CNS Neuroscience & Therapeutics最新文献

{"title":"Thalamic Volumes and Functional Networks Linked With Self-Regulation Dysfunction in Major Depressive Disorder","authors":"Zhang Ling,&nbsp;He Cancan,&nbsp;Liu Xinyi,&nbsp;Fan Dandan,&nbsp;Zhang Haisan,&nbsp;Zhang Hongxing,&nbsp;Xie Chunming","doi":"10.1111/cns.70116","DOIUrl":"10.1111/cns.70116","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Self-regulation (SR) dysfunction is a crucial risk factor for major depressive disorder (MDD). However, neural substrates of SR linking MDD remain unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Sixty-eight healthy controls and 75 MDD patients were recruited to complete regulatory orientation assessments with the Regulatory Focus Questionnaire (RFQ) and Regulatory Mode Questionnaire (RMQ). Nodal intra and inter-network functional connectivity (FC) was defined as FC sum within networks of 46 thalamic subnuclei (TS) or 88 AAL brain regions, and between the two networks separately. Group-level volumetric and functional difference were compared by two sample <i>t</i>-tests. Pearson's correlation analysis and mediation analysis were utilized to investigate the relationship among imaging parameters and the two behaviors. Canonical correlation analysis (CCA) was conducted to explore the inter-network FC mode of TS related to behavioral subscales. Network-based Statistics with machine learning combining powerful brain imaging features was applied to predict individual behavioral subscales.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>MDD patients showed no group-level volumetric difference in 46 TS but represented significant correlation of TS volume and nodal FC with behavioral subscales. Specially, inter-network FC of the orbital part of the right superior frontal gyrus and the left supplementary motor area mediated the correlation between RFQ/RMQ subscales and depressive severity. Furthermore, CCA identified how the two behaviors are linked via the inter-network FC mode of TS. More crucially, thalamic functional subnetworks could predict RFQ/RMQ subscales and psychomotor retardation for MDD individuals.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>These findings provided neurological evidence for SR affecting depressive severity in the MDD patients and proposed potential biomarkers to identify the SR-based risk phenotype of MDD individuals.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 11","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11551040/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142612906","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTP1B Modulates Carotid Plaque Vulnerability in Atherosclerosis Through Rab5-PDGFRβ-Mediated Endocytosis Disruption and Apoptosis","authors":"Xiao Zhang,&nbsp;Ran Xu,&nbsp;Tao Wang,&nbsp;Jiayao Li,&nbsp;Yixin Sun,&nbsp;Shengyan Cui,&nbsp;Zixuan Xing,&nbsp;Xintao Lyu,&nbsp;Ge Yang,&nbsp;Liqun Jiao,&nbsp;Wenjing Li","doi":"10.1111/cns.70071","DOIUrl":"10.1111/cns.70071","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Protein tyrosine phosphatase 1B (PTP1B) is a protein tyrosine phosphatase and modulates platelet-derived growth factor (PDGF)/platelet-derived growth factor receptor (PDGFR) signaling in vascular smooth muscle cells (VSMCs) via endocytosis. However, the related molecular pathways that participated in the interaction of endo-lysosome and the trafficking of PDGFR are largely unknown. This study aims to determine the subcellular regulating mechanism of PTP1B to the endo-lysosome degradation of PDGFR in atherosclerotic carotid plaques, thereby offering a potential therapeutic target for the stabilization of carotid plaques.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>The immunohistochemical staining technique was employed to assess the expression levels of both PDGFR-β and Caspase 3 in stable and vulnerable carotid plaques. Tunnel staining was utilized to quantify the apoptosis of carotid plaques. Live-cell imaging was employed to observe endocytic motility, while cell apoptosis was evaluated through Propidium Iodide staining. In an in vivo experiment, ApoE^−/− mice were administered a PTP1B inhibitor to investigate the impact of PTP1B on atherosclerosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The heightened expression of PDGFR-β correlates with apoptosis in patients with vulnerable carotid plaques. At the subcellular level of VSMCs, PDGFR-β plays a pivotal role in sustaining a balanced endocytosis system motility, regulated by the expression of Rab5, a key regulator of endocytic motility. And PTP1B modulates PDGFR-β signaling via Rab5-mediated endocytosis. Additionally, disrupted endocytic motility influences the interplay between endosomes and lysosomes, which is crucial for controlling PDGFR-β trafficking. Elevated PTP1B expression induces cellular apoptosis and impedes migration and proliferation of carotid VSMCs. Ultimately, mice with PTP1B deficiency exhibit a reduction in atherosclerosis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our results illustrate that PTP1B induces disruption in endocytosis and apoptosis of VSMCs through the Rab5-PDGFRβ pathway, suggesting a potential association with the heightened vulnerability of carotid plaques.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 11","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11549062/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142612919","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Transcranial Direct Current Stimulation Targeting Dorsolateral Prefrontal Cortex and Orbitofrontal Cortex on Somatic Symptoms in Patients With Major Depressive Disorder: A Randomized, Double-Blind, Controlled Clinical Trial","authors":"Shuxiang Shi,&nbsp;Haijing Huang,&nbsp;Mengke Zhang,&nbsp;Yiming Chen,&nbsp;Weichieh Yang,&nbsp;Fan Wang,&nbsp;Shuqi Kong,&nbsp;Ni Zhou,&nbsp;Zheyi Wei,&nbsp;Shentse Chen,&nbsp;Dongbin Lyu,&nbsp;Chenglin Wu,&nbsp;Qinte Huang,&nbsp;Qinting Zhang,&nbsp;Wu Hong","doi":"10.1111/cns.70110","DOIUrl":"10.1111/cns.70110","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>There is a lack of research on transcranial direct current stimulation (tDCS) for the treatment of somatic symptoms in major depressive disorder (MDD) and the suitable stimulating brain region. We investigated the efficacy of tDCS targeting the dorsolateral prefrontal cortex (DLPFC) versus orbitofrontal cortex (OFC) on depressive somatic symptoms and somatic anxiety in patients with MDD and aimed to identify the appropriate stimulating brain regions.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>In this randomized, double-blind, sham-controlled study, a total of 70 patients diagnosed with MDD were randomly allocated into DLPFC group, OFC group, and Sham group. Subjects participated in 2 weeks of 10 primary interventions and subsequently 2-week maintenance interventions weekly (20 min, 2 mA).</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The DLPFC group showed a more significant improvement in somatic symptoms compared to the Sham group at week 2. At the maintenance and follow-up stages, the DLPFC group outperformed the Sham and OFC groups, but the difference with the Sham group was not significant. Neither active group demonstrated superiority over the Sham group in improving depression and anxiety.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>In conclusion, the tDCS targeting DLPFC may be a potentially effective therapeutic target for alleviating somatic symptoms in patients with MDD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 11","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11549028/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142612890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Orexin-A Attenuates the Inflammatory Response in Sepsis-Associated Encephalopathy by Modulating Oxidative Stress and Inhibiting the ERK/NF-κB Signaling Pathway in Microglia and Astrocytes","authors":"Jing Guo,&nbsp;Dexun Kong,&nbsp;Junchi Luo,&nbsp;Tao Xiong,&nbsp;Fang Wang,&nbsp;Mei Deng,&nbsp;Zhuo Kong,&nbsp;Sha Yang,&nbsp;Jingjing Da,&nbsp;Chaofei Chen,&nbsp;Jinhai Lan,&nbsp;Liangzhao Chu,&nbsp;Guoqiang Han,&nbsp;Jian Liu,&nbsp;Ying Tan,&nbsp;Jiqin Zhang","doi":"10.1111/cns.70096","DOIUrl":"10.1111/cns.70096","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Oxidative stress-induced inflammation is a major pathogenic mechanism in sepsis-associated encephalopathy (SAE). We hypothesized that regulation of reactive oxygen species (ROS) by the neuropeptide orexin-A could prevent SAE-induced oxidative stress and inflammation. Therefore, the aim of this study was to investigate the effects of orexin-A on oxidative stress and inflammation in SAE in mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Adult male mice were treated with orexin-A (250 μg/kg, intranasal administration) to establish a cecal ligation perforation (CLP) model. We performed behavioral tests, observed neuronal damage in the hippocampal region, measured the levels of ROS, NOX2, and observed the structure of mitochondria by transmission electron microscopy. We then examined the inflammatory factors TNF-α and IL-1β, the activation of microglia and astrocytes, the expression of ERK/NF-κB, C3, and S100A10, and the presence of A1 type astrocytes and A2 type astrocytes.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Orexin-A treatment improved cognitive performance in CLP-induced SAE mice, attenuated neuronal apoptosis in the hippocampal region, ameliorated ROS levels and the extent of mitochondrial damage, and reduced protein expression of NOX2 in hippocampal tissue. In addition, orexin-A treatment significantly reduced microglia and astrocyte activation, inhibited the levels of P-ERK and NF-κB, and reduced the release of IL-1β and TNF-α, which were significantly increased after CLP. Finally, Orexin-A treatment significantly decreased the number of C3/glial fibrillary acidic protein (GFAP)-positive cells and increased the number of S100A10/GFAP-positive cells.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our data suggest that orexin-A reduces ROS expression by inhibiting CLP-induced NOX2 production, thereby attenuating mitochondrial damage and neuronal apoptosis. Its inhibition of microglial and A1-type astrocyte activation and inflammation was associated with the ERK/NF-κB pathway. These suggest that orexin-A may reduce cognitive impairment in SAE by reducing oxidative stress-induced inflammation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 11","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541240/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevention and Treatment of Alzheimer's Disease Via the Regulation of the Gut Microbiota With Traditional Chinese Medicine","authors":"Jinyao Long,&nbsp;Jiani Zhang,&nbsp;Xin Zeng,&nbsp;Min Wang,&nbsp;Ningqun Wang","doi":"10.1111/cns.70101","DOIUrl":"10.1111/cns.70101","url":null,"abstract":"<p>Alzheimer's disease (AD) is caused by a variety of factors, and one of the most important factors is gut microbiota dysbiosis. An imbalance in the gut mincrobiota have been shown to change the concentrations of lipopolysaccharide and short-chain fatty acids. These microorganisms synthesize substances that can influence the levels of a variety of metabolites and cause multiple diseases through the immune response, fatty acid metabolism, and amino acid metabolism pathways. Furthermore, these metabolic changes promote the formation of β-amyloid plaques and neurofibrillary tangles. Thus, the microbiota–gut–brain axis plays an important role in AD development. In addition to traditional therapeutic drugs such as donepezil and memantine, traditional Chinese medicines (TCMs) have also showed to significantly decrease the severity of AD symptoms and suppress the underlying related mechanisms. We searched for studies on the effects of different herbal monomers, single herbs, and polyherbal formulas on the gut microbiota of AD patients and identified the relevant pathways through which the gut microbiota affected AD. We conclude that improvements in the gut microbiota not only decrease the occurrence of inflammatory reactions but also reduce the deposition of central pathological products. Herbal monomers have a stronger effect on improving of central pathology. Polyherbal formulas have the most extensive effect on the gut microbiota in patients with AD. Among the effects of formulas, the anti-inflammatory effect is the most essential and is also the main concern regarding the use of TCMs in treating AD from the viewpoint of the gut microbiota. We hope that this review will be helpful for providing new ideas for the clinical application of TCMs in the treatment of AD.</p>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 11","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Local Neuronal Activity and the Hippocampal Functional Network Can Predict the Recovery of Consciousness in Individuals With Acute Disorders of Consciousness Caused by Neurological Injury","authors":"Xi Wang,&nbsp;Xingdong Liu,&nbsp;Lin Zhao,&nbsp;Zhiyan Shen,&nbsp;Kemeng Gao,&nbsp;Yu Wang,&nbsp;Danjing Yu,&nbsp;Lin Yang,&nbsp;Ying Wang,&nbsp;Yongping You,&nbsp;Jing Ji,&nbsp;Jiu Chen,&nbsp;Wei Yan","doi":"10.1111/cns.70108","DOIUrl":"10.1111/cns.70108","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Aims&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;There is limited research on predicting the recovery of consciousness in patients with acute disorders of consciousness (aDOC). The purpose of this study is to investigate the altered characteristics of the local neuronal activity indicated by the amplitude of low-frequency fluctuations (ALFF) and functional connectivity (FC) of the hippocampus network in patients with aDOC caused by neurological injury and to explore whether these characteristics can predict the recovery of consciousness.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Methods&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Thirty-seven patients with aDOC were included, all of whom completed resting-state functional magnetic resonance imaging (rsfMRI) scans. The patients were divided into two groups based on prognosis of consciousness recovery, 24 patients were in prolonged disorders of consciousness (pDOC) and 13 in emergence from minimally conscious state (eMCS) at 3 months after neurological injury. Univariable and multivariate logistic regression analyses were used to investigate the clinical indicators affecting patients' recovery of consciousness. The ALFF values and FC of the hippocampal network were compared between patients with pDOC and those with eMCS. Additionally, we employed the support vector machine (SVM) method to construct a predictive model for prognosis of consciousness based on the ALFF and FC values of the aforementioned differential brain regions. The accuracy (ACC), area under the curve (AUC), sensitivity, and specificity were used to evaluate the efficacy of the model.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Results&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The FOUR score at onset and the length of mechanical ventilation (MV) were found to be significant influential factors for patients who recovered to eMCS at 3 months after onset. Patients who improved to eMCS showed significantly increased ALFF values in the right calcarine gyrus, left lingual gyrus, right middle temporal gyrus, and right precuneus compared to patients in a state of pDOC. Furthermore, significant increases in FC values of the hippocampal network were observed in the eMCS group, primarily involving the right lingual gyrus and bilateral precuneus, compared to the pDOC group. The predictive model constructed using ALFF alone or ALFF combined with FC values from the aforementioned brain regions demonstrated high accuracies of 83.78% and 81.08%, respectively, with AUCs of 95% and 94%, sensitivities of 0.92 for both models, and specificities of 0.92 for both models in predicting the recovery of consciousness in patients with aDOC.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Conclusion&lt;/h3&gt;\u0000 ","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 11","pages":""},"PeriodicalIF":4.8,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541605/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142602404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin attenuates chronic sleep deprivation-induced cognitive deficits and HDAC3-Bmal1/clock interruption","authors":"Yujie Hu,&nbsp;Yefan Lv,&nbsp;Xiaoyan Long,&nbsp;Guoshuai Yang,&nbsp;Jinxia Zhou","doi":"10.1111/cns.14474","DOIUrl":"10.1111/cns.14474","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Aims</h3>\u0000 \u0000 <p>Sleep is predicted as a key modulator of cognition, but the underlying mechanisms are poorly understood. In this study, we investigated the effects of melatonin on chronic rapid eye movement sleep deprivation (CRSD)-induced cognitive impairment and circadian dysfunction in rat models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Thirty-six Sprague-Dawley male rats were divided into three groups: CRSD with saline treatment, CRSD with chronic melatonin injection (20 mg/kg/day), and non-sleep-deprived control. The cognitive behavioral tests as well as the expression of clocks and HDAC3 were evaluated in all groups.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CRSD significantly reduced recognition index in novel object location, increased escape latency and distance traveling in Morris water maze while melatonin treatment attenuated CRSD-induced hippocampal-dependent spatial learning and memory deficits. Furthermore, the mRNAs of <i>brain and muscle aryl hydrocarbon receptor nuclear translocator-like 1(Bmal1)</i> and <i>circadian locomotor output cycles kaput</i> (<i>Clock</i>) were globally down-regulated by CRSD with constant intrinsic oscillation in both hippocampus and peripheral blood. The protein levels of hippocampal Bmal1, Clock, and HDAC3 were also remarkably down-regulated following CRSD. Melatonin treatment reversed CRSD-induced alterations of Bmal1/Clock and HDAC3 on both mRNA levels and protein levels.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Our data indicate that melatonin treatment attenuates CRSD-induced cognitive impairment via regulating HDAC3-Bmal1/Clock interaction. These findings explore a broader understanding of the relationship between sleep and cognition and provide a potential new therapeutic target for cognitive impairment.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 3","pages":""},"PeriodicalIF":5.5,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cns.14474","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10653449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of TRPV1 in electroacupuncture-mediated signal to the primary sensory cortex during regulation of the swallowing function","authors":"Si Yuan,&nbsp;Bo Qiu,&nbsp;Ying Liang,&nbsp;Bing Deng,&nbsp;Jing Xu,&nbsp;Xiaorong Tang,&nbsp;Junshang Wu,&nbsp;Sheng Zhou,&nbsp;Zeli Li,&nbsp;Hongzhu Li,&nbsp;Qiuping Ye,&nbsp;Lin Wang,&nbsp;Shuai Cui,&nbsp;Chunzhi Tang,&nbsp;Wei Yi,&nbsp;Lulu Yao,&nbsp;Nenggui Xu","doi":"10.1111/cns.14457","DOIUrl":"10.1111/cns.14457","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>Electroacupuncture (EA) at the Lianquan (CV23) could alleviate swallowing dysfunction. However, current knowledge of its neural modulation focused on the brain, with little evidence from the periphery. Transient receptor potential channel vanilloid subfamily 1 (TRPV1) is an ion channel predominantly expressed in sensory neurons, and acupuncture can trigger calcium ion (Ca²⁺) wave propagation through active TRPV1 to deliver signals. The present study aimed to investigate whether TRPV1 mediated the signal of EA to the primary sensory cortex (S1) during regulation of swallowing function.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Blood perfusion was evaluated by laser speckle contrast imaging (LSCI), and neuronal activity was evaluated by fiber calcium recording and c-Fos staining. The expression of TRPV1 was detected by RNA-seq analysis, immunofluorescence, and ELISA. In addition, the swallowing function was assessed by in vivo EMG recording and water consumption test.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>EA treatment potentiated blood perfusion and neuronal activity in the S1, and this potentiation was absent after injecting lidocaine near CV23. TRPV1 near CV23 was upregulated by EA-CV23. The blood perfusion at CV23 was decreased in the TRPV1 hypofunction mice, while the blood perfusion and the neuronal activity of the S1 showed no obvious change. These findings were also present in post-stroke dysphagia (PSD) mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The TRPV1 at CV23 after EA treatment might play a key role in mediating local blood perfusion but was not involved in transferring EA signals to the central nervous system (CNS). These findings collectively suggested that TRPV1 may be one of the important regulators involved in the mechanism of EA treatment for improving swallowing function in PSD.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 3","pages":""},"PeriodicalIF":5.5,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cns.14457","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10634655","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of serum occludin levels and perihematomal edema volumes in intracranial hemorrhage patients","authors":"Shuhua Yuan,&nbsp;Qingfeng Ma,&nbsp;Chengbei Hou,&nbsp;Yue Zhao,&nbsp;Ke Jian Liu,&nbsp;Xunming Ji,&nbsp;Zhifeng Qi","doi":"10.1111/cns.14450","DOIUrl":"10.1111/cns.14450","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background and Purpose</h3>\u0000 \u0000 <p>Perihematomal edema (PHE) is one of the severe secondary damages following intracranial hemorrhage (ICH). Studies showed that blood–brain barrier (BBB) injury contributes to the development of PHE. Previous studies showed that occludin protein is a potential biomarker of BBB injury. In the present study, we investigated whether the levels of serum occludin on admission are associated with PHE volumes in ICH patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>This cross-sectional study included 90ICH patients and 32 healthy controls.The volumes of hematoma and PHE were assessed using non-contrast cranial CT within 30 min of admission. Blood samples were drawn on admission, and the levels of baseline serum occludin were detected using enzyme-linked immunosorbent assay. Partial correlation analysis and multiple linear regression analysis were performed to evaluate the association between serum occludin levels and PHE volumes in ICH patients.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The serum occludin levels in ICH patients were much higher than health controls (median 0.27 vs. 0.13 ng/mL, <i>p</i> &lt; 0.001). At admission, 34 ICH patients (37.78%) had experienced a severe PHE (≥30 mL), and their serum occludin levels were higher compared to those with mild PHE (&lt;30 mL) (0.78 vs. 0.21 ng/mL, <i>p</i> &lt; 0.001). The area under the receiver operating characteristics curve (ROC) of serum occludin level in predicting severe PHE was 0.747 (95% confidence interval CI 0.644–0.832, <i>p</i> &lt; 0.001). There was a significant positive correlation between serum occludin levels and PHE volumes (partial correlation <i>r</i> = 0.675, <i>p</i> &lt; 0.001). Multiple linear regression analysis showed that serum occludin levels remained independently associated with the PHE volumes after adjusting other confounding factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>The present study showed that serum occludin levels at admission were independently correlated with PHE volumes in ICH patients, which may provide a biomarker indicating PHE volume change.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 3","pages":""},"PeriodicalIF":5.5,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cns.14450","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10290374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"VIRMA promotes neuron apoptosis via inducing m6A methylation of STK10 in spinal cord injury animal models","authors":"Hongxiang Hong,&nbsp;Guanhua Xu,&nbsp;Guofeng Bao,&nbsp;Jinlong Zhang,&nbsp;Chu Chen,&nbsp;Jiajia Chen,&nbsp;Chunshuai Wu,&nbsp;Jiawei Jiang,&nbsp;Jiayi Huang,&nbsp;Haiming Huang,&nbsp;Zhiming Cui","doi":"10.1111/cns.14453","DOIUrl":"10.1111/cns.14453","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Spinal cord injury (SCI) occurs as a devastating neuropathic disease. The role of serine–threonine kinase 10 (STK10) in the development of SCI remains unclear.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Objective</h3>\u0000 \u0000 <p>This study aimed to investigate the action of m6A methylation on STK10 in the apoptosis of spinal cord neurons in the pathogenesis of SCI and the possible underlying mechanisms.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Rat model of SCI was established and subsequently evaluated for motor function, pathological conditions, and apoptosis of spinal cord neurons. And the effects of overexpression of STK10 on neuronal cells in animal models of spinal cord injury and glyoxylate deprivation (OGD) cell models were evaluated. m6A2Target database and SRAMP database were used to predict the m6A methylation sites of STK10. The methylation kits were used to detect overall m6A methylation. Finally, the interaction between STK10 and vir like m6A methyltransferase associated (VIRMA) was explored in animal and cellular models.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>STK10 is markedly decreased in spinal cord injury models and overexpression of STK10 inhibits neuronal apoptosis. VIRMA can induce m6A methylation of STK10. VIRMA is over-expressed in spinal cord injury models and negatively regulates the expression of STK10. m6A methylation and apoptosis of neuronal cells are reduced by the knockdown of VIRMA and STK10 shRNA have shown the opposite effects.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>VIRMA promotes neuronal apoptosis in spinal cord injury by regulating STK10 m6A methylation.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"30 3","pages":""},"PeriodicalIF":5.5,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/cns.14453","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10280486","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}