Neuroreport最新文献

{"title":"Preventive effect of aminocaproic acid combined with nimodipine on short-term rebleeding in patients with aneurysmal subarachnoid hemorrhage.","authors":"Qiong Zhao, Zhongyang Liu, Qingcheng Yang","doi":"10.1097/WNR.0000000000002127","DOIUrl":"10.1097/WNR.0000000000002127","url":null,"abstract":"<p><p>Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening and life-limiting disease with high mortality and disability rates. Herein, we aim to explore the preventive effect of aminocaproic acid combined with nimodipine on short-term rebleeding in patients with aSAH. Retrospectively, the medical data of patients with aSAH ( n  = 256) were collected. According to different treatment methods, patients were categorized into the aminocaproic acid + nimodipine group ( n  = 152) and the nimodipine group ( n  = 104), and were treated for 1 week. Baseline characteristics, incidence of rebleeding, average velocity of cerebral artery blood flow, cerebral vasospasm index, vascular endothelial function, complications, and adverse events were analyzed between the two groups. After 1-week treatment, compared to the nimodipine group, the aminocaproic acid + nimodipine group exhibited lower incidence of rebleeding, notable decreases in average velocity of cerebral artery blood flow and the cerebral vasospasm index, and downregulation of endothelin-1 and vascular endothelial growth factor ( P  < 0.05). There were no significant differences about complications and adverse events between the two groups. Aminocaproic acid combined with nimodipine is superior to nimodipine alone in preventing the short-term rebleeding in patients with aSAH, and has good safety.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"99-104"},"PeriodicalIF":1.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813805","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":"Artemisinin antagonizes cognitive disorder in hyperuricemia through glutamate receptor-interacting protein 1-suppressed pyroptosis.","authors":"Yanfang Chen, Shuangxi Chen, Huiqing Wang, Peng Cao","doi":"10.1097/WNR.0000000000002131","DOIUrl":"10.1097/WNR.0000000000002131","url":null,"abstract":"<p><p>The prevalence of hyperuricemia (HUA) is climbing worldwide and persistent elevation of serum uric acid impairs cognitive function. This study aimed to explore the mechanisms of Artemisinin (Art) antagonizing cognitive disorder in HUA by suppressing pyroptosis. A mouse model of HUA was established by intraperitoneal injection of 300 mg/kg potassium oxonate (PO) in C57BL/6 mice for 14 days. The mice were simultaneously treated with Art, an agonist of pyroptosis Polyphyllin VI (PPVI), or glutamate receptor-interacting protein 1 (GRIP1) knockdown lentiviral plasmid. After treatment, serum uric acid, IL-6, and TNF-ɑ levels were examined, as well as hippocampal IL-1β and IL-18 levels, and the cognitive function of mice was assessed by the Morris water maze test. Pathological changes in the CA1 of the hippocampus were observed. Cleave-caspase-1, GSDMD-N, and GRIP1 protein level in the hippocampus was quantified by western blot. After PO induction, the escape latency and the time spent in the target quadrant increased in mice, cell arrangement in CA1 hippocampus was loose and disorganized, with obvious inflammatory infiltration and serious damage being observed, and the mouse hippocampus had elevated cleaved-caspase-1, GSDMD-N, IL-1β, and IL-18. Art treatment reduced pyroptosis in the hippocampus and improved cognitive disorder in HUA mice. Administration of PPVI aggravated cognitive disorder in Art-treated HUA mice, and Art improved cognitive dysfunction in HUA mice by inhibiting pyroptosis through upregulation of GRIP1. Art blunts pyroptosis in the hippocampus of HUA mice suffering from cognitive disorder by upregulating GRIP1.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 3","pages":"145-152"},"PeriodicalIF":1.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458794","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":"Functional imaging of time on task and habituation in passive exposure to faces with emotional expression.","authors":"Karin Labek, Roberto Viviani","doi":"10.1097/WNR.0000000000002130","DOIUrl":"10.1097/WNR.0000000000002130","url":null,"abstract":"<p><p>The amygdala responds to emotional stimuli but habituates at repeated presentation. Much less is known about time-on-task effects during exposure to emotional stimuli in the cortex. Here, we identified the neural substrates that show habituation or cortical decreased activity in a task of repeated passive exposure to faces with negative emotional expressions. We found that in the amygdala, habituation selectively involved the central nucleus and extended posteriorly in the hippocampal-amygdaloid region, consistently with reduced motivational and attentional effects of repeated stimulation. In the cortex, decreases in activity with time on task involved a network including the temporoparietal junction, the postsplenial region, and the ventromedial prefrontal cortex, mostly located at the transition from task activations to deactivations. These effects were analogous to those reported as encoding of social cognition information, suggesting a role in developing task-based representations of input content.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 3","pages":"135-139"},"PeriodicalIF":1.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11867801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458837","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":"The potential of mitochondrially-targeted tetrapeptide in protecting against noise-induced hearing impairment.","authors":"Niranj A Kumar, Azmi Marouf, Kumar N Alagramam, Ruben Stepanyan","doi":"10.1097/WNR.0000000000002124","DOIUrl":"10.1097/WNR.0000000000002124","url":null,"abstract":"<p><p>Noise-induced hearing loss (NIHL) constitutes a significant global health issue for which there is no effective treatment. The loss of cochlear hair cells and associated synaptopathy are common causes of hearing impairment. One primary mechanism implicated in NIHL is the accumulation of reactive oxygen species (ROS), which ultimately overwhelms cochlear cells. ROS are detected in the cochlea immediately after noise exposure and persist for at least a week. Within cells, ROS are primarily generated in mitochondria as byproducts of cellular metabolism. Elamipretide is a synthetic tetrapeptide known to concentrate in mitochondria, improving mitochondrial function and reducing ROS production. To test the hypothesis that elamipretide treatment mitigates NIHL, 16-week-old male and female CBA/J mice were exposed to 8-16 kHz octave-band noise (OBN) at 98 dB SPL for 2 hours. Elamipretide was administered intraperitoneally immediately after noise exposure and continued for 2 weeks. Efficacy was evaluated based on auditory brainstem response (ABR) thresholds, wave amplitudes, and wave latencies in treated and control groups. Results showed that OBN-exposed mice exhibited an elevation in ABR thresholds at 16 and 32 kHz and a reduction in ABR wave-I amplitude at 32 kHz, although wave-I latencies were not affected at 16 or 32 kHz. Elamipretide treatment prevented the OBN-induced elevation of ABR thresholds and the attenuation of wave-I amplitude. These findings provide proof of concept that mitochondrial-targeted elamipretide can prevent NIHL in a mammalian model and highlight its potential to protect against NIHL in humans.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":" ","pages":"93-98"},"PeriodicalIF":1.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142813887","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":"A finite set of content-free pointers in visual working memory: magnetoencephalography (MEG) evidence.","authors":"Xinchi Yu, Ellen Lau","doi":"10.1097/WNR.0000000000002132","DOIUrl":"10.1097/WNR.0000000000002132","url":null,"abstract":"<p><p>Human visual working memory (VWM) is known to be capacity-limited, but the nature of this limit continues to be debated. Recent work has proposed that VWM is supported by a finite (~3) set of content-free pointers, acting as stand-ins for individual objects and binding features together. According to this proposal, the pointers do not represent features within themselves, but rather bind features represented elsewhere together. The current study set out to test if neural hallmarks resembling these content-free pointers can be observed with magnetoencephalography (MEG). Based on two VWM delay-match-to-sample experiments (N = 20 each) examining memory for simple and complex objects, we report a sustained response in MEG over right posterior cortex whose magnitude tracks the core hypothesized properties of this content-free pointer system: load-dependent, capacity-limited, and content-free. These results provide novel evidence for a finite set of content-free pointers underlying VWM.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 3","pages":"153-160"},"PeriodicalIF":1.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458806","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":"P2Y12-mediated HIV gp120 and ddC-induced neuropathic pain improved by esculin.","authors":"Zhihua Yi, Han Si, Shangdong Liang, Guilin Li, Yifan Dang, Congfa Zhou","doi":"10.1097/WNR.0000000000002125","DOIUrl":"10.1097/WNR.0000000000002125","url":null,"abstract":"<p><p>We studied whether esculin (ES) has the effect of alleviating peripheral neuropathic pain (NP) in rat models of HIV glycoprotein 120 (gp120) together with zalcitabine (2',3'-dideoxycytidine; ddC) treatment and explored the possible mechanism of it. The rats pain behaviors were evaluated by observing the paw withdrawal threshold (PWT) and the paw withdrawal latency (PWL). The rats were divided into a control group, sham group, gp120 combined with a ddC treatment group (gp120& ddC group), gp120&ddC combined with ES treatment group (gp120&ddC+ES group), which ES was administered intragastrically, and gp120&ddC combined with short hair RNA of P2Y12 receptor (rP2Y12) treatment group (gp120&ddC+shP2Y12 group), which shRNA of rP2Y12 was injected intrathecally with a dose of 25 µg/20 µl for every rat, and a negative control plasmid was administered to the gp120&ddC+nc group. Western blotting was used to measure the protein expression levels of the rP2Y12, the nuclear factor of activated T-cells type c1 (NFATc1), phospho-NFATc1 and the C-C motif chemokine ligand 3 (CCL3) in the L4-L6 dorsal root ganglia (DRG). Real-time quantitative PCR (RT-qPCR) was used to test the mRNA expression level of the CCL3. Double-labeling immunofluorescence was used to identify the co-localization of the rP2Y12 with glial fibrillary acidic protein (GFAP) in DRG. Fluorescence imaging with calcium indicator fluo-3 AM (7.5 μM) was performed to observe the change of intracellular calcium concentration ([Ca2+]i). Molecular docking was performed to identify the interaction between rP2Y12 and the ligand ES. We found that accompanied by the attenuation of mechanical allodynia and thermal hyperalgesia, rP2Y12 expression in the gp120+ddC+ES group of rats was downregulated compared with the gp120+ddC ones, as was the coexpression of the rP2Y12 and GFAP of satellite glial cells (SGCs) in DRG, and the CCL3 mRNA levels and protein expression were both decreased. In addition, mechanistic studies have found that there is a docking pocket between ES and the rP2Y12 protein, which causes ES to decrease the [Ca2+]i, thus increasing the phosphorylation level of NFATc1. Taken together, the results suggest that ES can combine with the rP2Y12, inhibit DRG SGCs activation caused by gp120&ddC, reduce [Ca2+]i, and prevent the NFATc1-mediated gene transcription of CCL3, finally relieving NP in rats treated with gp120&ddC.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 3","pages":"117-126"},"PeriodicalIF":1.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458839","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 effect of referential and emotional information on novel word learning: an fNIRS study.","authors":"Shan Li, Xue Sui, Yanbo Hu, Yutong Li","doi":"10.1097/WNR.0000000000002135","DOIUrl":"10.1097/WNR.0000000000002135","url":null,"abstract":"<p><p>The current study utilized functional near-infrared spectroscopy to examine the neural mechanisms underlying the effect of referential and emotional information on novel word learning. After learning the meaning of novel words in different sentences, participants were asked to complete a semantic consistency judgment task and a source judgment task. The behavioral data and neural data were recorded simultaneously. The results showed that: (1) referential information affected the novel word learning; (2) the interaction between referential and emotional information was significant; (3) these effects were associated with neural activities in the frontal and temporal lobe, mainly in the activation of the dorsolateral prefrontal cortex, the inferior frontal gyrus, the middle temporal gyrus, the superior temporal gyrus, and the premotor and supplementary motor cortex. The findings suggested that self-referential information could promote the novel word learning. Notably, referential and emotional information jointly affected the novel word learning in the frontal and temporal lobe, indicating the integrative contributions of both referential and emotional information to novel word learning.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 3","pages":"179-190"},"PeriodicalIF":1.6,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143458842","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":"Anxiety-like behaviors in rats exposed to the single and combined program of running exercise and environmental enrichment.","authors":"Farnaz Ghayourbabaei, Mohaya Farzin, Zakieh Keshavarzi, Ehsan Saburi, Mohammad Amin Khodadadegan, Vahid Hajali","doi":"10.1097/WNR.0000000000002117","DOIUrl":"10.1097/WNR.0000000000002117","url":null,"abstract":"<p><p>Exercise (Ex) and environmental enrichment (EE) as the nondrug solutions have positive effects on cognitive behaviors and also increase the ability to cope with anxiety, fear, and stress. In this research, we decided to investigate the simultaneous effect of Ex and EE on anxiety-like behaviors and hippocampal neurogenesis markers in healthy rats. A total of 40 male Wistar rats were divided into four treatment groups: control, EE, Ex, and EE + Ex. Animals in EE groups were housed in large cages (50 × 50 × 50 cm) equipped with toys and objects of different shapes for 3 weeks. Ex-animals were forced to run on a treadmill once a day for 3 consecutive weeks. Open field (OF) and elevated plus maze (EPM) tests were used to evaluate anxiety behaviors. The hippocampal expression of early neurogenesis markers, doublecortin, and sex determining region Y-box 2, were measured using real-time-PCR. Ex and EE animals separately did not show any significant performance in reducing anxiety levels, neither in EPM nor in OF compared with the control group. When animals were treated with EE and Ex simultaneously, they showed significantly reduced anxiety in both EPM and OF tests compared with the control as well as Ex and EE groups separately. Both treatments in combination were also more effective than individual groups in increasing the neurogenesis molecular markers within the hippocampus. This study proposes that Ex in combination with cognitive engagement is more efficient in alleviating anxiety responses and that can develop a nonpharmacological and multidomain policy that may prevent or delay psychophysiological symptoms.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 1","pages":"31-38"},"PeriodicalIF":1.6,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801848","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":"Differences in embodied cognition between the arrow-orientation and the arrow-position recognition tasks: evidence from event-related potentials.","authors":"WenJing Qi, Jin Gong, Li Sui","doi":"10.1097/WNR.0000000000002116","DOIUrl":"10.1097/WNR.0000000000002116","url":null,"abstract":"<p><p>Embodied cognition is known to play a role in verbal semantic processing. However, its involvement in nonverbal semantic elements, such as arrows, is less understood. Two spatial recognition tasks, specifically arrow-orientation recognition and arrow-position recognition, were employed using directional arrows in various spatial arrangements as visual stimuli. Stimuli were categorized into congruent (where orientation and position align), incongruent 1 (where orientation and position are directly opposing), and incongruent 2 (where orientation and position are unrelated) groups for both tasks. To investigate neural processes, event-related potentials (ERPs) were recorded and analyzed during task performance. Additionally, standardized low-resolution electromagnetic tomography (sLORETA) was utilized to examine brain electrical activity during ERP intervals. The analysis revealed significant ERP component differences between congruent and incongruent conditions across both spatial tasks, highlighting a Stroop-like interference effect. Notably, the arrow-orientation task showed marked enhancements in P3 and N400 components, as well as heightened brain activity in the frontal lobe, anterior cingulate cortex, and insula, compared with the arrow-position task. These findings suggest that embodied cognition is involved in both spatial arrow recognition tasks. The unique role of embodied cognition in these contexts is primarily reflected in the modulation of the P3-N400 complex, indicating differentiated cognitive processing.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 1","pages":"39-46"},"PeriodicalIF":1.6,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801851","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":"Paclitaxel-induced cognitive decline was attenuated by necroptosis inhibition.","authors":"Lan-Lan Liu, Shuang Zhao, Zhao Li, Hui-Zhou Li, Dong-Yang Ma, Xin Liu, Gui-Ying Wang, Xiu-Li Wang","doi":"10.1097/WNR.0000000000002121","DOIUrl":"10.1097/WNR.0000000000002121","url":null,"abstract":"<p><p>Anti-cancer agent paclitaxel induces cognitive impairment. Paclitaxel can induce limited neuron apoptosis and wide scope of neuroinflammation, but its precise mechanisms remain unclear. In this study, we determined paclitaxel causes necroptosis, a programmed cell death, via activation of the RIPK1-RIPK3-MLKL signaling pathway in hippocampal neurons (HT22 cells). Flow cytometric analysis, propidium iodide staining, and western blotting techniques were used to evaluate paclitaxel-induced necroptosis. Cell viability was determined using the Cell Counting Kit-8 assay, and the Ca2+ levels were measured using a Fluo-4 AM fluorescent probe. The number of cells positive for both annexin V and propidium iodide staining was significantly higher in paclitaxel-treated than vehicle-treated HT22 cells. Additionally, the nuclei of paclitaxel-treated cells exhibited more diffused necrotic propidium iodide staining than the vehicle-treated cells. The expression of necroptosis-associated proteins, including receptor-interacting protein kinase (RIPK)1, RIPK3, mixed lineage kinase domain-like protein (MLKL), and phosphorylated (p)-MLKL, were increased following paclitaxel treatment. Treating HT22 cells with necrostatin-1, a specific inhibitor for RIPK1, effectively decreased paclitaxel-induced necroptosis through lowering intracellular Ca2+ overload. In addition, administration of necrostatin-1 to paclitaxel-treated mice rescued cognitive impairments, as assessed by novel object recognition and Morris water maze tests. Necrostatin-1 also reduced the increases in necroptosis-associated protein levels of RIPK1, RIPK3, MLKL, and p-MLKL in hippocampal tissue of paclitaxel-treated mice. Paclitaxel induces cognitive deficits through RIPK1-mediated necroptosis. The inhibition of necroptosis may be a potential therapeutic approach to reduce paclitaxel-induced cognitive deficits.</p>","PeriodicalId":19213,"journal":{"name":"Neuroreport","volume":"36 1","pages":"61-69"},"PeriodicalIF":1.6,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142801854","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}