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| 1 | Caspase-3 activation as a bifurcation point between plasticity and cell death显示文摘Death-mediating proteases such as caspases and caspase-3 in particular,have been implicated in neurodegenerative processes,aging and Alzheimer's disease.However,emerging evidence suggests that in addition to their classical role in cell death,caspases play a key role in modulating synaptic function.It is remarkable that active caspases-3,which can trigger widespread damage and degeneration,aggregates in structures as delicate as synapses and persists in neurons without causing acute cell death.Here,we evaluate this dichotomy,and discuss the hypothesis that caspase-3 may be a bifurcation point in cellular signaling,able to orient the neuronal response to stress down either pathological/apoptotic pathways or towards physiological cellular remodeling.We propose that temporal,spatial and other regulators of caspase activity are key determinants of the ultimate effect of caspase-3 activation in neurons.This concept has implications for differential roles of caspase-3 activation across the lifespan.Specifically,we propose that limited caspase-3 activation is critical for synaptic function in the healthy adult brain while chronic activation is involved in degenerative processes in the aging brain. | Shikha Snigdha Erica D Smith G Aleph Prieto Carl W Cotman | 2012 | Neuroscience Bulletin2012，28，1： | 91 |
| 2 | Prevalence of Autism Spectrum Disorder in China:A Nationwide Multi-center Population-based Study Among Children Aged 6 to 12 Years显示文摘This study aimed to obtain the first national estimate of the prevalence of autism spectrum disorder(ASD) in Chinese children.We targeted the population of 6 to 12-year-old children for this prevalence study by multistage convenient cluster sampling.The Modified Chinese Autism Spectrum Rating Scale was used for the screening process.Of the target population of 142,086 children,88.5%(n=125,806) participated in the study.A total of 363 children were confirmed as having ASD.The observed ASD prevalence rate was 0.29%(95% CI:0.26%-0.32%) for the overall population.After adjustment for response rates,the estimated number of ASD cases was867 in the target population sample,thereby achieving an estimated prevalence of 0.70%(95% CI:0.64%-0.74%).The prevalence was significantly higher in boys than in girls(0.95%;95% CI:0.87%-1.02% versus 0.30%;95%CI:0.26%-0.34%;P <0.001).Of the 363 confirmed ASD cases,43.3% were newly diagnosed,and most of those(90.4%) were attending regular schools,and 68.8% of the children with ASD had at least one neuropsychiatric comorbidity.Our findings provide reliable data on the estimated ASD prevalence and comorbidities in Chinese children. | Hao Zhou Xiu Xu Weili Yan Xiaobing Zou Lijie Wu Xuerong Luo Tingyu Li Yi Huang Hongyan Guan Xiang Chen Meng Mao Kun Xia Lan Zhang Erzhen Li Xiaoling Ge Lili Zhang Chunpei Li Xudong Zhang Yuanfeng Zhou Ding Ding Andy Shih Eric Fombonne Yi Zheng Jisheng Han Zhongsheng Sun Yong-hui Jiang Yi Wang LATENT-NHC Study Team | 2020 | Neuroscience Bulletin2020，36，9： | 158 |
| 3 | Oxidative stress in Alzheimer's disease显示文摘Oxidative stress plays a significant role in the pathogenesis of Alzheimer's disease(AD), a devastating disease of the elderly. The brain is more vulnerable than other organs to oxidative stress, and most of the components of neurons(lipids, proteins, and nucleic acids) can be oxidized in AD due to mitochondrial dysfunction, increased metal levels, infl ammation, and β-amyloid(Aβ) peptides. Oxidative stress participates in the development of AD by promoting Aβ deposition, tau hyperphosphorylation, and the subsequent loss of synapses and neurons. The relationship between oxidative stress and AD suggests that oxidative stress is an essential part of the pathological process, and antioxidants may be useful for AD treatment. | Zhichun Chen Chunjiu Zhong | 2014 | Neuroscience Bulletin2014，30，2： | 66 |
| 4 | Dual Functions of Microglia in Ischemic Stroke显示文摘Ischemic stroke is a leading cause of morbidity and mortality worldwide. Resident microglia are the principal immune cells of the brain, and the first to respond to the pathophysiological changes induced by ischemic stroke. Traditionally, it has been thought that microglial activation is deleterious in ischemic stroke, and therapies to suppress it have been intensively explored. However,increasing evidence suggests that microglial activation is also critical for neurogenesis, angiogenesis, and synaptic remodeling, thereby promoting functional recovery after cerebral ischemia. Here, we comprehensively review the dual role of microglia during the different phases of ischemic stroke, and the possible mechanisms controlling the post-ischemic activity of microglia. In addition, we discuss the dynamic interactions between microglia and other cells, such as neurons, astrocytes, oligodendrocytes,and endothelial cells within the brain parenchyma and the neurovascular unit. | Chuan Qin Luo-Qi Zhou Xiao-Tong Ma Zi-Wei Hu Sheng Yang Man Chen Dale B. Bosco Long-Jun Wu Dai-Shi Tian | 2019 | Neuroscience Bulletin2019，35，5： | 64 |
| 5 | Wilson's Disease in China显示文摘Wilson's disease(WD) is an autosomal recessive disorder of copper metabolism. Its incidence is higher in China than in western countries. ATP7 B is the causative gene and encodes a P-type ATPase, which participates in the synthesis of holoceruloplasmin and copper excretion. Disease-causing variants of ATP7 B disrupt the normal structure or function of the enzyme and cause copper deposition in multiple organs,leading to diverse clinical manifestations. Given the variety of presentations, misdiagnosis is not rare. Genetic diagnosis plays an important role and has gradually become a routine test in China. The first Chinese spectrum of disease-causing mutations of ATP7 B has been established. As a remediable hereditary disorder, most WD patients have a good prognosis with an early diagnosis and chelation treatment. However, clinical trials are relatively few in China, and most treatments are based on the experience of experts and evidences from other countries. It is necessary to study and develop appropriate regimens specific for Chinese WD patients. | Juan-Juan Xie Zhi-Ying Wu | 2017 | Neuroscience Bulletin2017，33，3： | 54 |
| 6 | Biomarkers for Parkinson's Disease:Recent Advancement显示文摘As a multi-factorial degenerative disease,Parkinson's disease(PD) leads to tremor, gait rigidity,and hypokinesia, thus hampering normal living. As this disease is usually detected in the later stages when neurons have degenerated completely, cure is on hold, ultimately leading to death due to the lack of early diagnostic techniques. Thus, biomarkers are required to detect the disease in the early stages when prevention is possible.Various biomarkers providing early diagnosis of the disease include those of imaging, cerebrospinal fluid,oxidative stress, neuroprotection, and inflammation. Also,biomarkers, alone or in combination, are used in the diagnosis and evolution of PD. This review encompasses various biomarkers available for PD and discusses recent advances in their development. | Sharvari Lotankar Kedar S Prabhavalkar Lokesh K Bhatt | 2017 | Neuroscience Bulletin2017，33，5： | 41 |
| 7 | Regulation of Pain and Itch by TRP Channels显示文摘Nociception is an important physiological process that detects harmful signals and results in pain perception. In this review, we discuss important experimental evidence involving some TRP ion channels as molecular sensors of chemical, thermal, and mechanical noxious stimuli to evoke the pain and itch sensations.Among them are the TRPA1 channel, members of the vanilloid subfamily(TRPV1, TRPV3, and TRPV4), and finally members of the melastatin group(TRPM2, TRPM3,and TRPM8). Given that pain and itch are pro-survival,evolutionarily-honed protective mechanisms, care has to be exercised when developing inhibitory/modulatory compounds targeting specific pain/itch-TRPs so that physiological protective mechanisms are not disabled to a degree that stimulus-mediated injury can occur. Such events have impeded the development of safe and effective TRPV1-modulating compounds and have diverted substantial resources. A beneficial outcome can be readily accomplished via simple dosing strategies, and also by incorporating medicinal chemistry design features during compound design and synthesis. Beyond clinical use,where compounds that target more than one channel might have a place and possibly have advantageous features,highly specific and high-potency compounds will be helpful in mechanistic discovery at the structure-function level. | Carlene Moore Rupali Gupta Sven-Eric Jordt Yong Chen Wolfgang B.Liedtke | 2018 | Neuroscience Bulletin2018，34，1： | 39 |
| 8 | An Overview of Autism Spectrum Disorder, Heterogeneity and Treatment Options显示文摘Since the documented observations of Kanner in1943, there has been great debate about the diagnoses, the sub-types, and the diagnostic threshold that relates to what is now known as autism spectrum disorder(ASD).Re?ecting this complicated history, there has been continual re?nement from DSM-III with ‘Infantile Autism' to the current DSM-V diagnosis. The disorder is now widely accepted as a complex, pervasive, heterogeneous condition with multiple etiologies, sub-types, and developmental trajectories. Diagnosis remains based on observation of atypical behaviors, with criteria of persistent de?cits in social communication and restricted and repetitive patterns of behavior. This review provides a broad overview of the history, prevalence, etiology, clinical presentation, and heterogeneity of ASD. Factors contributing to heterogeneity, including genetic variability, comorbidity, and gender are reviewed. We then explore current evidencebased pharmacological and behavioral treatments for ASD and highlight the complexities of conducting clinical trials that evaluate therapeutic ef?cacy in ASD populations.Finally, we discuss the potential of a new wave of research examining objective biomarkers to facilitate the evaluation of sub-typing, diagnosis, and treatment response in ASD. | Anne Masi Marilena M.De Mayo Nicholas Glozier Adam J.Guastella | 2017 | Neuroscience Bulletin2017，33，2： | 33 |
| 9 | Gastrodin Attenuates Pentylenetetrazole-Induced Seizures by Modulating the Mitogen-Activated Protein Kinase-Associated Inflammatory Responses in Mice显示文摘Gastrodin, the major component isolated from the rhizome of the Chinese traditional medicinal herb Gastrodia elata(‘‘Tianma''), has a long history in the treatment of epilepsy and other neurological disorders.However, the molecular mechanisms are not clear. Here,we found that gastrodin ameliorated pentylenetetrazole(PTZ)-induced epileptic seizures with improvement of the electroencephalographic pattern in mice. Further studies demonstrated that gastrodin decreased the levels of the pro-inflammatory cytokines interleukin-1b and tumor necrosis factor-a while increasing interleukin-10, an antiinflammatory cytokine in the brain. Furthermore, gastrodin attenuated the PTZ-induced microglial activation along with inhibition of mitogen-activated protein kinases,c AMP response element binding protein, and NF-j B. Our data suggest that gastrodin attenuates seizures by modulating the mitogen-activated protein kinase-associated inflammatory responses. | Liming Chen Xinan Liu Hua Wang Min Qu | 2017 | Neuroscience Bulletin2017，33，3： | 31 |
| 10 | Emerging role of Toll-like receptors in the control of pain and itch显示文摘Toll-like receptors (TLRs) are germline-encoded pattern-recognition receptors that initiate innate immune responses by recognizing molecular structures shared by a wide range of pathogens, known as pathogen-associated molecular patterns (PAMPs). After tissue injury or cellular stress, TLRs also detect endogenous ligands known as danger-associated molecular patterns (DAMPs). TLRs are expressed in both non-neuronal and neuronal cell types in the central nervous system (CNS) and contribute to both infectious and non-infectious disorders in the CNS. Following tissue insult and nerve injury, TLRs (such as TLR2, TLR3, and TLR4) induce the activation of microglia and astrocytes and the production of the proinflammatory cytokines in the spinal cord, leading to the development and maintenance of inflammatory pain and neuropathic pain. In particular, primary sensory neurons, such as nociceptors, express TLRs (e.g., TLR4 and TLR7) to sense exogenous PAMPs and endogenous DAMPs released after tissue injury and cellular stress. These neuronal TLRs are new players in the processing of pain and itch by increasing the excitability of primary sensory neurons. Given the prevalence of chronic pain and itch and the suffering of affected people, insights into TLR signaling in the nervous system will open a new avenue for the management of clinical pain and itch. | Tong Liu Yong-Jing Gao Ru-Rong Ji | 2012 | Neuroscience Bulletin2012，28，2： | 30 |
| 11 | Hydroxysafflor yellow A improves learning and memory in a rat model of vascular dementia by increasing VEGF and NR1 in the hippocampus显示文摘Hydroxysafflor yellow A(HSYA) has angiogenesisregulating and neuro-protective effects, but its effects on vascular dementia(VaD) are unknown. In this study, 30 adult Sprague-Dawley rats were randomly allocated to five groups: normal, sham-operation, VaD alone(bilateral carotid artery occlusion), VaD plus saline(control), and VaD plus HSYA. One week after operation, the HSYA group received one daily tail-vein injection of 0.6 mg/100 g HSYA for two weeks. Five weeks after operation, the spatial memory of all five groups was evaluated by the water maze task, and synaptic plasticity in the hippocampus was assessed by the long-term potentiation(LTP) method. Vascular endothelial growth factor(VEGF) and N-methyl-Daspartic acid receptor 1(NR1) expression in the hippocampus was detected via Western blot. We found that, compared with the group with VaD alone, the group with HSYA had a reduced escape latency in the water maze(P <0.05), and the LTP at CA3-CA1 synapses in the hippocampus was enhanced(P <0.05). Western blot in the late-phase VaD group showed slight up-regulation of VEGF and downregulation of NR1 in the hippocampus, while HSYA significantly up-regulated both VEGF and NR1. Theseresults suggested that HSYA promotes angiogenesis and increases synaptic plasticity, thus improving spatial learning and memory in the rat model of VaD. | Nan Zhang Mengya Xing Yiyi Wang Hao Liang Zhuo Yang Fudong Shi Yan Cheng | 2014 | Neuroscience Bulletin2014，30，3： | 30 |
| 12 | Clinical Research on Alzheimer's Disease: Progress and Perspectives显示文摘Alzheimer's disease(AD), the most common type of dementia, is becoming a major challenge for global health and social care. However, the current understanding of AD pathogenesis is limited, and no early diagnosis and disease-modifying therapy are currently available. During the past year, significant progress has been made in clinical research on the diagnosis, prevention, and treatment of AD.In this review, we summarize the latest achievements,including diagnostic biomarkers, polygenic hazard score,amyloid and tau PET imaging, clinical trials targeting amyloid-beta(Ab), tau, and neurotransmitters, early intervention, and primary prevention and systemic intervention approaches, and provide novel perspectives for further efforts to understand and cure the disease. | Bin-Lu Sun Wei-Wei Li Chi Zhu Wang-Sheng Jin Fan Zeng Yu-Hui Liu Xian-Le Bu Jie Zhu Xiu-Qing Yao Yan-Jiang Wang | 2018 | Neuroscience Bulletin2018，34，6： | 29 |
| 13 | 脑小血管病的临床特点及病理生理机制(英文)显示文摘小血管病与慢性脑循环障碍相关,占缺血性卒中的20%-30%,也是大部分脑出血和脑病的病因所在。与小血管病相关的疾病包括Binswanger病、多发小灶中风和微出血,这些疾病在老年人中的发病率极高,且往往导致认知减退或血管性痴呆、步态和平衡障碍、情绪低落、尿失禁等。小血管病相关性脑病预示着老年人跌倒、致残和死亡的几率增加,因此其临床特点和病理生理机制正日益受到关注。本文对脑小血管病的危险因素、发病机制、病理以及临床表现作一综述。 | 张爱娟 于新军 王梅 | 2010 | Neuroscience Bulletin2010，26，3： | 27 |
| 14 | The glial scar in spinal cord injury and repair显示文摘Glial scarring following severe tissue damage and inflammation after spinal cord injury (SCi) is due to an extreme, uncontrolled form of reactive astrogliosis that typically occurs around the injury site. The scarring process includes the misalignment of activated astrocytes and the deposition of inhibitory chondroitin sulfate proteoglycans. Here, we first discuss recent developments in the molecular and cellular features of glial scar formation, with special focus on the potential cellular origin of scar-forming cells and the molecular mechanisms underlying glial scar formation after SCi. Second, we discuss the role of glial scar formation in the regulation of axonal regeneration and the cascades of neuro-inflammation. Last, we summarize the physical and pharmacological approaches targeting the modulation of glial scarring to better understand the role of glial scar formation in the repair of SCi. | Yi-Min Yuan Cheng He | 2013 | Neuroscience Bulletin2013，29，4： | 28 |
| 15 | Sleep and Cognitive Abnormalities in Acute Minor Thalamic Infarction显示文摘In order to characterize sleep and the cognitive patterns in patients with acute minor thalamic infarction(AMTI), we enrolled 27 patients with AMTI and 12 matched healthy individuals. Questionnaires about sleep and cognition as well as polysomnography(PSG) were performed on days 14 and 90 post-stroke. Compared to healthy controls, in patients with AMTI, hyposomnia was more prevalent; sleep architecture was disrupted as indicated by decreased sleep efficiency, increased sleep latency, and decreased non-rapid eye movement sleep stages 2 and 3;more sleep-related breathing disorders occurred; and cognitive functions were worse, especially memory. While sleep apnea and long-delay memory recovered to a large extent in the patients, other sleep and cognitive function deficit often persisted. Patients with AMTI are at an increased risk for hyposomnia, sleep structure disturbance,sleep apnea, and memory deficits. Although these abnormalities improved over time, the slow and incomplete improvement suggest that early management should be considered in these patients. | Wei Wu Linyang Cui Ying Fu Qianqian Tian Lei Liu Xuan Zhang Ning Du Ying Chen Zhijun Qiu Yijun Song Fu-Dong Shi Rong Xue | 2016 | Neuroscience Bulletin2016，32，4： | 28 |
| 16 | Neuronal autophagy in cerebral ischemia显示文摘Autophagy has evolved as a conserved process for the bulk degradation and recycling of cytosolic components, such as long-lived proteins and organelles. In neurons, autophagy is important for homeostasis and protein quality control and is maintained at relatively low levels under normal conditions, while it is upregulated in response to pathophysiological conditions, such as cerebral ischemic injury. However, the role of autophagy is more complex. It depends on age or brain maturity, region, severity of insult, and the stage of ischemia. Whether autophagy plays a beneficial or a detrimental role in cerebral ischemia depends on various pathological conditions. In this review, we elucidate the role of neuronal autophagy in cerebral ischemia. | Feng Xu Jin-Hua Gu Zheng-Hong Qin | 2012 | Neuroscience Bulletin2012，28，5： | 26 |
| 17 | Experimental animal models and infl ammatory cellular changes in cerebral ischemic and hemorrhagic stroke显示文摘Stroke,including cerebral ischemia,intracerebral hemorrhage,and subarachnoid hemorrhage,is the leading cause of long-term disability and death worldwide. Animal models have greatly contributed to our understanding of the risk factors and the pathophysiology of stroke,as well as the development of therapeutic strategies for its treatment. Further development and investigation of experimental models,however,are needed to elucidate the pathogenesis of stroke and to enhance and expand novel therapeutic targets. In this article,we provide an overview of the characteristics of commonly-used animal models of stroke and focus on the infl ammatory responses to cerebral stroke,which may provide insights into a framework for developing effective therapies for stroke in humans. | Tao Yan Michael Chopp Jieli Chen | 2015 | Neuroscience Bulletin2015，31，6： | 26 |
| 18 | Olfactory Dysfunction as an Early Biomarker in Parkinson's Disease显示文摘Olfactory dysfunction is common in Parkinson's disease(PD) and often predates the diagnosis by years,reflecting early deposition of Lewy pathology, the histologic hallmark of PD, in the olfactory bulb. Clinical tests are available that allow for the rapid characterization of olfactory dysfunction, including tests of odor identification,discrimination, detection, and recognition thresholds,memory, and tests assessing the build-up of odor intensity across increasing suprathreshold stimulus concentrations.The high prevalence of olfactory impairment, along with the ease and low cost of assessment, has fostered great interest in olfaction as a potential biomarker for PD.Hyposmia may help differentiate PD from other causes of parkinsonism, and may also aid in the identification of‘‘pre-motor'' PD due to the early pathologic involvement of olfactory pathways. Olfactory function is also correlated with other non-motor features of PD and may serve as a predictor of cognitive decline. In this article, we summarize the existing literature on olfaction in PD, focusing on the potential for olfaction as a biomarker for early or differential diagnosis and prognosis. | Michelle E.Fullard James F.Morley John E.Duda | 2017 | Neuroscience Bulletin2017，33，5： | 26 |
| 19 | Up-Regulation of Trem2 Inhibits Hippocampal Neuronal Apoptosis and Alleviates Oxidative Stress in Epilepsy via the PI3K/Akt Pathway in Mice显示文摘Epilepsy is a chronic and severe neurological disorder that has negative effects on the autonomous activities of patients. Functionally, Trem2(triggering receptor expressed on myeloid cells-2) is an immunoglobulin receptor that affects neurological and psychiatric genetic diseases. Based on this rationale, we aimed to assess the potential role of Trem2 integration with the PI3 K/Akt pathway in epilepsy. We used microarray-based gene expression profiling to identify epilepsy-related differentially-expressed genes. In a mouse hippocampal neuron model of epilepsy, neurons were treated with lowMg^2+ extracellular fluid, and the protein and mRNA expression of Trem2 were determined. Using a gain-offunction approach with Trem2, neuronal apoptosis and its related factors were assessed by flow cytometry, RT-qPCR,and Western blot analysis. In a pilocarpine-induced epileptic mouse model, the malondialdehyde(MDA) and8-hydroxy-20-deoxyguanosine(8-OHdG) content and superoxide dismutase(SOD) and glutathione-peroxidase(GSH-Px) activity in the hippocampus were determined,and the protein expression of Trem2 was measured. In addition, the regulatory effect of Trem2 on the PI3 K/Akt pathway was analyzed by inhibiting this pathway in both the cell and mouse models of epilepsy. Trem2 was found to occupy a core position and was correlated with epilepsy.Trem2 was decreased in the hippocampus of epileptic miceand epileptic hippocampal neurons. Of crucial importance,overexpression of Trem2 activated the PI3 K/Akt pathway to inhibit neuronal apoptosis. Moreover, activation of the PI3 K/Akt pathway through over-expression of Trem2 alleviated oxidative stress, as shown by the increased expression of SOD and GSH-Px and the decreased expression of MDA and 8-OHdG. The current study defines the potential role of Trem2 in inhibiting the development of epilepsy, indicating that Trem2 up-regulation alleviates hippocampal neuronal injury and oxidative stress, and inhibits neuronal apoptosis in epilepsy by activating the PI3 K/Akt pathway. | Ai-Hua Liu Min Chu Yu-Ping Wang | 2019 | Neuroscience Bulletin2019，35，3： | 25 |
| 20 | Local synchronization and amplitude of the fluctuation of spontaneous brain activity in attention-deficit/hyperactivity disorder:a resting-state fMRI study显示文摘Regional homogeneity(ReHo)and the amplitude of low-frequency fluctuation(ALFF)are two approaches to depicting different regional characteristics of resting-state functional magnetic resonance imaging(RS-fMRI)data.Whether they can complementarily reveal brain regional functional abnormalities in attention-deficit/hyperactivity disorder(ADHD)remains unknown.In this study,we applied ReHo and ALFF to 23 medication-na ve boys diagnosed with ADHD and 25 age-matched healthy male controls using whole-brain voxel-wise analysis.Correlation analyses were conducted in the ADHD group to investigate the relationship between the regional spontaneous brain activity measured by the two approaches and the clinical symptoms of ADHD.We found that the ReHo method showed widely-distributed differences between the two groups in the fronto-cingulo-occipitocerebellar circuitry,while the ALFF method showed a difference only in the right occipital area.When a larger smoothing kernel and a more lenient threshold were used for ALFF,more overlapped regions were found between ALFF and ReHo,and ALFF even found some new regions with group differences.The ADHD symptom scores were correlated with the ReHo values in the right cerebellum,dorsal anterior cingulate cortex and left lingual gyrus in the ADHD group,while no correlation was detected between ALFF and ADHD symptoms.In conclusion,ReHo may be more sensitive to regional abnormalities,at least in boys with ADHD,than ALFF.And ALFF may be complementary to ReHo in measuring local spontaneous activity.Combination of the two may yield a more comprehensive pathophy-siological framework for ADHD. | Li An Qing-Jiu Cao Man-Qiu Sui Li Sun Qi-Hong Zou Yu-Feng Zang Yu-Feng Wang | 2013 | Neuroscience Bulletin2013，29，5： | 24 |
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