Keystone Symposia Meetings on Neurodegenerative Diseases and Axonal Connections
Keystone Symposia Meetings on Neurodegenerative Diseases and Axonal Connections
批准号:
7614758
负责人:
ANDREW D ROBERTSON
金额:
$1.05万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2009
资助国家:
美国
项目状态:
已结题
起止时间:
2009-01-01 至 2009-12-31
关键词:
AddressAdultAffectAlzheimer&aposs DiseaseAmericanAmyotrophic Lateral SclerosisAreaAxonBiochemistryBiologyCell Death Signaling ProcessCharacteristicsClinicalCollaborationsColoradoComplexCuesDevelopmentDiseaseEventGenomicsGoalsImageIndividualInjuryLearningLogicMedicalMolecularNatural regenerationNervous System PhysiologyNeuraxisNeurodegenerative DisordersNeurologicNeuronsParkinson DiseasePathogenesisPathologicPatternPhysiologicalProcessProteomicsResearchResearch PersonnelScientistTherapeuticTimeTrainingaxon growthcostdisease-causing mutationextracellularmeetingsnervous system disorderneural circuitnovel therapeuticspredictive modelingpublic health relevancerelating to nervous systemrepairedresponsesymposium
中文摘要
描述(由申请人提供):本提案旨在为2009年2月17日至22日在科罗拉多州基斯顿举行的题为“神经退行性疾病:新的分子机制”(由Valina L. Dawson和David M. Holtzman组织)和“轴突连接:发育和再生的分子线索”的2009年基斯顿专题会议提供支持。联合举办这些会议——包括一个共同的主题演讲和三个共同的全体会议,加上相当多的共享非结构化时间——提供了一个独特的机会,可以深入讨论神经系统疾病的发病机制,并就控制轴突生长和再生的正常生物学的分子和生理机制进行高水平的讨论。神经退行性疾病会议的重点是我们对神经退行性疾病的病因和病理进展的理解的重大进展。对致病突变的识别为开发新的预测模型和接近新的治疗方法提供了前所未有的机会。生物化学、基因组学、蛋白质组学和成像技术的进步促进了对复杂疾病提出和回答复杂问题的能力,以及对神经退行性疾病具有独特的细胞死亡信号级联反应的认识,这些细胞死亡信号级联反应可以共享一些共同的分子事件。本次会议将强调了解可能的共同机制以及神经退行性疾病的独特特征,如阿尔茨海默病(AD),帕金森病(PD),三重重复疾病,肌萎缩侧索硬化症(ALS)等。轴突连接:发育和再生的分子线索会议重点关注神经系统的正常功能,特别是发育过程中复杂连接模式的形成。如果这种连接随后因损伤或变性而丢失,则成人中枢神经系统中的轴突无法再生,这是一个重大的临床挑战。在过去的几年里,在确定轴突发育和再生的分子机制方面取得了巨大的进展,尽管这些复杂的过程还有很多有待了解。在识别细胞外调节因子的新类别,理解细胞外信息被神经元转导成适当反应的机制,以及学习神经连接形成的潜在分子逻辑方面,正在取得快速进展。这些同时举行的会议将汇集轴突发育、退化和再生领域的研究人员;促进这些领域之间的思想、信息交流和合作;在这些令人兴奋和热门的研究领域培养年轻科学家的问题、方法和机会;并促进理解神经回路形成的基本机制和开发治疗性修复的新策略的科学和转化目标。公共卫生相关性:在美国,神经系统疾病影响了大约5000万美国人,每年在医疗和相关费用方面的费用估计为4000亿美元。不幸的是,对于患有神经系统疾病的人来说,几乎没有治疗方法。同样,成人中枢神经系统(CNS)的损伤或退化可导致轴突无法再生,这是一个重大的临床挑战,因为神经系统的功能依赖于发育过程中形成的复杂连接模式。这些同时举行的会议将汇集轴突发育、退化和再生领域的研究人员;促进这些领域之间的思想、信息交流和合作;在这些令人兴奋和热门的研究领域培养年轻科学家的问题、方法和机会;并促进理解神经回路形成的基本机制和开发治疗性修复的新策略的科学和转化目标。
英文摘要
DESCRIPTION (provided by applicant): This proposal is to request support for a pair of concurrent 2009 Keystone Symposia meetings entitled Neurodegenerative Diseases: New Molecular Mechanisms (organized by Valina L. Dawson and David M. Holtzman), and Axonal Connections: Molecular Cues for Development and Regeneration (organized by John G. Flanagan, Marie T. Filbin and Liqun Luo), to be held in Keystone, Colorado from February 17 - 22, 2009. Holding these meetings jointly - including a common keynote address and three shared plenary sessions plus considerable shared unstructured time - provides a unique opportunity for bridging an in-depth discussion of neurological disease pathogenesis with a high-level discourse on the molecular and physiological mechanisms governing the normal biology of axon growth and regeneration. The meeting on Neurodegenerative Diseases focuses on significant advances in our understanding of the causes and pathologic progression of neurodegenerative diseases. Identification of disease-causing mutations has provided unprecedented opportunities to develop new and predictive models and move closer to new therapeutic treatments. Technological advances in biochemistry, genomics, proteomics and imaging have facilitated the ability to pose and answer complex questions in complex disease, as well as an appreciation that neurodegenerative diseases have distinct cell death signaling cascades that can share some common molecular events. This meeting will emphasize understanding possible common mechanisms as well as the distinct characteristics of neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), triple repeat diseases, amyotrophic lateral sclerosis (ALS) and others. The meeting on Axonal Connections: Molecular Cues for Development and Regeneration focuses on the normal functioning of the nervous system and, in particular, formation of the complex pattern of connections during development. If such connections are subsequently lost through injury or degeneration, axons in the adult CNS fail to regenerate, creating a major clinical challenge. The last several years have seen tremendous progress in identifying molecular mechanisms for axon development and regeneration, although much remains to be learned about these complex processes. Rapid progress is being made in identifying new classes of extracellular regulators, understanding the mechanisms by which this extracellular information is transduced by the neuron into appropriate responses, and learning the underlying molecular logic for the formation of neural connectivity. These concurrent meetings will bring together researchers in the fields of axon development, degeneration and regeneration; promote exchange of ideas, information and collaboration among these fields; train young scientists in the questions, approaches, and opportunities in these exciting and topical research areas; and promote scientific and translational goals of understanding the basic mechanisms for the formation of neural circuits and developing new strategies for therapeutic repair. PUBLIC HEALTH RELEVANCE: In the USA, neurological disorders affect approximately 50 million Americans and cost an estimated $400 billion annually in medical and related expenses. Unfortunately there are few therapies for individuals who suffer from neurologic disease. Likewise, injury or degeneration in the adult central nervous system (CNS) can cause axons to fail to regenerate, creating a major clinical challenge as the functioning of the nervous system depends on the complex pattern of connections formed during development. These concurrent meetings will bring together researchers in the fields of axon development, degeneration and regeneration; promote exchange of ideas, information and collaboration among these fields; train young scientists in the questions, approaches, and opportunities in these exciting and topical research areas; and promote scientific and translational goals of understanding the basic mechanisms for the formation of neural circuits and developing new strategies for therapeutic repair.
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