetrazolium chloride staining. Gene expression levels of NLRP3 and GSDMD were quantified by RT-qPCR, and protein expressions of NLRP3, GSDMD, caspase-1, IL-1β, and IL-18 were evaluated via Western blotting, immunohistochemistry, immunofluorescence staining, and ELISA. On day 1, compared with the MCAO group, the MCAO+EA and MCAO+MCC950 groups exhibited significantly reduced mRNA and protein expressions of NLRP3 and GSDMD ( P  < 0.05), as well as decreased levels of caspase-1, IL-1β, and IL-18 ( P  < 0.05). However, no significant differences were observed in neurological deficit scores or cerebral infarction volume. By day 7, both the MCAO+EA and MCAO+MCC950 groups showed significant improvements in neurological function ( P  < 0.05), reductions in cerebral infarction volume ( P  < 0.05), and further decreases in the expression of NLRP3, GSDMD, caspase-1, IL-1β, and IL-18 ( P  < 0.05). EA at the Baihui and Dazhui acupoints alleviates neurological deficits in ischemic stroke rats by inhibiting the NLRP3/caspase-1 inflammatory pathway and reducing the expression of apoptosis-related proteins such as NLRP3, GSDMD, caspase-1, IL-1β, and IL-18.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"456-466"},"PeriodicalIF":1.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12080364/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079170","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":"Electroacupuncture promotes functional recovery after spinal cord injury in rats by regulating P2X4R/p38 MAPK signaling pathway and suppressing inflammatory responses.","authors":"Xiang Wang, Yimin Gao, Jianzhong Huo","doi":"10.1097/WNR.0000000000002163","DOIUrl":"10.1097/WNR.0000000000002163","url":null,"abstract":"<p><p>This study aimed to investigate whether electroacupuncture can modulate the purinergic P2X4 receptor (P2X4R)/p38 mitogen-activated protein kinase (MAPK) pathway, thereby reducing inflammatory responses and facilitating functional recovery in a rat model of spinal cord injury (SCI). The SCI model was developed in female rats. The electroacupuncture intervention began on the seventh day after modeling, mainly Jiaji, Dazhui, and Mingmen. Sensory function was evaluated via the mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL), while motor function was measured using the Basso, Beattie, and Bresnahan (BBB) scoring system and footprint analysis. To analyze the protein expression related to the P2X4R/p38 MAPK signaling pathways, methods such as immunohistochemistry, immunofluorescence analysis, quantitative real-time PCR, and western blotting were utilized. To evaluate the levels of inflammatory cytokines, ELISAs were utilized. Additionally, after hematoxylin and eosin staining, histological alterations in spinal cord tissue were investigated. The results showed that MWT, TWL, and BBB scores were decreased, while P2X4R, phosphorylated-p38 MAPK, and phosphorylated nuclear factor κB p65 expression levels were increased, tumor necrosis factor-α, interleukin (IL)-1β, and IL-6 levels were elevated, and histopathological damage was more pronounced after SCI. However, electroacupuncture treatment effectively reversed these pathological changes. We demonstrate that electroacupuncture can alleviate SCI in rats by inhibiting the activation of the P2X4R/p38 MAPK pathway and reducing inflammatory response.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"443-455"},"PeriodicalIF":1.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983492","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":"Inhibition of autophagy in the amygdala ameliorates anxiety-like behaviors induced by morphine-protracted withdrawal in male mice.","authors":"Shuang Han, Chenchen Zhu, Dengjun Min, Zicheng Li","doi":"10.1097/WNR.0000000000002166","DOIUrl":"10.1097/WNR.0000000000002166","url":null,"abstract":"<p><strong>Objective: </strong>Morphine withdrawal triggers a range of negative affective states, wherein anxiety is typically common, significantly contributing to the morphine relapse. To date, the exact mechanism underlying morphine withdrawal-induced anxiety has remained unclear. Previous studies have proposed that autophagy is involved in the pathogenesis of morphine addiction and anxiety; however, the possible relationship between autophagy and morphine withdrawal-induced anxiety has not been explored before. In this study, we aimed to reveal the potential role of autophagy in anxiety-like behaviors elicited by protracted morphine withdrawal, and which brain region is involved.</p><p><strong>Methods: </strong>We established the model mice of anxiety by chronic intermittent escalating-dose morphine administration for 7 days and then withdrawing for 4 days. Anxious behaviors were detected using the Open field test and the Elevated plus maze test. Western blot was performed to measure the change of autophagy-associated proteins (ATG5, Beclin-1, LC3) in different brain regions.</p><p><strong>Results: </strong>Our results showed that intraperitoneal injection of an autophagy inhibitor 3-Methyladenine attenuated protracted morphine withdrawal-induced anxiety-like behaviors in male mice. Moreover, protracted morphine withdrawal predominantly promoted autophagy in the amygdala, rather than other related brain regions, suggesting the crucial involvement of amygdala in autophagy-mediated anxiety after morphine withdrawal. We further validated that 3-Methyladenine can effectively reduce autophagy-associated protein levels in the relevant brain region.</p><p><strong>Conclusion: </strong>These findings indicated that protracted morphine withdrawal-elicited autophagy in the amygdala contributes to the anxiety-like behaviors and may have implications for the future treatment of this disorder.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"487-496"},"PeriodicalIF":1.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12084013/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144007081","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":"Network centrality alterations in patients with moyamoya disease after combined revascularization surgery: a resting-state fMRI study.","authors":"Yuanyuan Wang, Jian Li, Feng Lin, Junwei Gao, Zihe Xu, Jie Liu, Xianjun Zeng","doi":"10.1097/WNR.0000000000002154","DOIUrl":"10.1097/WNR.0000000000002154","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to explore alterations in brain network characteristics among patients with moyamoya disease (MMD) before and after combined revascularization surgery (CRS).</p><p><strong>Methods: </strong>This investigation enrolled 20 MMD patients alongside 20 age- and sex-matched healthy controls (HCs). All participants underwent MRI scans. Additionally, MMD patients were subjected to comprehensive clinical assessments. Degree centrality (DC) analysis was utilized to assess the connectivity features of the entire brain network. The study also examined correlations between DC values in MMD patients before- (pre-CRS) and after-CRS (post-CRS) and various clinical indicators.</p><p><strong>Results: </strong>Compared with HCs, pre-CRS MMD patients showed abnormal DC values in multiple brain regions, mainly including the cerebellum, frontal lobe, temporal lobe, and cingulate gyrus. One year after CRS treatment, the DC values of the bilateral cerebellum posterior lobe showed a reverse increase. In addition, the DC value of the right cerebellum posterior lobe in pre-CRS MMD patients was positively correlated with the Montreal cognitive assessment scores.</p><p><strong>Conclusions: </strong>CRS treatment can effectively improve the functional network damage of the bilateral cerebellum posterior lobes caused by MMD, and it is expected to provide a new neuroimaging marker for the evaluation of CRS treatment efficacy.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"435-442"},"PeriodicalIF":1.6,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028694","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}