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  • 1.

    【2hr】A Longitudinal Investigation of Sleep and Daytime Wakefulness in Children and Youth With Concussion

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    机译 患有脑震荡的儿童和青少年的睡眠和白天清醒度的纵向调查
    摘要：A high proportion of adults who sustain a concussion identify changes in their sleep during the acute stage, typically reporting an increased need for sleep or nonrestful sleep. Our understanding of sleep following concussion is less well understood within a pediatric population. In this study, we investigated the trajectory of sleep and daytime sleepiness in a prospective cohort of 40 children and youth (6–18 years old) with concussion, 40 age-and sex-matched healthy children and youth, and 40 with upper-extremity orthopedic injury. Evaluations occurred during the acute stage (<2 weeks) and at 3-, 6-, and 12-month postinjury using the Sleep Disturbance Scale for Children and the Postconcussion Symptom Scale. There were no significant differences within- or between-group differences in sleep across all four time points with analysis of the groups as a whole. When groups were divided by age (6–11 and 12– < 18 years), there was a significant difference in the ability to initiate sleep for the younger concussed group during the acute stage, compared with healthy controls, as well as significantly greater daytime nap duration that decreased over time. Significant correlations were also found between the frequency and duration of daytime naps and Postconcussion Symptom Scale total score and subscores (cognitive, physical/migraine, mood, and sleep) in the concussed group during the acute stage. Our results suggest that in a group with noncomplicated concussion, children and youth have transient alterations in daytime sleepiness that are related to concussion symptoms. Younger children may be more vulnerable to disturbances in sleep and daytime wakefulness.
  • 2.

    【2hr】Sildenafil Inhibits Myelin Expression and Myelination of Oligodendroglial Precursor Cells

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    机译 西地那非抑制少突胶质前体细胞的髓鞘表达和髓鞘形成。
    摘要：Phosphodiesterases (PDEs) have previously been implicated in oligodendrocyte maturation and myelination of central nervous system axons. Sildenafil citrate is a phosphodiesterase inhibitor known to block PDE5, which also reduces inflammation in the experimental autoimmune encephalomyelitis demyelinating model. To find out whether this inhibitor might exert beneficial effects on central nervous system myelin repair activities, we investigated to what degree sildenafil modulates differentiation and maturation of cultured primary rat oligodendroglial precursor cells (OPCs). To this end, gene and protein expression of 2′,3′-cyclic-nucleotide 3′-phosphodiesterase, myelin basic protein, and myelin oligodendrocyte glycoprotein, as well as of negative regulators of myelin expression (Hes1, Hes5, Id2, Id4, Rock2, and p57Kip2) were measured in OPCs treated with sildenafil. Moreover, the subcellular distribution of the p57kip2 protein was determined after sildenafil treatment, as this revealed to be an early predictor of the oligodendroglial differentiation capacity. In vitro myelination assays were done to measure the myelination capacity of oligodendrocytes treated with sildenafil. We found that sildenafil significantly diminished myelin gene expression and protein expression. Moreover, sildenafil also increased the expression of Id2 and Id4 negative transcriptional regulators, and the degree of OPCs with cytoplasmic p57kip2 protein localization was reduced, providing evidence that the PDE blocker impaired the differentiation capacity. Finally, sildenafil also interfered with the establishment of internodes as revealed by in vitro myelination assays. We therefore conclude that blocking PDE5 activities exerts a negative impact on intrinsic oligodendroglial differentiation processes.
  • 3.

    【2hr】Astrocyte and Neuronal Pannexin1 Contribute Distinctly to Seizures

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    机译 星形胶质细胞和神经元Pannexin1明显地有助于癫痫发作。
    摘要：ATP- and adenosine-mediated signaling are prominent types of glia–glia and glia–neuron interaction, with an imbalance of ATP/adenosine ratio leading to altered states of excitability, as seen in epileptic seizures. Pannexin1 (Panx1), a member of the gap junction family, is an ATP release channel that is expressed in astrocytes and neurons. Previous studies provided evidence supporting a role for purinergic-mediated signaling via Panx1 channels in seizures; using mice with global deletion of Panx1, it was shown that these channels contribute in maintenance of seizures by releasing ATP. However, nothing is known about the extent to which astrocyte and neuronal Panx1 might differently contribute to seizures. We here show that targeted deletion of Panx1 in astrocytes or neurons has opposing effects on acute seizures induced by kainic acid. The absence of Panx1 in astrocytes potentiates while the absence of Panx1 in neurons attenuates seizure manifestation. Immunohistochemical analysis performed in brains of these mice, revealed that adenosine kinase (ADK), an enzyme that regulates extracellular levels of adenosine, was increased only in seized GFAP-Cre:Panx1f/f mice. Pretreating mice with the ADK inhibitor, idotubercidin, improved seizure outcome and prevented the increase in ADK immunoreactivity. Together, these data suggest that the worsening of seizures seen in mice lacking astrocyte Panx1 is likely related to low levels of extracellular adenosine due to the increased ADK levels in astrocytes. Our study not only reveals an unexpected link between Panx1 channels and ADK but also highlights the important role played by astrocyte Panx1 channels in controlling neuronal activity.
  • 4.

    【2hr】Heme Oxygenase 1 in Schwann Cells Regulates Peripheral Nerve Degeneration Against Oxidative Stress

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    机译 雪旺细胞中的血红素加氧酶1调节抗氧化应激的周围神经变性。
    摘要：During Wallerian degeneration, Schwann cells lose their characteristic of myelinating axons and shift into the state of developmental promyelinating cells. This recharacterized Schwann cell guides newly regrowing axons to their destination and remyelinates reinnervated axons. This Schwann cell dynamics during Wallerian degeneration is associated with oxidative events. Heme oxygenases (HOs) are involved in the oxidative degradation of heme into biliverdin/bilirubin, ferrous iron, and carbon monoxide. Overproduction of ferrous iron by HOs increases reactive oxygen species, which have deleterious effects on living cells. Thus, the key molecule for understanding the exact mechanism of Wallerian degeneration in the peripheral nervous system is likely related to oxidative stress-mediated HOs in Schwann cells. In this study, we demonstrate that demyelinating Schwann cells during Wallerian degeneration highly express HO1, not HO2, and remyelinating Schwann cells during nerve regeneration decrease HO1 activation to levels similar to those in normal myelinating Schwann cells. In addition, HO1 activation during Wallerian degeneration regulates several critical phenotypes of recharacterized repair Schwann cells, such as demyelination, transdedifferentiation, and proliferation. Thus, these results suggest that oxidative stress in Schwann cells after peripheral nerve injury may be regulated by HO1 activation during Wallerian degeneration and oxidative-stress-related HO1 activation in Schwann cells may be helpful to study deeply molecular mechanism of Wallerian degeneration.
  • 5.

    【2hr】Altered Brain Expression of Insulin and Insulin-Like Growth Factors in Frontotemporal Lobar Degeneration: Another Degenerative Disease Linked to Dysregulation of Insulin Metabolic Pathways

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    机译 额颞叶变性中胰岛素和类似胰岛素的生长因子的大脑表达改变：与胰岛素代谢途径失调有关的另一种退行性疾病。
    摘要：BackgroundFrontotemporal lobar degeneration (FTLD) is the third most common dementing neurodegenerative disease with nearly 80% having no known etiology.
  • 6.

    【2hr】Global Brain Transcriptome Analysis of a Tpp1Neuronal Ceroid Lipofuscinoses Mouse Model

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    机译 Tpp1的全球脑转录组分析。神经元类脂脂肪藻糖小鼠模型
    摘要：In humans, homozygous mutations in the TPP1 gene results in loss of tripeptidyl peptidase 1 (TPP1) enzymatic activity, leading to late infantile neuronal ceroid lipofuscinoses disease. Using a mouse model that targets the Tpp1 gene and recapitulates the pathology and clinical features of the human disease, we analyzed end-stage (4 months) transcriptional changes associated with lack of TPP1 activity. Using RNA sequencing technology, Tpp1 expression changes in the forebrain/midbrain and cerebellum of 4-month-old homozygotes were compared with strain-related controls. Transcriptional changes were found in 510 and 1,550 gene transcripts in forebrain/midbrain and cerebellum, respectively, from Tpp1-deficient brain tissues when compared with age-matched controls. Analysis of the differentially expressed genes using the Ingenuity™ pathway software, revealed increased neuroinflammation activity in microglia and astrocytes that could lead to neuronal dysfunction, particularly in the cerebellum. We also observed upregulation in the production of nitric oxide and reactive oxygen species; activation of leukocyte extravasation signals and complement pathways; and downregulation of major transcription factors involvedin control of circadian rhythm. Several of these expression changes wereconfirmed by independent quantitative polymerase chain reaction and histologicalanalysis by mRNA in situ hybridization, which allowed for anin-depth anatomical analysis of the pathology and provided independentconfirmation of at least two of the major networks affected in this model. Theidentification of differentially expressed genes has revealed new lines ofinvestigation for this complex disorder that may lead to novel therapeutictargets.
  • 7.

    【2hr】Role of Connexin 36 in Autoregulation of Oxytocin Neuronal Activity in Rat Supraoptic Nucleus

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    机译 连接蛋白36在大鼠视上核中催产素神经元活性的自动调节中的作用。
    摘要：In the supraoptic nucleus (SON), the incidence of dye coupling among oxytocin (OT) neurons increases significantly in nursing mothers. However, the type(s) of connexin (Cx) involved is(are) unknown. In this study, we specifically investigated whether Cx36 plays a functional role in the coupling between OT neurons in the SON of lactating rats. In this brain region, Cx36 was mainly coimmunostained with vasopressin neurons in virgin female rats, whereas in lactating rats, Cx36 was primarily colocalized with OT neurons. In brain slices from lactating rats, application of quinine (0.1 mM), a selective blocker of Cx36, significantly reduced dye coupling among OT neurons as well as the discharge/firing frequency of spikes/action potentials and their amplitude, and transiently depolarized the membrane potential of OT neurons in whole-cell patch-clamp recordings. However, quinine significantly reduced the amplitude, but not frequency, of inhibitory postsynaptic currents in OT neurons; the duration of excitatory postsynaptic currents was reduced but not their frequency and amplitude. Furthermore, the excitatory effect of OT (1 pM) on OT neurons was significantly weakened and delayed by quinine, and burst firing was absent in the presence of this inhibitor. Lastly, Western blotting analysis revealed that the presence of combined, but not alone, quinine and OT significantly reduced the amount of Cx36 in the SON. Thus, Cx36-mediated junctional communication plays a crucial role in autoregulatory control of OT neuronal activity, likely by acting at the postsynaptic sites. The level of Cx36 is modulated by its own activity and the presence of OT.
  • 8.

    【2hr】Higher Level of Mismatch in APOEε4 Carriers for Amyloid-Beta Peptide Alzheimer’s Disease Biomarkers in Cerebrospinal Fluid

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    机译 APOE中的不匹配程度更高脑脊液中淀粉样蛋白-贝塔肽阿尔茨海默氏病生物标志物的ε4载体
    摘要：Cerebrospinal fluid (CSF) biomarkers are widely used in the diagnosis of dementia. Even though there is a causal correlation between apolipoprotein E (APOE) genotype and amyloid-beta (Aβ), the determination of APOE is currently not supported by national or international guidelines. We compared parallel measured CSF biomarkers of two independent laboratories from 126 patients who underwent clinical dementia diagnostics regarding the APOE genotype. APOE ε4 reduces Aβ1-42 (Aβ42) and Aβ42 to Aβ 1-40 ratio (Aβ42/40) but not total Tau or phospho-181 Tau CSF levels. Higher discordance rates were observed for Aβ42 and subsequently for Aβ42/40 in APOE ε4 carriers compared with noncarriers, and the correlation between the two laboratories was significantly lower for Aβ42 in APOE ε4 positive patients compared with patients without APOE ε4. These observations demonstrate that the evaluation of CSF Aβ biomarkers needs to be interpreted carefully in the clinical context. Different immunoassays, disparate cutoff values, and APOE should be respected.
  • 9.

    【2hr】Small Interference RNA Targeting Connexin-43 Improves Motor Function and Limits Astrogliosis After Juvenile Traumatic Brain Injury

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    机译 靶向连接蛋白-43的小干扰RNA可改善运动功能并限制青少年脑外伤后的星形胶质化。
    摘要：Juvenile traumatic brain injury (jTBI) is the leading cause of death and disability for children and adolescents worldwide, but there are no pharmacological treatments available. Aquaporin 4 (AQP4), an astrocytic perivascular protein, is increased after jTBI, and inhibition of its expression with small interference RNA mitigates edema formation and reduces the number of reactive astrocytes after jTBI. Due to the physical proximity of AQP4 and gap junctions, coregulation of AQP4 and connexin 43 (Cx43) expressions, and the possibility of water diffusion via gap junctions, we decided to address the potential role of astrocytic gap junctions in jTBI pathophysiology. We evaluated the role of Cx43 in the spread of the secondary injuries via the astrocyte network, such as edema formation associated with blood–brain barrier dysfunctions, astrogliosis, and behavioral outcome. We observed that Cx43 was altered after jTBI with increased expression in the perilesional cortex and in the hippocampus at several days post injury. In a second set of experiments, cortical injection of small interference RNA against Cx43 decreased Cx43 protein expression, improved motor function recovery, and decreased astrogliosis but did not result in differences in edema formation as measured via T2-weighted imaging or diffusion-weighted imaging at 1 day or 3 days. Based on our findings, we can speculate that while decreasing Cx43 has beneficial roles, it likely does not contribute to the spread of edema early after jTBI.
  • 10.

    【2hr】MicroRNAs 145 and 148a Are Upregulated During Congenital Zika Virus Infection

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    机译 先天性寨卡病毒感染期间MicroRNA 145和148a上调。
    摘要：Zika virus (ZIKV) is an arthropod-borne virus (arbovirus) member of the Flaviviridae family, which has been associated with the development of the congenital Zika syndrome (CZS). RNA viruses, such as flaviviruses, have been reported to exert a profound impact on host microRNAs (miRNAs). Cellular miRNAs modulated by ZIKV may help identify cellular pathways of relevance to pathogenesis. Here, we screened 754 human cellular miRNAs modulated by ZIKV infection (Brazilian PE strain) in a neuroblastoma cell line. Seven miRNAs (miR-99a*, miR-126*, miR-190b, miR-361-3p, miR-522-3p, miR-299-5p, and miR-1267) were downregulated during ZIKV infection, while miR-145 was upregulated. Furthermore, 11 miRNAs were exclusively expressed in ZIKV-infected (miR-148a, miR-342-5p, miR-598, and miR-708-3p) or mock cells (miR-208, miR-329, miR-432-5p, miR-488, miR-518b, miR-520g, and miR-767-5p). Furthermore, in silico analysis indicated that some central nervous system, cellular migration, and adhesion function-related biological processes were overrepresented in the list of target genes of the miRNAs regulated in ZIKV-infected cells, especially for miR-145 and miR-148a. The induction of miR-145 and miR-148a was confirmed in postmortem brain samples from stillborn with severe CZS. Finally, we determined the expression regulation of microcephaly related genes through RNA interference pathway caused by ZIKV directly on neuron cells.
  • 11.

    【2hr】Identification of the Molecular Events Involved in the Development ofPrefrontal Cortex Through the Analysis of RNA-Seq Data FromBrainSpan

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    机译 鉴定参与发展的分子事件前额叶皮层通过分析来自RNA序列的数据脑跨度
    摘要：Human brain development is a complex process that follows sequential orchestration of gene expression, begins at conceptual stages, and continues into adulthood. Altered profile of gene expression drives many cellular and molecular events required for development. Here, the molecular events during development of human prefrontal cortex (PFC) (as an important executive part of the brain) were investigated. First, the RNA-sequencing data of BrainSpan were used to obtain differentially expressed genes between each two developmental stages and then, the relevant biological processes and signaling pathways were deduced by gene set enrichment analysis. In addition, the changes in transcriptome landscape of PFC during development were analyzed and the potential biological processes underlie the changes were found. Comparison of the four regions of PFC based on their biological processes showed that additional to common biological processes and signaling pathways, each PFC region had its own molecular characteristics, conforming their previously reported functional roles in brain physiology. The most heterogeneity in transcriptome between the PFC regions was observed at the time of birth which was concurrent with the activity of some region-specific regulatory systems suchas DNA methylation, transcription regulation, RNA splicing, and presence ofdifferent transcription factors and microRNAs. In conclusion, this study usedbioinformatics to present a comprehensive molecular overview on PFC developmentwhich may explain the etiology of brain neuropsychiatric disorders originatedfrom malfunctioning of PFC.
  • 12.

    【2hr】Blood Flow Deficits and Cerebrovascular Changes in a Dietary Model of Hyperhomocysteinemia

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    机译 高同型半胱氨酸饮食模型中的血流不足和脑血管变化
    摘要：Elevated homocysteine in the blood, or hyperhomocysteinemia, is a recognized risk factor for multiple causes of dementia including Alzheimer’s disease. While reduction of homocysteine levels can generally be accomplished in a straightforward manner, the evidence regarding the cognitive benefits of this approach is less clear. To identify adjunct therapeutic targets that might more effectively restore cognition, the present series of experiments characterizes early and later cerebrovascular changes in a model of hyperhomocysteinemia. Sex-balanced groups of adult C57BL/6J mice were administered a diet deficient in vitamins B6, B12, and B9 (folate) and supplemented with excess methionine. They were subsequently assessed for changes in cerebral blood flow, memory, blood–brain barrier permeability, and selected vascular-associated genes. Blood flow deficits and barrier permeability changes occurred alongside changes in memory and in genes associated with metabolism, endothelial nitric oxide signaling, barrier integrity, and extracellular matrix remodeling. Significant sexually dimorphic responses to the diet were also detected. Taken together, these data deepen our understanding of a major contributor to dementia burden.
  • 13.

    【2hr】Intracerebroventricular Infusion of Gangliosides Augments theAdult Neural Stem Cell Pool in Mouse Brain

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    机译 脑室内注入神经节苷脂可增强小鼠脑中的成人神经干细胞池
    摘要：We previously reported that ganglioside GD3 is the predominant species in neural stem cells (NSCs) and reduced postnatal NSC pools are observed in both the subventricular zone and dentate gyrus (DG) of GD3-synthase knockout (GD3S-KO) mouse brains. Specifically, deficiency of GD3 in GD3S-KO animals revealed a dramatic reduction in cellularity in the DG of the hippocampus of the developing mouse brain, resulting in severe behavioral deficits in these animals. To further evaluate the functional role of GD3 in postnatal brain, we performed rescue experiments by intracerebroventricular infusion of ganglioside GD3 in adult GD3S-KO animals and found that it could restore the NSC pools and enhance the NSCs for self-renewal. Furthermore, 5xFAD mouse model was utilized, and GD3 restored NSC numbers and GM1 promoted neuronal differentiation. Our results thus demonstrate that exogenously administered gangliosides are capable to restore the function of postnatal NSCs. Since ganglioside expression profiles are associated not only with normal brain development but also with pathogenic mechanisms of diseases, such as Alzheimer’s disease, we anticipatethat the administration of exogenous gangliosides, such as GD3 andGM1, may represent a novel and effective strategy for promoting adultneurogenesis in damaged brain for disease treatment.
  • 14.

    【2hr】Subacute Transplantation of Native and Genetically Engineered Neural Progenitors Seeded on Microsphere Scaffolds Promote Repair and Functional Recovery After Traumatic Brain Injury

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    机译 亚急性移植的自然和遗传工程神经祖细胞植入微球支架上促进创伤性脑损伤后修复和功能恢复。
    摘要：There is intense interest and effort toward regenerating the brain after severe injury. Stem cell transplantation after insult to the central nervous system has been regarded as the most promising approach for repair; however, engrafting cells alone might not be sufficient for effective regeneration. In this study, we have compared neural progenitors (NPs) from the fetal ventricular zone (VZ), the postnatal subventricular zone, and an immortalized radial glia (RG) cell line engineered to conditionally secrete the trophic factor insulin-like growth factor 1 (IGF-1). Upon differentiation in vitro, the VZ cells were able to generate a greater number of neurons than subventricular zone cells. Furthermore, differentiated VZ cells generated pyramidal neurons. In vitro, doxycycline-driven secretion of IGF-1 strongly promoted neuronal differentiation of cells with hippocampal, interneuron and cortical specificity. Accordingly, VZ and engineered RG-IGF-1-hemagglutinin (HA) cells were selected for subsequent in vivo experiments. To increase cell survival, we delivered the NPs attached to a multifunctional chitosan-based scaffold. The microspheres containing adherent NPs were injected subacutely into the lesion cavity of adult rat brains that had sustained controlled cortical impact injury. At 2 weeks posttransplantation, the exogenously introduced cells showed a reduction in stem cell or progenitor markers and acquired mature neuronal and glial markers. In beam walking tests assessing sensorimotor recovery, transplanted RG cells secreting IGF-1 contributed significantly to functional improvement while native VZ or RG cells did not promote significant recovery. Altogether, these results support the therapeutic potential of chitosan-based multifunctional microsphere scaffolds seeded with genetically modified NPs expressing IGF-1 to promote repair and functional recovery after traumatic brain injuries.
  • 15.

    【2hr】2018 Reviewer Thank You

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    机译 2018 Reviewer谢谢
    • 作者：
    • 刊名：ASN NEURO
    • 2019年第期
    摘要：
  • 16.

    【2hr】Abstracts of the 2018 Meeting of ArgentineSociety for Research in Neurosciences

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    机译 2018年阿根廷神经科学研究协会会议摘要
    • 作者：
    • 刊名：ASN NEURO
    • 2019年第期
    摘要：

    Cognition, Behavior, and Memory

    P153. Dopamine D2 Receptors of the Central Amygdala Regulate Unconditioned Fear in Mice

    Eric Casey1, Alexxai V. Kravitz2, Elena Avale1 and Marcelo Rubinstein1,3 1Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina2National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health and National Institute on Alcohol Abuse and Alcoholism, National Institutes of Health, Bethesda, MD, USA3Instituto de Investigaciones en Ingeniería Genética y Biología Molecular, Consejo Nacional de Investigaciones Científicas y Técnicas and Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, ArgentinaPresenting author: Eric Casey,
  • 17.

    【2hr】Amyloid Beta-Related Alterations to Glutamate Signaling DynamicsDuring Alzheimer’s Disease Progression

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    机译 淀粉样蛋白相关谷氨酸信号动力学的变化。在阿尔茨海默氏病进展期间
    摘要：Alzheimer’s disease (AD) ranks sixth on the Centers for Disease Control and Prevention Top 10 Leading Causes of Death list for 2016, and the Alzheimer’s Association attributes 60% to 80% of dementia cases as AD related. AD pathology hallmarks include accumulation of senile plaques and neurofibrillary tangles; however, evidence supports that soluble amyloid beta (Aβ), rather than insoluble plaques, may instigate synaptic failure. Soluble Aβ accumulation results in depression of long-term potentiation leading to cognitive deficits commonly characterized in AD. The mechanisms through which Aβ incites cognitive decline have been extensively explored, with a growing body of evidence pointing to modulation of the glutamatergic system. The period of glutamatergic hypoactivation observed alongside long-term potentiation depression and cognitive deficits in later disease stages may be the consequence of a preceding period of increased glutamatergic activity. This review will explore the Aβ-related changes to the tripartite glutamate synapse resulting in altered cell signaling throughout disease progression, ultimately culminating in oxidative stress, synaptic dysfunction, and neuronal loss.
  • 18.

    【2hr】Alterations of Calcium Channels in a Mouse Model of Huntington’s Disease and Neuroprotection by Blockage of CaV1 Channels

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    机译 亨廷顿舞蹈病小鼠模型中钙通道的改变和CaV1通道的阻断对神经的保护
    摘要：Huntington’s disease (HD) is a neurodegenerative autosomal dominant disorder, characterized by symptoms of involuntary movement of the body, loss of cognitive function, psychiatric disorder, leading inevitably to death. It has been previously described that higher levels of brain expression of Cav1 channels are involved in major neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Our results demonstrate that a bacterial artificial chromosome (BAC)-mediated transgenic mouse model (BACHD mice) at the age of 3 and 12 months exhibits significantly increased Cav1.2 protein levels in the cortex, as compared with wild-type littermates. Importantly, electrophysiological analyses confirm a significant increase in L-type Ca2+ currents and total Ca2+ current density in cortical neurons from BACHD mice. By using an in vitro assay to measure neuronal cell death, we were able to observe neuronal protection against glutamate toxicity after treatment with Cav1 blockers, in wild-type and, more importantly, in BACHD neurons. According to our data, Cav1 blockers may offer an interesting strategy for the treatment of HD. Altogether, our results show that mutant huntingtin (mHtt) expression may cause a dysregulation of Cav1.2 channels and we hypothesize that this contributes to neurodegeneration during HD.
  • 19.

    【2hr】Erythropoietin as a Neuroprotective Molecule: An Overview of Its Therapeutic Potential in Neurodegenerative Diseases

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    机译 促红细胞生成素作为一种神经保护分子：在神经退行性疾病中治疗潜力的概述
    摘要：Erythropoietin (EPO) is a cytokine mainly induced in hypoxia conditions. Its major production site is the kidney. EPO primarily acts on the erythroid progenitor cells in the bone marrow. More and more studies are highlighting its secondary functions, with a crucial focus on its role in the central nervous system. Here, EPO may interact with up to four distinct isoforms of its receptor (erythropoietin receptor [EPOR]), activating different signaling cascades with roles in neuroprotection and neurogenesis. Indeed, the EPO/EPOR axis has been widely studied in the neurodegenerative diseases field. Its potential therapeutic effects have been evaluated in multiple disorders, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, spinal cord injury, as well as brain ischemia, hypoxia, and hyperoxia. EPO is showing great promise by counteracting secondary neuroinflammatory processes, reactive oxygen species imbalance, and cell death in these diseases. Multiple studies have been performed both in vitro and in vivo, characterizing the mechanisms through which EPO exerts its neurotrophic action. In some cases, clinical trials involving EPO have been performed, highlighting its therapeutic potential. Together, all these works indicate the potential beneficial effects of EPO.
  • 20.

    【2hr】2019 Academic Annual Meeting and the Frontier Seminar on “Glial CellFunction and Disease” (Nantong, China)

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    机译 2019年学术年会暨“胶质细胞”前沿研讨会功能与疾病”（中国南通）
    摘要：The contribution of glial activities to the functions, diseases, and repair of the central nervous system has received increasing attention in neuroscience studies. To promote the research of glial cells and increase cooperation with peers, the 2019 Academic Annual Meeting and the Frontier Seminar on “Glial Cell Function and Disease” was held in Nantong City, Jiangsu Province, China from May 24 to 26. The meeting was organized by Drs. Yong-Jing Gao and Jia-Wei Zhou of the Chinese Society of Neuroscience Glia Branch. The conference focused on the physiological and pathological functions of astrocytes, microglia, and oligodendrocytes with 25 speakers in two plenary speeches and five sections of more than 180 participants engaged in glial cell research. In the two plenary lectures, Yutian Wang from the University of British Columbia and Xia Zhang from the University of Ottawa presented “Development of NMDAR (N-methyl-D-aspartic acid receptor)-positive allosteric modulators as novel therapeutics for brain disorders” and “Mechanisms underlying cannabinoid regulation of brain function and disease,” respectively. The five sections included microglia and disease, astrocytes and disease, glioma treatment and glial imaging, oligodendrocytes and disease, and glial–neuronal interactions and disease. This meeting allowedextensive and in-depth academic exchanges on the latest research andexperimental techniques, represented the highest achievements of Chinesescholars on glial cells, and promoted the cooperation between peers in thefields of glia studies.
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