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Neural Regeneration Research 2024年第8期19卷 1759-1767页

作者： Zihang Zhou Yalong Yan Heng Gu Ruiao Sun Zihan Liao Ke Xue Chuanxi Tang department of neurobiology Xuzhou Key Laboratory of NeurobiologyXuzhou Medical UniversityXuzhouJiangsu ProvinceChina

Parkinson’s disease can affect not only motor functions but also cognitive abilities,leading to cognitive impairment.One common issue in Parkinson’s disease with cognitive dysfunction is the difficulty in executive functioning.Executive functions help us plan,organize,and control our actions based on our goals.The brain area responsible for executive functions is called the prefrontal co rtex.It acts as the command center for the brain,especially when it comes to regulating executive functions.The role of the prefrontal cortex in cognitive processes is influenced by a chemical messenger called dopamine.However,little is known about how dopamine affects the cognitive functions of patients with Parkinson’s disease.In this article,the authors review the latest research on this topic.They start by looking at how the dopaminergic syste m,is alte red in Parkinson’s disease with executive dysfunction.Then,they explore how these changes in dopamine impact the synaptic structure,electrical activity,and connection components of the prefrontal cortex.The authors also summarize the relationship between Parkinson’s disease and dopamine-related cognitive issues.This information may offer valuable insights and directions for further research and improvement in the clinical treatment of cognitive impairment in Parkinson’s disease.

关键词： dopamine dopamine receptor dopamine transporter executive dysfunction neural network neural oscillation prefrontal cortex synaptic plasticity

Post-transcriptional mechanisms controlling neurogenesis and direct neuronal reprogramming

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Neural Regeneration Research 2024年第9期19卷 1929-1939页

作者： Elsa Papadimitriou Dimitra Thomaidou department of neurobiology Hellenic Pasteur InstituteAthensGreece

Neurogenesis is a tightly regulated process in time and space both in the developing embryo and in adult neurogenic niches.A drastic change in the transcriptome and proteome of radial glial cells or neural stem cells towards the neuronal state is achieved due to sophisticated mechanisms of epigenetic,transcriptional,and post-transcriptional regulation.Understanding these neurogenic mechanisms is of major importance,not only for shedding light on very complex and crucial developmental processes,but also for the identification of putative reprogramming factors,that harbor hierarchically central regulatory roles in the course of neurogenesis and bare thus the capacity to drive direct reprogramming towards the neuronal fate.The major transcriptional programs that orchestrate the neurogenic process have been the focus of research for many years and key neurogenic transcription factors,as well as repressor complexes,have been identified and employed in direct reprogramming protocols to convert non-neuronal cells,into functional neurons.The post-transcriptional regulation of gene expression during nervous system development has emerged as another important and intricate regulatory layer,strongly contributing to the complexity of the mechanisms controlling neurogenesis and neuronal function.In particular,recent advances are highlighting the importance of specific RNA binding proteins that control major steps of mRNA life cycle during neurogenesis,such as alternative splicing,polyadenylation,stability,and translation.Apart from the RNA binding proteins,microRNAs,a class of small non-coding RNAs that block the translation of their target mRNAs,have also been shown to play crucial roles in all the stages of the neurogenic process,from neural stem/progenitor cell proliferation,neuronal differentiation and migration,to functional maturation.Here,we provide an overview of the most prominent post-transcriptional mechanisms mediated by RNA binding proteins and microRNAs during the neurogenic process,giving particular emphasis on

关键词： direct neuronal reprogramming in vivo glia-to-neuron conversion microRNAs neurogenesis post-transcriptional regulation RNA binding proteins

Pipeline Embolization Device for intracranial aneurysms presenting with mass effect:a large Chinese cohort

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Stroke & Vascular Neurology 2024年第1期9卷 50-58页

作者： Yang Zhao Junlin Lu Hongqi Zhang Tianxiao LI Donglei Song Sheng Guan Aisha Maimaitili Yunyan Wang Wenfeng Feng Yang Wang Jieqing Wan Guohua Mao Huaizhang Shi Xinjian Yang Jianmin Liu Yuanli Zhao department of neurosurgery Beijing Tiantan HospitalCapital Medical UniversityBeijingChina department of neurosurgery Peking University International HospitalBeijingChina department of neurosurgery West China HospitalSichuan UniversityChengduSichuanChina department of neurosurgery Xuanwu HospitalCapital Medical UniversityBeijingChina department of Interventional Neuroradiology Zhengzhou University People's HospitalZhengzhouHenanChina department of neurosurgery Shanghai Donglei Brain HospitalShanghaiChina department of Interventional Neuroradiology The First Affiliated Hospital of Zhengzhou UniversityZhengzhouHenanChina department of neurosurgery The First Affiliated Hospital of Xinjiang Medical UniversityUrumqiXinjiangChina department of neurosurgery Qilu Hospital of Shandong University QingdaoJinanShandongChina department of neurosurgery Nanfang HospitalSouthern Medical UniversityGuangzhouGuangdongChina department of neurosurgery The First Affiliated Hospital of Nanchang UniversityNanchangJiangxiChina department of neurosurgery Renji HospitalSchool of MedicineShanghai Jiao Tong UniversityShanghaiChina department of neurosurgery The Second Affiliated Hospital of Nanchang UniversityNanchangJiangxiChina department of neurosurgery The First Affiliated Hospital of Harbin Medical UniversityHarbinHeilongjiangChina department of neurosurgery Changhai HospitalNaval Medical UniversityShanghaiChina

Background Unruptured intracranial aneurysm treatment aims to reduce the risk of aneurysm rupture and bleeding,relieves symptoms and improve the quality of life for patients.This study aimed to assess the safety and efficacy of Pipeline Embolization Device(PED,Covidien/Medtronic,Irvine,CA)treatment for intracranial aneurysms presenting with mass effect in real-world settings.Methods We selected patients from the PED in China Post-Market Multi-Center Registry Study with mass effect presentation.The study endpoints included postoperative mass effect deterioration and mass effect relief at follow-up(3–36 months).We conducted multivariate analysis to identify factors associated with mass effect relief.Subgroup analyses by aneurysm location,size and form were also performed.Results This study included 218 patients with a mean age of 54.3±11.8 years and a female predominance of 74.0%(162/218).The postoperative mass effect deterioration rate was 9.6%(21/218).During a median follow-up period of 8.4 months,the mass effect relief rate was 71.6%(156/218).Notably,immediate aneurysm occlusion following treatment was significantly associated with mass effect relief(OR 0.392,95%CI,0.170 to 0.907,p=0.029).Subgroup analysis demonstrated that adjunctive coiling contributed to mass effect relief in cavernous aneurysms,while dense embolism impeded symptom relief in aneurysms<10mm and saccular aneurysms.Conclusions Our data confirmed the efficacy of PED in relieving mass effect.The findings of this study provide support for endovascular treatment to alleviate mass effect in unruptured intracranial aneurysms.Trial registration number NCT03831672.

关键词： aneurysm intracranial Irvine

Intranasal administration of stem cell-derived exosomes for central nervous system diseases

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Neural Regeneration Research 2024年第6期19卷 1249-1255页

作者： Shuho Gotoh Masahito Kawabori Miki Fujimura department of neurosurgery Hokkaido University Graduate School of Medicine

Exosomes, lipid bilayer-enclosed small cellular vesicles, are actively secreted by various cells and play crucial roles in intercellular communication. These nanosized vesicles transport internalized proteins, mRNA, miRNA, and other bioactive molecules. Recent findings have provided compelling evidence that exosomes derived from stem cells hold great promise as a therapeutic modality for central nervous system disorders. These exosomes exhibit multifaceted properties including antiapoptotic, anti-inflammatory, neurogenic, and vasculogenic effects. Furthermore, exosomes offer several advantages over stem cell therapy, such as high preservation capacity, low immunogenicity, the ability to traverse the blood-brain barrier, and the potential for drug encapsulation. Consequently, researchers have turned their attention to exosomes as a novel therapeutic avenue. Nonetheless, akin to the limitations of stem cell treatment, the limited accumulation of exosomes in the injured brain poses a challenge to their clinical application. To overcome this hurdle, intranasal administration has emerged as a non-invasive and efficacious route for delivering drugs to the central nervous system. By exploiting the olfactory and trigeminal nerve axons, this approach enables the direct transport of therapeutics to the brain while bypassing the blood-brain barrier. Notably, exosomes, owing to their small size, can readily access the nerve pathways using this method. As a result, intranasal administration has gained increasing recognition as an optimal therapeutic strategy for exosomebased treatments. In this comprehensive review, we aim to provide an overview of both basic and clinical research studies investigating the intranasal administration of exosomes for the treatment of central nervous system diseases. Furthermore, we elucidate the underlying therapeutic mechanisms and offer insights into the prospect of this approach.

关键词： central nervous system disease exosome extracellular vesicle intranasal administration stem cell

Clinical features, treatment strategies and outcomes of craniocervical junction arteriovenous fistulas: a cohort study of 193 patients

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Stroke & Vascular Neurology 2024年第1期9卷 18-29页

作者： Yongjie Ma Zihao Song Yinqing Wang Jiachen Wang Chuan He Guilin Li Peng Zhang Tao Hong Liyong Sun Peng Hu Ming Ye Hongqi Zhang department of neurosurgery Xuanwu Hospital Capital Medical University

Background Craniocervical junction(CCJ)arteriovenous fistulas(AVFs)are rare.The current treatment strategies for AVFs with different angioarchitecture need to be clarified.The present study aimed to analyse the correlation between angioarchitecture and clinical characteristics,share our experience in treating this disease and identify risk factors associated with subarachnoid haemorrhage(SAH)and poor outcomes.Methods A total of 198 consecutive patients with CCJ AVFs from our neurosurgical centre were retrospectively reviewed.The patients were grouped according to their clinical manifestations,and their baseline clinical characteristics,angioarchitecture,treatment strategies and outcomes were summarised.Results The patients’median age was 56 years(IQR 47–62 years).The majority of patients were men with 166(83.8%)patients.The most common clinical manifestation was SAH(52.0%),followed by venous hypertensive myelopathy(VHM)(45.5%).The most common CCJ AVFs type was dural AVF,with 132(63.5%)fistulas.The most frequent fistula location was C-1(68.7%)and dural branch of vertebral artery(70.2%)was the most involved arterial feeders for fistulas.The most common direction of venous drainage was descending intradural drainage(40.9%),followed by ascending intradural drainage(36.5%).Microsurgery was the most common treatment strategy applied for 151(76.3%)patients,15(7.6%)patients were treated with interventional embolisation only,and 27(13.6%)received both interventional embolisation and microsurgical treatment.The learning curve for microsurgery only was analysed by cumulative summation method,and the turning point was the 70th case,and blood loss in post-group was lower than that in pre-group(p=0.034).At the last follow-up,there were 155(78.3%)patients with favourable outcomes(modified Rankin Scale(mRS)<3).Age≥56(OR 2.038,95%CI 1.039 to 3.998,p=0.038),VHM as the clinical manifestation(OR 4.102,95%CI 2.108 to 7.982,p<0.001)and pretreatment mRS≥3(OR 3.127,95%CI 1.617 to 6.047,p<0.001)were significantly associated with poor out

关键词： patients treatment hypertensive

Focusing on the tetra-partite synapse in Parkinson’s disease research using human patient-derived neurons

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Neural Regeneration Research 2024年第5期19卷 979-981页

作者： Diogo Cordeiro Tchelet Stern Shani Stern University of Haifa Sagol Department of NeurobiologyHaifaIsrael

Parkinson’s disease(PD)was first described as a neurological disease by Dr.James Parkinson in 1817 as a“shaking palsy”.Since that time,much more is known about the pathophysiology of PD yet the disease is still uncurable.The hallmark of the disease is often considered Lewy body neural inclusions in the substantia nigra pars compacta and other brain areas,although not all patients have these inclusions.The patients exhibit massive neuronal cell loss in the substantia nigra pars compacta,which is associated with the motor symptoms of tremor,bradykinesia,rigidity,and postural instability.PD is the second most common neurodegenerative disease after Alzheimer’s disease with a prevalence of around 1%of individuals over the age of 60.

关键词： patients Alzheimer Focus

miR-200b-3p accelerates progression of pituitary adenomas by negatively regulating expression of RECK

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Oncology Research 2024年第5期32卷 933-941页

作者： XIAOXI WANG YANFEI JIA QIANG LI QIANG YANG YINGFENG LIU BEIFENG WEI XIANG NIU YINJIE ZHANG XIAODONG LUO ZIYU ZHAO PENG WANG department of neurosurgery Tianshui First People’s HospitalTianshuiChina department of neurosurgery The Second Affiliated Hospital of Lanzhou UniversityLanzhouChina

MicroRNA(miR)-200b-3p has been associated with many tumors,but its involvement in pituitary adenoma is unclear.This study investigated the molecular mechanism underlying miR-200b-3p regulation in pituitary adenomas to provide a theoretical basis for treatment.Bioinformatics was used to analyze pituitary adenoma-related genes and screen new targets related to RECK and miRNA.As well,the relationship between miR-200b-3p and RECK protein was verified using a double-luciferase reporter gene assay.The expression of miR-200b-3p in clinical samples was analyzed by in situ hybridization.Transfection of the miR-200b-3p inhibitor and small interfering-RECK(si-RECK)was verified by qPCR.GH3 cell viability and proliferation were detected using CCK8 and EdU assays.Apoptosis was detected by flow cytometry and western blotting.Wound healing and Transwell assays were used to detect cell migration and invasion.The effects of miR-200b-3p and RECK on GH3 cells were verified using salvage experiments.miR-200b-3p was highly expressed in pituitary tumor tissue.Inhibitors of miR-200b-3p inhibited cell proliferation promoted cell apoptosis,inhibited invasion and migration,and inhibited the expression of matrix metalloproteinases.Interestingly,miR-200b-3p negatively regulated RECK.The expression of RECK in pituitary adenoma tissues was lower than that in neighboring tissues.Si-RECK rescued the function of miR-200b-3p inhibitors in the above cellular behaviors,and miR-200b-3p accelerated the development of pituitary adenoma by negatively regulating RECK expression.In summary,this study investigated the molecular mechanism by which miR-200b-3p regulates the progression of pituitary adenoma through the negative regulation of RECK.The findings provide a new target for the treatment of pituitary adenoma.

关键词： Pituitary adenomas miR-200b-3p RECK Matrix metalloproteinase

Upper extremity motor function before and after the cerebrospinal fluid tap test in patients with idiopathic normal pressure hydrocephalus: A retrospective study

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中华医学杂志(英文版) 2024年第7期137卷 877-879页

作者： Liu Caiyan Wei Junji Dong Liling Mao Chenhui Li Jie Huang Xinying Hou Bo Feng Feng Cui Liying Gao Jing department of Neurology Peking Union Medical College Hospital Chinese Academy of Medical Sciences Beijing 100730 China department of neurosurgery department of neurosurgery and Radiology

ATAT1 deficiency enhances microglia/macrophage-mediated erythrophagocytosis and hematoma absorption following intracerebral hemorrhage

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Neural Regeneration Research 2024年第5期19卷 1072-1077页

作者： Yihua Zhang Ping Huang Min Cao Yi Chen Xinhu Zhao Xuzhi He Lunshan Xu department of neurosurgery Daping HospitalArmy Medical UniversityChongqingChina

MIcroglia/macrophage-mediated erythrophagocytosis plays a crucial role in hematoma clearance after intracerebral hemorrhage.Dynamic cytoskeletal changes accompany phagocytosis.However,whether and how these changes are associated with microglia/macrophage-mediated erythrophagocytosis remain unclear.In this study,we investigated the function of acetylatedα-tubulin,a stabilized microtubule form,in microglia/macrophage erythrophagocytosis after intracerebral hemorrhage both in vitro and in vivo.We first assessed the function of acetylatedα-tubulin in erythrophagocytosis using primary DiO GFP-labeled red blood cells co-cultured with the BV2 microglia or RAW264.7 macrophage cell lines.Acetylatedα-tubulin expression was significantly decreased in BV2 and RAW264.7 cells during erythrophagocytosis.Moreover,silencingα-tubulin acetyltransferase 1(ATAT1),a newly discoveredα-tubulin acetyltransferase,decreased Ac-α-tub levels and enhanced the erythrophagocytosis by BV2 and RAW264.7 cells.Consistent with these findings,in ATAT1-/-mice,we observed increased ionized calcium binding adapter molecule 1(Iba1)and Perls-positive microglia/macrophage phagocytes of red blood cells in peri-hematoma and reduced hematoma volume in mice with intracerebral hemorrhage.Additionally,knocking out ATAT1 alleviated neuronal apoptosis and pro-inflammatory cytokines and increased anti-inflammatory cytokines around the hematoma,ultimately improving neurological recovery of mice after intracerebral hemorrhage.These findings suggest that ATAT1 deficiency accelerates erythrophagocytosis by microglia/macrophages and hematoma absorption after intracerebral hemorrhage.These results provide novel insights into the mechanisms of hematoma clearance and suggest ATAT1 as a potential target for the treatment of intracerebral hemorrhage.

关键词： acetylatedα-tubulin α-tubulin acetyltransferase 1(ATAT1) erythrophagocytosis hematoma absorption intracerebral hemorrhage macrophage microglia

Mitochondrial dysfunction and quality control lie at the heart of subarachnoid hemorrhage

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Neural Regeneration Research 2024年第4期19卷 825-832页

作者： Jiatong Zhang Qi Zhu Jie Wang Zheng Peng Zong Zhuang Chunhua Hang Wei Li department of neurosurgery Nanjing Drum Tower HospitalAffiliated Hospital of Medical SchoolNanjing University department of neurosurgery Nanjing Drum Tower HospitalClinical College of Nanjing Medical University

The dramatic increase in intracranial pressure after subarachnoid hemorrhage leads to a decrease in cerebral perfusion pressure and a reduction in cerebral blood flow.Mitochondria are directly affected by direct factors such as ischemia,hypoxia,excitotoxicity,and toxicity of free hemoglobin and its degradation products,which trigger mitochondrial dysfunction.Dysfunctional mitochondria release large amounts of reactive oxygen species,inflammatory mediators,and apoptotic proteins that activate apoptotic pathways,further damaging cells.In response to this array of damage,cells have adopted multiple mitochondrial quality control mechanisms through evolution,including mitochondrial protein quality control,mitochondrial dynamics,mitophagy,mitochondrial biogenesis,and intercellular mitochondrial transfer,to maintain mitochondrial homeostasis under pathological conditions.Specific interventions targeting mitochondrial quality control mechanisms have emerged as promising therapeutic strategies for subarachnoid hemorrhage.This review provides an overview of recent research advances in mitochondrial pathophysiological processes after subarachnoid hemorrhage,particularly mitochondrial quality control mechanisms.It also presents potential therapeutic strategies to target mitochondrial quality control in subarachnoid hemorrhage.

关键词： mitochondrial biogenesis mitochondrial dynamics mitochondrial dysfunction mitochondrial fission and fusion mitochondrial quality control mitophagy subarachnoid hemorrhage