Unifying Mechanisms of Neurological Disorders: Scientific, Translational, and Cli

神经系统疾病的统一机制：科学、转化和气候

• 批准号: 7920278
• 负责人: Joan Marie Cranmer
• 金额: $ 4万
• 依托单位: UNIV OF ARKANSAS FOR MED SCIS
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7920278
• 关键词: Address; Affect; Animals; Area; Award; Basic Science; Characteristics; Chemicals; Clinical Medicine; Data; Development; Disease; Educational workshop; Environmental Exposure; Environmental Risk Factor; Epidemiology; Epigenetic Process; Epilepsy; Event; Exposure to; Female; Functional disorder; Gender; Genes; Genetic; Glean; Goals; Health; Human; Huntington Disease; International; Ion Channel; Knowledge; Lead; Link; Location; Mediation; Mentors; Migraine; Mitochondria; Mutation; Nature; Nervous System Physiology; Neurodevelopmental Disorder; Neuronal Dysfunction; Neurotoxins; Oregon; Parkinson Disease; Pathogenesis; Pathway interactions; Pattern; Pharmaceutical Preparations; Play; Postdoctoral Fellow; Prevention; Probability; Process; Proteins; Reporting; Research; Research Personnel; Rewards; Risk; Role; Scientist; Series; Sex Characteristics; Students; Therapeutic; Therapeutic Intervention; Time; Touch sensation; Toxic Environmental Substances; Toxicology; Translational Research; chronic pain; critical period; design; gene environment interaction; insight; male; meetings; mitochondrial dysfunction; nervous system disorder; neuropathology; neurotoxicology; novel strategies; planetary Atmosphere; posters; protein aggregation; public health relevance; response; sex; social; symposium

DESCRIPTION (provided by applicant): The Twenty-Sixth International Eurotoxicology Conference (NEUROTOX 26) addressing the theme of "Unifying Mechanisms of Neurological Disorders" will be held June 6-11, 2010 in Portland, Oregon. The meeting location is the Portland Marriott Downtown Waterfront Hotel where greatly reduced conference rates have been negotiated. The International Neurotoxicology Conference is an annual event that focuses on a timely and provocative theme that has a high probability of advancing the field by being addressed by an interdisciplinary, international group of scientists in the unique "atmosphere" and organized format of this established Conference Series - while at the same time providing an opportunity for presenting new data related to the general interdisciplinary field of neurotoxicology. The Specific Aims identified in the proposal will be accomplished by conducting a 4 day conference according to a varied format similar to previous conferences in this series which has proven to be highly successful. Each conference has its own "special touch" unique to the venue and consists of Tutorials, Symposia, Platform Sessions, -Workshops, Panel Discussions, Roundtables, Debates, Poster Session, Pre- and Postdoctoral Student Competition and Awards Banquet and social events as well as novel approaches to facilitate networking and mentoring. NEUROTOX 26 will not be simply an occasion to present data. It will also coalesce human, experimental animal, methodological, and epidemiological research by offering a well-recognized venue where previously unconnected investigators can come together and where commonalties can emerge. Traditionally the Neurotoxicology Conference places special emphasis on nurturing, promoting and rewarding pre- and post-doctoral students and young investigators. Extra effort is extended to mentor students and help them network with the leaders in the field. Justification for the Theme: Over the past several years, research into neurological disease and disorders has evolved to recognize that there are often overlapping similarities in seemingly different disease states. Although genetic factors have long been a primary focus in neurological disease, identification of single genes involved in more than a small fraction of cases in a variety of neurological disorders has proven difficult. These findings have led to the emerging recognition that environmental factors or gene-environment interactions are likely to play a pivotal role in disease pathogenesis. Thus, understanding common mechanisms and genetic and environmental factors that contribute to manifestation of neuronal dysfunction has the potential to provide insight into the pathophysiology of neurological disorders and ultimately lead to better prevention and treatment of disease. In order to accomplish the goal of understanding common mechanisms and contributors to neurological disease, we are proposing to convene a conference entitled "Unifying Mechanisms of Neurological Disorders". Through this conference, we plan to bring together experts in clinical medicine, basic science, toxicology, and translational research to explore common mechanisms of neurological disease with the goal of facilitating interactions and the transfer of knowledge between groups that have not historically interacted to a significant degree. We have chosen to focus on two major common mechanisms associated with a number of neurological disease states and three emerging areas of research that have the potential to benefit from increased focus. First, we will explore the role of mitochondrial dysfunction, which is a hallmark of several devastating neurological disease such as Parkinson's, Alzheimers, Huntington's, and ALS. The salient questions relating to mitochondrial function in disease to be assessed in this session will include the role of mitochondrial dysfunction in pathogenesis, the role of environmental factors and gene-environment interactions, and how mitochondrial function can be targeted for therapeutic intervention. The second major common mechanism of focus will be on the role of protein aggregation and misfolding in neurological disease. Protein aggregation and misfolding have been linked to a variety of neurological disorders, both genetic and idiopathic in origin. However, there is currently controversy as to whether this process is a cause or consequence of the disease process. This session will bring together experts in neuropathology, clinical medicine, and basic researchers to evaluate the role of protein aggregation and misfolding in neurological disease and what information relating to pathogenesis and treatment that can be gleaned from examining common mechanisms affecting these pathways. The three emerging areas that we have chosen for focus include channelopathies, gender, and epigentics. Channelopathies are thought to play an important role in epilepsy, chronic pain, and migraine. Although most of the focus has been on the role of genetic alterations in channel proteins, a variety of environmental toxicants target ion channels, which suggests the potential for environmental exposures to contribute to channelopathies. The IOM report, "Does Sex Matter" (2001) emphasized the need for examining differences between male and female responses in the research enterprise because of wide gaps between males and females in disease patterns and in response to therapeutic practices and drugs. This symposium is designed to exemplify both current knowledge of sex differences in environmenal chemical vulnerability and to propose insight into the relationship between the environmental exposures, gender, and the development of neurological disease. Finally, we will explore the role of epigenetic alterations in neurological disorders. Emerging evidence suggests that epigenetic alterations resulting from environmental exposures during critical periods of development may play a significant role in neurodevelopmental disorders. This session is designed to assess the current state of knowledge in this and identify common mechanisms involving epigenetic alterations that may provide insight into disease pathogenesis and ultimately, therapeutic intervention. PUBLIC HEALTH RELEVANCE: The health relatedness of this application is that he results of this conference will contribute to a fuller understanding of the true risk posed by exposure to a variety of neurotoxicants on human neurological diseases or disorders. Exposure to a variety of neurotoxicants has been associated with characteristic derangements of nervous system function, some fleeting in nature and others virtually permanent. Furthermore, exposure to neurotoxicants has been hypothesized to play a role in the development of many neurological diseases and disorders. NEUROTOXICOLOGY 26 will focus on common mechanisms in neurological disease and the role of environmental exposures and gene-environment interactions in the development of neurological disease and disorders.

描述（由申请人提供）：第26届国际欧洲毒理学会议（Neurotox 26）介绍了“神经疾病统一机制”主题，将于2010年6月6日至11日在俄勒冈州的波特兰举行。会议地点是波特兰万豪市中心海滨酒店，在那里已经谈判了会议率大大降低。国际神经毒理学会议是一年一度的活动，重点是及时挑衅的主题，该主题很有可能通过由跨学科的，国际科学家的国际科学家集团解决，以独特的“气氛”和这个既定的会议系列的有组织的格式来提高领域 - 同时提供了与一般互化型NeuroToxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of Neuroxic of neuroToxic的新数据。该提案中确定的具体目的将通过根据与本系列中以前的会议相似的各种形式进行为期4天的会议来实现，事实证明，该会议非常成功。每次会议都有自己独特的“特殊触摸”，包括教程，研讨会，平台会议， - 工作坊，小组讨论，圆桌讨论，辩论，辩论，海报会议，预科课程和博士后学生竞争以及奖励宴会和社交活动，以及促进网络和培训的新方法。 Neurotox 26将不仅仅是显示数据的场合。它还将通过提供一个公认的场地，以前未连接的研究人员可以聚集在一起，并且可以在共同点可以出现的地方结合人类，实验动物，方法论和流行病学研究。传统上，神经毒理学会议特别强调了培养，促进和奖励博士后学生和年轻研究人员。额外的努力将扩大到指导学生，并帮助他们与该领域的领导者建立联系。主题的理由：在过去的几年中，对神经疾病和疾病的研究已经发展为认识到，看似不同的疾病状态中经常有重叠的相似性。尽管遗传因素长期以来一直是神经系统疾病的主要重点，但事实证明，在多种神经系统疾病中涉及的单个基因的鉴定已被证明很困难。这些发现导致了新兴的认识，即环境因素或基因环境相互作用可能在疾病发病机理中起关键作用。因此，理解有助于神经元功能障碍表现的常见机制以及遗传和环境因素有可能洞悉神经系统疾病的病理生理学，并最终导致更好的预防和治疗疾病。为了实现理解共同机制和神经疾病的贡献者的目标，我们提议召集一个名为“神经疾病的统一机制”的会议。通过这次会议，我们计划将临床医学，基础科学，毒理学和转化研究专家汇集在一起​​，以探索神经系统疾病的共同机制，目的是促进相互作用，并在没有历史上相互作用的群体之间转移知识。我们选择专注于与许多神经系统疾病状态和三个新兴研究领域相关的两个主要常见机制，它们有可能受益于增加的关注点。首先，我们将探索线粒体功能障碍的作用，这是几种毁灭性神经系统疾病的标志，例如帕金森氏症，阿尔茨海默氏症，亨廷顿和ALS。与线粒体在本届会议中的疾病中有关的显着问题将包括线粒体功能障碍在发病机理中的作用，环境因素和基因环境相互作用的作用以及如何将线粒体功能靶向治疗介入。重点的第二个主要共同机制将是蛋白质聚集和在神经系统疾病中的折叠的作用。蛋白质的聚集和错误折叠与各种神经系统疾病有关，均与遗传性和特发性有关。但是，目前关于此过程是疾病过程的原因还是结果存在争议。本届会议将汇集神经病理学，临床医学和基础研究人员的专家，以评估蛋白质聚集和错误折叠在神经系统疾病中的作用，以及哪些与发病机理和治疗有关的信息可以从检查影响这些途径的常见机制中收集。我们选择重点的三个新兴领域包括通道病，性别和表观观念。人们认为通道病在癫痫，慢性疼痛和偏头痛中起着重要作用。尽管大多数重点是遗传改变在通道蛋白中的作用，但各种环境有毒物质靶向离子通道，这表明环境暴露有助于导致通道病。 IOM报告“做性问题”（2001年）强调了研究企业中男性和女性反应之间的差异的必要性，因为男性与女性之间的疾病模式中的差距很大，并且对治疗实践和药物的反应。该研讨会旨在体现当前对环境化学脆弱性性别差异的了解，并提出对环境暴露，性别和神经系统疾病发展之间关系的见解。最后，我们将探讨表观遗传改变在神经系统疾病中的作用。新兴的证据表明，在关键发展期间环境暴露引起的表观遗传改变可能在神经发育障碍中起重要作用。本届会议旨在评估当前的知识状态，并确定涉及表观遗传学改变的共同机制，这些机制可能会洞悉疾病发病机理，并最终是治疗性干预。 公共卫生相关性：本申请的健康相关性是，他的成绩将有助于更深入地了解人类神经疾病或疾病的各种神经毒性的真正风险。暴露于多种神经毒性剂与神经系统功能的特征危险有关，有些人自然而过，而另一些实际上是永久的。此外，假设暴露于神经毒性中，可以在许多神经系统疾病和疾病的发展中发挥作用。神经毒理学26将重点关注神经系统疾病中的常见机制以及环境暴露和基因环境相互作用在神经系统疾病和疾病发展中的作用。