当前的神经血管研究为发表科学严谨的研究提供了一个跨平台，这些研究解决了神经科学中神经元和血管起源的疾病机制。该杂志作为一个国际论坛，出版新颖和原创作品以及及时的神经科学研究文章、细胞发育障碍、可塑性和退化学科的全长/迷你评论，弥合了基础科学研究和临床发现之间的差距。当前的神经血管研究强调阐明疾病机制，包括细胞和分子，这可能会影响神经元和血管疾病的独特治疗策略的发展。

Current Neurovascular Research is an interdisciplinary platform dedicated to publishing scientifically rigorous research that explores the mechanisms of neuron and vascular-related diseases in neuroscience. As an international forum, the journal publishes novel and original research findings, as well as timely articles, full-length and mini-reviews in the fields of neuroscience, cellular developmental disorders, plasticity, and degeneration, aiming to bridge the gap between basic scientific research and clinical discoveries. Current Neurovascular Research emphasizes elucidating disease mechanisms, including cellular and molecular studies, which may advance the development of unique therapeutic strategies for neuron and vascular diseases.

《Current Neurovascular Research》是一个跨学科的平台，致力于发表科学严谨的研究，探讨神经科学中神经元和血管相关疾病的机制。作为一个国际论坛，该杂志发布新颖且原创的研究成果，以及及时的神经科学研究文章、细胞发育障碍、可塑性和退化领域的全长和迷你评论，旨在弥合基础科学研究与临床发现之间的差距。《Current Neurovascular Research》强调阐明疾病机制，包括细胞和分子层面的研究，这些研究可能会推动针对神经元和血管疾病的独特治疗策略的发展。

Current Neurovascular Research

Alcohol abuse is a major health problem worldwide, resulting to extensive admissions in many general hospitals. The overall economic cost of alcohol abuse is enormous worldwide. As a small molecule, alcohol can easily cross membrane barriers and reach different parts of the body very quickly. Attainment of its equilibrium concentration in different cellular compartments depends on the respective water content. Alcohol can affect several parts of the brain, but, in general, contracts brain tissues, destroys brain cells, as well as depresses the central nervous system. Excessive drinking over a prolonged period of time can cause serious problems with cognition and memory. Alcohol interacts with the brain receptors, interfering with the communication between nerve cells, and suppressing excitatory nerve pathway activity. Neuro-cognitive deficits, neuronal injury, and neurodegeneration are well documented in alcoholics, yet the underlying mechanisms remain elusive. The effect can be both direct and/ or indirect. In this review we highlighted the role of alcoholism on the CNS and its impact on human health.

Sukhes Mukherjee

Alcoholism and its Effects on the Central Nervous System

酒精中毒及其对中枢神经系统的影响

Coronary artery stenosis (CAS) ≥50% often coexists in patients with ischemic
stroke, which leads to a significant increase in the occurrence of major vascular events after
stroke. This study aimed to develop a nomogram for diagnosing the presence of ≥50% asymptomatic
CAS in patients with ischemic stroke.
A primary cohort was established that included 275 non-cardioembolic ischemic stroke
patients who were admitted from January 2011 to April 2013 to a teaching hospital in southern China.
The preoperative data were used to construct two models by the best subset regression and the
forward stepwise regression methods, and a nomogram between these models was established. The
assessment of the nomogram was carried out by discrimination and calibration in an internal cohort.
Out of the two models, model 1 contained eight clinical-related variables and exhibited the
lowest Akaike Information Criterion value (322.26) and highest concordance index 0.716 (95% CI,
0.654-0.778). The nomogram showed good calibration and significant clinical benefit according to
calibration curves and the decision curve analysis.
The nomogram, composed of age, sex, NIHSS score on admission, hypertension history,
fast glucose level, HDL cholesterol level, LDL cholesterol level, and presence of ≥50% cervicocephalic
artery stenosis, can be used for prediction of ≥50% asymptomatic coronary artery disease
(CAD). Further studies are needed to validate the effectiveness of this nomogram in other populations.

Youming Long

Jie Yang

Xinguang Yang

Jun Wen

Jiayi Huang

Lihong Jiang

Sha Liao

Chun Lian

Haiyan Yao

Li Huang

Development of a Nomogram for Predicting Asymptomatic Coronary
Artery Disease in Patients with Ischemic Stroke

用于预测缺血性卒中患者无症状冠状动脉疾病列线图的开发

Objective: This study was conducted to evaluate the effects of anti-vascular endothelial growth factor (VEGF) antibody (bevacizumab) on vascular leakage and fibrosis in a monkey choroidal neovascularization (CNV) model. The relationship between fibrotic tissue and subretinal hyper-reflective material (SHRM), in optical coherence tomography (OCT) images, was also investigated. Methods: Experimental CNV was induced in male cynomolgus monkeys by laser photocoagulation. Intravitreal injection of bevacizumab at 0.5 mg/eye/dosing was initiated 2 weeks before or after laser irradiation and thereafter, conducted intermittently at 2- or 3-week intervals. Fluorescein fundus angiography (FA) and OCT imaging were conducted weekly from 2 to 7 weeks after laser irradiation. CNV leakage was evaluated by an established grading method using FA images. To assess the fibrosis and scarring, Masson’s trichrome specimens of each CNV lesion were prepared, and morphometric analysis was conducted using an image analysis software. Results: The effects of bevacizumab on vascular leakage were shown using an established evaluation method. Morphometric analysis of Masson’s trichrome-stained (MT) specimens revealed that collagen fiber synthesis was suppressed by bevacizumab pre-treatment (-29.2%) or post-treatment (-19.2%). SHRM was detected in OCT images in a monkey CNV model, and a significant correlation between the SHRM area in the OCT images and the collagen fiber area in the MT specimens was noted. Conclusion: In the established cynomolgus monkey CNV model, bevacizumab prevented blood leakage but could not completely suppress fibrosis. SHRM in the OCT images reflected retinal fibrous tissue in a laser-induced CNV monkey model. This model might be useful for elucidating the pathology and development therapy for neovascularization or fibrosis.

Satoshi Inagaki

Masamitsu Shimazawa

Koji Hamaguchi

Wataru Otsu

Tomoaki Araki

Yuji Sasaki

Yosuke Numata

Hideshi Tsusaki

Hideaki Hara

Anti-vascular Endothelial Growth Factor Antibody Limits the Vascular Leakage and Decreases Subretinal Fibrosis in a Cynomolgus Monkey Choroidal Neovascularization Model

抗血管内皮生长因子抗体限制血管渗漏并减少食蟹猴脉络膜新生血管模型中的视网膜下纤维化

Multiple viral pathogens can pose a significant health risk to individuals. As a recent example, the &amp;#946;-coronavirus family virion, SARS-CoV-2, has quickly evolved as a pandemic leading to coronavirus disease 2019 (COVID-19) and has been declared by the World Health Organization as a Public Health Emergency of International Concern. To date, no definitive treatment or vaccine application exists for COVID-19. Although new investigations seek to repurpose existing antiviral treatments for COVID-19, innovative treatment strategies not normally considered to have antiviral capabilities may be critical to address this global concern. One such avenue that may prove to be exceedingly fruitful and offer exciting potential as new antiviral therapy involves the mechanistic target of rapamycin (mTOR) and its associated pathways of mTOR Complex 1 (mTORC1), mTOR Complex 2 (mTORC2), and AMP activated protein kinase (AMPK). Recent work has shown that mTOR pathways in conjunction with AMPK may offer valuable targets to control cell injury, oxidative stress, mitochondrial dysfunction, and the onset of hyperinflammation, a significant disability associated with COVID-19. Furthermore, pathways that can activate mTOR may be necessary for anti-hepatitis C activity, reduction of influenza A virus replication, and vital for type-1 interferon responses with influenza vaccination. Yet, important considerations for the development of safe and effective antiviral therapy with mTOR pathways exist. Under some conditions, mTOR can act as a double edge sword and participate in virion replication and virion release from cells. Future work with mTOR as a potential antiviral target is highly warranted and with a greater understanding of this novel pathway, new treatments against several viral pathogens may successfully emerge.

Kenneth Maiese

The Mechanistic Target of Rapamycin (mTOR): Novel Considerations as an Antiviral Treatment

雷帕霉素机制靶点（mTOR）：作为抗病毒治疗的全新考量

Background: Stroke, primarily known as ischemic stroke, is a leading cause of mortality and disability worldwide. Reperfusion after the ischemia stroke resolves is necessary for maintaining the health of brain tissues; however, it also induces inflammation and oxidative stress, resulting in brain injury. This study aimed to investigate the role of circ0001679 in the pathology of I/R (Ischemia/Reperfusion)-induced brain injury and explore its therapeutic potential for I/R injury. Methods: The Oxygen-Glucose Deprivation/Re-oxygenation (OGD/R) model was employed in primary mouse astrocytes, and the Middle Cerebral Artery Occlusion (MCAO) model was established in mice to mimic ischemia-reperfusion-induced injury. Si-circ0001679, anti-miR- 216, and TLR4 ORF-clone were transfected either in cells or mice to study the molecular mechanisms during I/R-induced injury. Inflammation and oxidative stress were monitored after treatment. Results: Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress. Conclusion: This study unveiled a novel regulatory axis of circ0001679-miR-216-TLR4 in I/Rinduced brain injury. Targeting circ0001679 may represent a promising therapeutic strategy for I/R-induced brain injury. result: Upregulated gene expression of circ0001679 was noticed in both OGD/R-treated primary mouse astrocytes and MCAO-induced mouse brain tissue. Silencing circ0001679 reduced cellular damage, inflammation, and oxidative stress induced by OGD/R treatment. Knocking down of circ0001679 alone with either miR-216 inhibition or TLR4 overexpression increased the inflammation response and oxidative stress compared to circ0001679 silencing only. Moreover, inhibition of circ0001679 attenuated brain injury in MCAO-treated mice via reduced infarction, neuronal damage, apoptosis, inflammation, and oxidative stress.

Chenrui Zhang

Liaoyu Li

Feng Wang

Hailong Du

Xiaoliang Wang

Xiaoyu Gu

Xinlei Liu

Haie Han

Jianliang Wu

Jianping Sun

Inhibition of Circ0001679 Alleviates Ischemia/Reperfusion-induced Brain Injury via miR-216/TLR4 Regulatory Axis

抑制Circ0001679通过miR-216/TLR4调控轴减轻缺血/再灌注诱导的脑损伤

Curr Neurovasc Res

Wnt Signaling, Musculoskeletal Disease, and the Onset of Dementia and Alzheimer's Disease

Wnt信号通路、肌肉骨骼疾病与痴呆和阿尔茨海默病的发病

Objective: The aim of this study was to explore the primary changes in corneal nerve fiber structure and its influencing factors in patients with primary glaucoma. Method: A retrospective analysis was conducted in this study. A total of 51 patients with primary glaucoma who were diagnosed and treated in our hospital from March 2020 to March 2022 were selected as the research objects and designated as the glaucoma group. In addition, 51 patients with normal eyes were chosen as the control group. The characteristic changes of corneal nerve fibers, the thickness of the nerve fiber layer, and the number of ganglion cell complexes and dendritic cells were measured. Multivariate logistic regression analysis was performed to analyze the influencing factors of ganglion fiber structure change. Result: Compared with the control group, the length of corneal nerve fibers and the density of corneal nerve fibers in the glaucoma group were significantly shortened, the number of branches was significantly reduced, the curvature was significantly increased, and the number of dendritic cells was significantly increased (P &lt;0.05). Compared with the control group, the thickness of the upper, lower, nasal, temporal, and peripheral nerve fiber layers in the glaucoma group was obviously reduced (P &lt;0.05). Compared with the control group, the thickness of the above inferior, nasal, temporal, and peripheral nerve fiber layers in the glaucoma group was significantly reduced (P &lt;0.05). Compared with the control group, the above, below, and mean ganglion cell complex thickness in the glaucoma group was significantly reduced (P &lt;0.05). Logistic regression analysis showed that intraocular pressure and the number of dendritic cells were risk factors for ganglion fiber structure change. In contrast, nerve fiber layer thickness and ganglion cell complex were protective factors for ganglion fiber structure change (P &lt;0.05). Conclusion: There were primary changes in the structure of corneal nerve fibers in patients with primary glaucoma, which were more slender, tortuous, and sparse, and the primary changes in nerve fiber structure could be affected by intraocular pressure, the number of dendritic cells, the thickness of the nerve fiber layer, and the ganglion cell complex.

Mingming Cai

Jie Zhang

Lin Xie

Primary Changes in Corneal Nerve Fiber Structure in Patients with Primary Glaucoma and Related Influencing Factors

原发性青光眼患者角膜神经纤维结构的主要变化及相关影响因素

Ischemic stroke due to Large Vessel Occlusion (LVO) represents a critical and time-sensitive neurological emergency. Advancements in imaging technology and endovascular therapies have transformed the management of LVO. Nonetheless, thrombectomy failure diminishes the chances of patients achieving a favorable clinical outcome.

Beny Rilianto

Ricky Gusanto Kurniawan

Bambang Tri Prasetyo

Nurfadilah M. Rajab

Abrar Arham

Thrombectomy Failure and Associated Factors for Large-vessel Occlusion Stroke

大血管闭塞性卒中血栓切除术失败及关联因素

Background: Electroacupuncture (EA) exerts a protective role in Blood-Brain Barrier (BBB) damage after ischemic stroke, but whether this effect involves the regulation of the pericytes in vitro is unclear. Methods: The in vitro BBB models were established with brain microvascular endothelial cells (BMECs) and pericytes, and the co-cultured cells were randomly divided into three groups: the control group, oxygen-glucose deprivation/reoxygenation (OGD/R) group and EA group. OGD/R was performed to simulate cerebral ischemia-reperfusion in vitro. EA serum was prepared by EA treatment at the “Renzhong” (GV26) and “Baihui” (GV20) acupoints in middle cerebral artery occlusion/ reperfusion rats. Furthermore, the characteristics of BMECs and pericytes were identified with immunohistochemistry staining. The cell morphology of the BBB model was observed using an inverted microscope. The function of BBB was measured with transendothelial electrical resistance (TEER) and sodium fluorescein, and the viability, apoptosis, and migration of pericytes were detected by cell counting kit-8, flow cytometry, and Transwell migration assay. Results: BMECs were positive staining for Factor-VIII, and pericytes were positive staining for the α-SMA and NG2. EA serum improved cell morphology of the BBB model increased TEER, and decreased sodium fluorescein in OGD/R condition. Besides, EA serum alleviated pericytes” apoptosis rate and migration number, and enhanced pericytes' viability rate in OGD/R condition. Conclusion: EA serum protects against BBB damage induced by OGD/R in vitro, and this protection might be achieved by attenuating pericytes apoptosis and migration, as well as enhancing pericytes viability. The findings provided new evidence for EA as a medical therapy for ischemic stroke.

Hanrui Zhang

Hequn Lyv

Yaoting Feng

Yongjun Peng

Electroacupuncture Serum Protects Blood-brain Barrier Damage after Ischemic Stroke BY Regulating the Pericytes in vitro

电针血清通过体外调节周细胞保护缺血性卒中后的血脑屏障损伤

Abbreviation	CNR
Journal Impact	1.94
Quartiles(Global)	NEUROSCIENCES(Q3)

ISSN	1567-2026, 1875-5739
h-index	60

Publication Information	Publisher: Bentham Science Publishers，Publishing cycle: Quarterly，Journal Type: journal，Open Access Journals: No
Basic data	Year of publication: 2004，Proportion of original research papers: 100.00%，Self Citation Rate:10.00%， Gold OA Rate: 2.23%
Average review cycle	网友分享经验：平均3月
Average recruitment ratio	网友分享经验：约50%

Current Neurovascular Research

Journal Citation Format

A journal article with 1 author

A journal article with 2 authors

A journal article with 3 authors

A journal article with 5 or more authors

Books Citation Format

Thesis Citation Format

Web sites Citation Format

Patent Citation Format

Staying up late manually editing references? ivySCI automatically matches journals and helps you generate references with a single click.

Share Submission Experience

Alcoholism and its Effects on the Central Nervous System

Development of a Nomogram for Predicting Asymptomatic Coronary Artery Disease in Patients with Ischemic Stroke

Anti-vascular Endothelial Growth Factor Antibody Limits the Vascular Leakage and Decreases Subretinal Fibrosis in a Cynomolgus Monkey Choroidal Neovascularization Model

The Mechanistic Target of Rapamycin (mTOR): Novel Considerations as an Antiviral Treatment

Inhibition of Circ0001679 Alleviates Ischemia/Reperfusion-induced Brain Injury via miR-216/TLR4 Regulatory Axis

Inhibition of Circ0001679 Alleviates Ischemia/Reperfusion-induced Brain Injury via miR-216/TLR4 Regulatory Axis

Wnt Signaling, Musculoskeletal Disease, and the Onset of Dementia and Alzheimer's Disease

Primary Changes in Corneal Nerve Fiber Structure in Patients with Primary Glaucoma and Related Influencing Factors

Thrombectomy Failure and Associated Factors for Large-vessel Occlusion Stroke

Electroacupuncture Serum Protects Blood-brain Barrier Damage after Ischemic Stroke BY Regulating the Pericytes in vitro