CNS Neuroscience & Therapeutics最新文献

{"title":"Effect of Different Treatments on Retinal Thickness Changes in Patients With Multiple Sclerosis: A Review","authors":"Armin Adibi,&nbsp;Iman Adibi,&nbsp;Milad Javidan","doi":"10.1111/cns.70225","DOIUrl":"10.1111/cns.70225","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Multiple sclerosis (MS) is an autoimmune disorder affecting the central nervous system, with varying clinical manifestations such as optic neuritis, sensory disturbances, and brainstem syndromes. Disease progression is monitored through methods like MRI scans, disability scales, and optical coherence tomography (OCT), which can detect retinal thinning, even in the absence of optic neuritis. MS progression involves neurodegeneration, particularly trans-synaptic degeneration, which extends beyond the initial injury site. This review focuses on the impact of different MS treatments on retinal thickness as assessed by OCT.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Injectable drugs, such as interferon beta and glatiramer acetate (GA), have a relatively modest impact on retinal atrophy. Oral medications like Fingolimod, Teriflunomide, and Dimethyl fumarate also have different impacts on retinal thickness. Fingolimod has been shown to protect against retinal thinning but may lead to macular edema. DMF-treated patients had less ganglion cell–inner plexiform layer thinning than GA-treated patients but more thinning compared to natalizumab-treated patients and healthy controls. Teriflunomide's impact on retinal layers remains unexplored in human studies. Monoclonal antibodies, including Alemtuzumab, Rituximab, Ocrelizumab, and Natalizumab, had protective effects on retinal layer atrophy. Alemtuzumab-treated patients showed significantly less atrophy compared to interferon- and GA-treated patients. Rituximab initially increased atrophy rates in the first months but subsequently demonstrated potential neuroprotective effects. Ocrelizumab slowed the rate of inner nuclear layer thinning in progressive forms of the disease. Natalizumab is considered the most effective in reducing retinal layer atrophy, particularly the peripapillary retinal nerve fiber layer.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>It's important to note that the effectiveness of these treatments may vary depending on MS subtype and individual factors. Future research should explore the long-term effects of these treatments on retinal layers and their correlations with overall disease progression and disability in MS patients.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11759887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031707","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":"Deep-Learning Generated Synthetic Material Decomposition Images Based on Single-Energy CT to Differentiate Intracranial Hemorrhage and Contrast Staining Within 24 Hours After Endovascular Thrombectomy","authors":"Tianyu Wang,&nbsp;Caiwen Jiang,&nbsp;Weili Ding,&nbsp;Qing Chen,&nbsp;Dinggang Shen,&nbsp;Zhongxiang Ding","doi":"10.1111/cns.70235","DOIUrl":"10.1111/cns.70235","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>To develop a transformer-based generative adversarial network (trans-GAN) that can generate synthetic material decomposition images from single-energy CT (SECT) for real-time detection of intracranial hemorrhage (ICH) after endovascular thrombectomy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Materials</h3>\u0000 \u0000 <p>We retrospectively collected data from two hospitals, consisting of 237 dual-energy CT (DECT) scans, including matched iodine overlay maps, virtual noncontrast, and simulated SECT images. These scans were randomly divided into a training set (<i>n</i> = 190) and an internal validation set (<i>n</i> = 47) in a 4:1 ratio based on the proportion of ICH. Additionally, 26 SECT scans were included as an external validation set. We compared our trans-GAN with state-of-the-art generation methods using several physical metrics of the generated images and evaluated the diagnostic efficacy of the generated images for differentiating ICH from contrast staining.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>In comparison with other generation methods, the images generated by trans-GAN exhibited superior quantitative performance. Meanwhile, in terms of ICH detection, the use of generated images from both the internal and external validation sets resulted in a higher area under the receiver operating characteristic curve (0.88 vs. 0.68 and 0.69 vs. 0.54, respectively) and kappa values (0.83 vs. 0.56 and 0.51 vs. 0.31, respectively) compared with input SECT images.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our proposed trans-GAN provides a new approach based on SECT for real-time differentiation of ICH and contrast staining in hospitals without DECT conditions.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11758448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031704","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":"NOTCH3 Mutation Causes Glymphatic Impairment and Promotes Brain Senescence in CADASIL","authors":"Chunyi Li,&nbsp;Hui Li,&nbsp;Xuejiao Men,&nbsp;Yuge Wang,&nbsp;Xinmei Kang,&nbsp;Mengyan Hu,&nbsp;Xiaotao Su,&nbsp;Shisi Wang,&nbsp;Danli Lu,&nbsp;Shishi Shen,&nbsp;Huipeng Huang,&nbsp;Xiaohui Deng,&nbsp;Yuxin Liu,&nbsp;Lei Zhang,&nbsp;Wei Cai,&nbsp;Aimin Wu,&nbsp;Zhengqi Lu","doi":"10.1111/cns.70140","DOIUrl":"10.1111/cns.70140","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>The aim of this study is to investigate the role of glymphatic function of cerebral autosomal dominant arteriopathy, subcortical infarcts, and leukoencephalopathy (CADASIL), the most common monogenic small vessel disease caused by <i>NOTCH3</i> mutation, and to explore potential therapeutic strategies to improve glymphatic function.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We assessed glymphatic influx and efflux function in CADASIL mouse models (<i>Notch3</i>^R170C) and correlated these findings with brain atrophy in CADASIL patients. We also investigated the underlying mechanisms of glymphatic impairment, focusing the expression of AQP4 in astrocytic endfeet.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>CADASIL mouse exhibited both impaired glymphatic influx and efflux, which impedes waste clearance and promotes brain senescence. In accordance, brain atrophy in CADASIL patients is associated with perivascular space enlargement, indicating that glymphatic impairment contributes to advanced brain senescence in CADASIL. The glymphatic malfunction in CADASIL is attributed to diminished AQP4 expression in astrocytic endfeet, which is the core mediator of glymphatic activity. Mechanistically, AQP4 expression is regulated by NOTCH3-RUNX1-CMYB signaling. Reinforcing AQP4 expression in astrocytes by AAV-based therapy resumes the glymphatic functions in CADASIL mice, which further prevents brain senescence.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>We propose that to improve glymphatic function by reinforcing AQP4 expression is a promising therapeutic strategy in CADASIL.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11760990/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031710","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":"CD4-Derived Double-Negative T Cells Ameliorate Alzheimer's Disease-Like Phenotypes in the 5×FAD Mouse Model","authors":"Yuanzi Xie,&nbsp;Jing Liu,&nbsp;Zongren Hou,&nbsp;Huan Wang,&nbsp;Kailun Liu,&nbsp;Xiaowei Chen,&nbsp;Zhen Fan,&nbsp;Da Li,&nbsp;Can Li,&nbsp;Yuhualei Pan,&nbsp;Yushang Zhao,&nbsp;Yanbing Zhu,&nbsp;Baoyang Hu","doi":"10.1111/cns.70187","DOIUrl":"10.1111/cns.70187","url":null,"abstract":"&lt;div&gt;\u0000 \u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Background&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;Alzheimer's disease (AD) is a debilitating neurodegenerative disorder that is difficult to predict and is typically diagnosed only after symptoms manifest. Recently, CD4&lt;sup&gt;+&lt;/sup&gt; T cell-derived double-negative T (DNT) cells have shown strong immuno-regulatory properties in both in vitro and in vivo neuronal inflammation studies. However, the effectiveness of DNT cells in treating on AD are not yet fully understood.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Objective&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;This study's aims were three-fold, to (1) evaluate the efficacy of CD4&lt;sup&gt;+&lt;/sup&gt; T cell-derived DNT cells treatment on AD mice, (2) understand how DNT treatment make changes in different cell types of 5FAD mice, (3) identify the side effects of DNT treatment.&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;We performed tail vein injection of transformed and amplified CD4&lt;sup&gt;+&lt;/sup&gt; T cell-derived DNT cells into 5 × FAD mice, while using WT mice and saline injection 5FAD mice as controls. DNT suspensions or NaCl alone were administered to 5 × FAD mice at the 6 months of age. For intravenous injection (&lt;i&gt;n&lt;/i&gt; = 10 for both DNT and control injections), 5 × FAD mice were injected with a total of 5 × 10&lt;sup&gt;6&lt;/sup&gt; DNT cells suspended in 200 μL of 0.9% NaCl or 0.9% NaCl alone via the lateral tail vein. Behavioral tests and pathology tests were carried out 30 days after cell transplantation.&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;Through qualitative analysis, we identified 6 main themes. DNT from young wild-type mice enhance the capability of spatial learning and memory in AD mice. DNT cell treatment rejuvenates the microglial function. DNT cell treatment improves the state of oligodendrocytes. DNT cell treatment finetunes the activation of the immune system. DNT cell treatment improves the synaptic plasticity and increases the complexity of neurons. DNT cell treatment reduces the density of amyloid Beta plaques deposition in the cortex and hippocampus of 5 × FAD mice.&lt;/p&gt;\u0000 &lt;/section&gt;\u0000 \u0000 &lt;section&gt;\u0000 \u0000 &lt;h3&gt; Discussion&lt;/h3&gt;\u0000 \u0000 &lt;p&gt;The findings from this study reveal that DNT treatment improved spatial memory and learning abilities, reduced Aβ deposition, and enhanced synaptic plasticity, contrasting with previous reports on thymus-derived DNT cells. Additionally, CD4&lt;sup&gt;+&lt;/sup&gt; T cell-derived DNT therapy exhibited anti-inflammatory effects and modulated microglial function, promoting a neuroprotective environment. Notably, DNT treatment also reduced tau pat","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143021341","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":"Molecular Symphony of Mitophagy: Ubiquitin-Specific Protease-30 as a Maestro for Precision Management of Neurodegenerative Diseases","authors":"Ankit Siwach,&nbsp;Harit Patel,&nbsp;Amit Khairnar,&nbsp;Pathik Parekh","doi":"10.1111/cns.70192","DOIUrl":"10.1111/cns.70192","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Introduction</h3>\u0000 \u0000 <p>Mitochondrial dysfunction stands as a pivotal feature in neurodegenerative disorders, spurring the quest for targeted therapeutic interventions. This review examines Ubiquitin-Specific Protease 30 (USP30) as a master regulator of mitophagy with therapeutic promise in Alzheimer's disease (AD) and Parkinson's disease (PD). USP30's orchestration of mitophagy pathways, encompassing PINK1-dependent and PINK1-independent mechanisms, forms the crux of this exploration.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Method</h3>\u0000 \u0000 <p>A systematic literature search was conducted in PubMed, Scopus, and Web of Science, selecting studies that investigated USP's function, inhibitor design, or therapeutic efficacy in AD and PD. Inclusion criteria encompassed mechanistic and preclinical/clinical data, while irrelevant or duplicate references were excluded. Extracted findings were synthesized narratively.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>USP30 modulates interactions with translocase of outer mitochondrial membrane (TOM) 20, mitochondrial E3 ubiquitin protein ligase 1 (MUL1), and Parkin, thus harmonizing mitochondrial quality control. Emerging novel USP30 inhibitors, racemic phenylalanine derivatives, N-cyano pyrrolidine, and notably, benzosulphonamide class compounds, restore mitophagy, and reduce neurodegenerative phenotypes across diverse models with minimal off-target effects. Modulation of other USPs also influences neurodegenerative disease pathways, offering additional therapeutic avenues.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>In highlighting the nuanced regulation of mitophagy by USP30, this work heralds a shift toward more precise and effective treatments, paving the way for a new era in the clinical management of neurodegenerative disorders.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143057430","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":"The Association Between Aspartate Transaminase to Alanine Transaminase Ratio and Perioperative Ischemic Stroke in Patients With Diabetes: A Retrospective Cohort Study","authors":"Siyuan Liu,&nbsp;Binbin Wang,&nbsp;Libin Ma,&nbsp;Huikai Yang,&nbsp;Min Liu,&nbsp;Yuxiang Song,&nbsp;Zhikang Zhou,&nbsp;Jingsheng Lou,&nbsp;Daming Zhou,&nbsp;Jiangbei Cao,&nbsp;Yanhong Liu,&nbsp;Weidong Mi,&nbsp;Yulong Ma","doi":"10.1111/cns.70223","DOIUrl":"10.1111/cns.70223","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Patients with diabetes are at a high risk for perioperative ischemic stroke (PIS). The use of biomarkers to identify high-risk patients and predict PIS may provide considerable reference value in clinical decision-making. The aspartate transaminase/alanine transaminase ratio (De Ritis ratio) has been proven to be associated with specific diabetic complications. However, the association between the De Ritis ratio and PIS has not been evaluated in this population. This retrospective cohort study aimed to evaluate the association between the preoperative De Ritis ratio and PIS in patients with type 2 diabetes undergoing noncardiovascular surgery.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Data from surgical patients were collected from January 2008 to August 2019. A total of 27,643 patients with type 2 diabetes mellitus (DM) undergoing noncardiovascular surgery under general anesthesia were screened. The optimal De Ritis ratio cutoff value was identified using the receiver operating characteristic (ROC) curve. Logistic regression models were used to evaluate the association between the preoperative De Ritis ratio and PIS. Propensity score matching (PSM), sensitivity analyses, and subgroup analyses were performed to further validate the robustness of this association.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>A total of 151 patients experienced PIS. A De Ritis ratio ≥ 1.04 was associated with an elevated risk of PIS after adjusting for baseline characteristics (OR [95% CI]: 2.25 [1.59–3.21]; <i>p</i> &lt; 0.001), intraoperative parameters (2.50 [1.80–3.49]; <i>p</i> &lt; 0.001), and all confounding variables (2.29 [1.61–3.29]; <i>p</i> &lt; 0.001). In the propensity score-matched cohort, the association between the De Ritis ratio and PIS remained significant (2.04 [1.38–3.05]; <i>p</i> &lt; 0.001). These associations were also consistently maintained in the sensitivity and subgroup analyses.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>An elevated De Ritis ratio is strongly associated with a higher risk of PIS in patients with type 2 DM undergoing noncardiovascular surgery. This may provide additional information on PIS risk assessment in patients with type 2 DM undergoing noncardiovascular surgery.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142996709","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":"Modulating Anxiety-Like Behaviors in Neuropathic Pain: Role of Anterior Cingulate Cortex Astrocytes Activation","authors":"Qingqing Zhou,&nbsp;Qi Zhong,&nbsp;Zhuang Liu,&nbsp;Ziyue Zhao,&nbsp;Jie Wang,&nbsp;Zongze Zhang","doi":"10.1111/cns.70227","DOIUrl":"10.1111/cns.70227","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aims</h3>\u0000 \u0000 <p>The comorbidity of anxiety-like symptoms in neuropathic pain (NP) is a significant yet often overlooked health concern. Anxiety sufferers may have a lower tolerance for pain, but which is difficult to treat. Accumulating evidence suggests a strong link between astrocytes and the manifestation of NP with concurrent anxiety-like behaviors. And the anterior cingulate cortex (ACC) has emerged as a key player in pain modulation and related emotional processing. However, the complex mechanisms that astrocytes in ACC influence anxiety behavior in mouse models of NP remain largely unexplored.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>Utilizing the traditional spared nerve injury (SNI) surgical model, we employed chemogenetic approaches, immunofluorescence, and western blot to investigate the functional significance and interactive dynamics between ACC astrocytes and excitatory neurons.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Our results revealed that SNI surgery induces NP and delayed anxiety-like behaviors, accompanied by increased astrocyte activity in the ACC. Chemogenetic manipulation demonstrated that inhibiting astrocytes alleviates anxiety symptoms, while activating them exacerbates anxiety-like behaviors, affecting local excitatory neurons and synapse density. Direct manipulation of ACC excitatory neurons also significantly impacted anxiety-like behaviors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our results highlight the pivotal role of ACC astrocytes in modulating anxiety-like behavior, suggesting a novel therapeutic strategy for anxiety associated with NP by targeting astrocyte function.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11751476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142996957","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":"Evaluating Brain Activity in Patients With Chronic Disorders of Consciousness After Traumatic Brain Injury Using EEG Microstate Analysis During Hyperbaric Oxygen Therapy","authors":"Long Xu,&nbsp;Jiameng Wang,&nbsp;Cong Wang,&nbsp;Qianqian Ge,&nbsp;Ziqi Ren,&nbsp;Chen He,&nbsp;Yun Liu,&nbsp;Bo Wang,&nbsp;Yaling Liu,&nbsp;Lianbi Xue,&nbsp;Jianghong He,&nbsp;Xudong Zhao,&nbsp;Qiuhong Yu","doi":"10.1111/cns.70220","DOIUrl":"10.1111/cns.70220","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Hyperbaric oxygen (HBO) therapy is an efficacious intervention for patients with prolonged disorders of consciousness (pDOC). Electroencephalographic (EEG) microstate analysis can provide an assessment of the global state of the brain. Currently, the misdiagnosis rate of consciousness-level assessments in patients with pDOC is high. Therefore, we aimed to assess the consciousness levels and outcomes of patients by analyzing changes in EEG signals during HBO therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>EEG data were collected from 32 patients with traumatic brain injury before and after 20 min of HBO therapy. EEG data were obtained during HBO therapy sessions. Modified k-means clustering was used to segment EEG signals into microstates. A paired sample t test was used to compare the microstate characteristics before and during HBO therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>The duration, occurrence, and coverage of microstate D significantly increased in the minimally conscious state (MCS) group after therapy. Significant increases in the same parameters were observed in microstate A among patients in the unresponsive wakefulness state group. Furthermore, patients with greater improvements in Coma Recovery Scale-Revised scores (i.e., improvements of more than three points) showed significant increases in the duration, occurrence, and coverage of microstate D. Both the MCS group and the improvement group presented significant increases in the duration, occurrence, and coverage of microstate D during therapy.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>Microstate D may be associated with the recovery of consciousness levels in patients. This study verified the safety and feasibility of real-time EEG during HBO therapy for patients with pDOC. The changes in EEG microstate characteristics during HBO therapy can serve as a significant complement to electroencephalographic assessment indices for patients with pDOC and may be useful for predicting the recovery of consciousness levels.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11746936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997025","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":"Correction to “Cinchonine and Cinchonidine Alleviate Cisplatin-Induced Ototoxicity by Regulating PI3K-AKT Signaling”","authors":"","doi":"10.1111/cns.70228","DOIUrl":"10.1111/cns.70228","url":null,"abstract":"<p>D. Tang, X. Wang, J. Wu, Y. Li, C. Li, X. Qiao, L. Fan, Y. Chen, H. Zhu, Z. Zhang, and Y. He, “Cinchonine and Cinchonidine Alleviate Cisplatin-Induced Ototoxicity by Regulating PI3K-AKT Signaling,” <i>CNS Neuroscience &amp; Therapeutics</i> 30, no. 2 (2024): e14403, https://doi.org/10.1111/cns.14403.</p><p>We apologize for this error.</p>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11744361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997020","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":"Electroacupuncture Pretreatment Reduces Ischemic Brain Injury by Inhibiting the Lactate Production and Its Derived Protein Lactylation Formation","authors":"Xin-Ru Pan,&nbsp;Yao-Dan Zhang,&nbsp;Yuan-Hui Gan,&nbsp;Jia-Hang Zhang,&nbsp;Su-Jin Gao,&nbsp;Xiao-Shuang Feng,&nbsp;Jia-Xin Xie,&nbsp;Yu-Fei Wang,&nbsp;Xin-Xiao Zhang,&nbsp;Peng-Fei Wang,&nbsp;Shu-Guang Yu,&nbsp;Yong Tang,&nbsp;Xiao-Yi Xiong","doi":"10.1111/cns.70231","DOIUrl":"10.1111/cns.70231","url":null,"abstract":"<div>\u0000 \u0000 \u0000 <section>\u0000 \u0000 <h3> Aim</h3>\u0000 \u0000 <p>Given that electroacupuncture (EA) pretreatment inhibits lactate production and lactate-derived lysine lactation (Kla) aggravates ischemic brain injury, we aimed to investigate whether the formation of Kla protein is involved in EA pretreatment to alleviate ischemic brain injury.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>EA was performed on the Baihui acupoint (GV20) of male C57BL/6J mice before receiving the permanent middle cerebral artery occlusion (pMCAO) surgery. Western blot and immunofluorescent staining were used to observe neuronal survival, astrocyte activation, and protein Kla levels, and the lactate levels in ischemic brains were assayed with a commercial kit. TTC staining and neurological function scores are performed to evaluate the brain damage in mice.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>We found that the increased lactate content and protein Kla levels were significantly decreased in ischemic brain tissue of mice after receiving EA pretreatment, and accompanied by the reduction of astrocyte activation and neuronal injury and death. Meantime, we found that EA pretreatment was effective in reversing the worsening of ischemic brain injury caused by lactate supplementation. However, EA pretreatment did not further reduce the lactate content and protein Kla levels and ameliorate brain injury in ischemic stroke mice after inhibition of glycolysis.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusion</h3>\u0000 \u0000 <p>Our study reveals that EA pretreatment reduced ischemic brain damage by inhibiting lactate production and its derived protein Kla formation in mice with ischemic stroke.</p>\u0000 </section>\u0000 </div>","PeriodicalId":154,"journal":{"name":"CNS Neuroscience & Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11746925/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142997023","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}