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Washington University Center for Translational Neuroscience

华盛顿大学转化神经科学中心

基本信息

批准号：
8334855
负责人：
DAVID M. HOLTZMAN
金额：
$ 76万
依托单位：
WASHINGTON UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2006
资助国家：
美国
起止时间：
2006-09-25 至 2013-08-31
项目状态：
已结题

项目摘要

The overarching goal of this grant, entitled "Washington University Center for Translational Neuroscience- WUCTN" is to support centralized resources, facilities, and expertise shared by neuroscience investigators at Washington University in order to facilitate discovery of fundamental mechanisms of disorders of the nervous system and to translate this understanding into treatments and cures. Core A, Administration, will organize and facilitate interaction among the 6 other cores: Core B, Biospecimen and Clinical Data Acquisition; Core C, Molecular Analysis; Core D, Viral Vectors; Core E, Optical imaging; Core F, Functional Assessment; and Core G, Informatics. By pooling and organizing resources and expertise, the enormous breadth and collaborative spirit of the Washington University neuroscience community that spans virtually every department, can take advantage of economies of scale, confront challenges too large for individual investigators, and develop an infrastructure that will serve the user group of over 120 investigators. The WUCTN will capitalize on the development and resources of 3 new initiatives at Washington University: Biomed 21, the Hope Center for Neurological Disorders, and the Neurological Clinical Research Unit as well as utilize the support and expertise of the long established McDonnell Neuroscience Centers to assist in supporting the personnel and infrastructure being requested in this proposal. In addition, we will work together with several ongoing NIH funded centers at Washington University including the Alzheimer's Disease Research Center, the Conte Center for research on the neurobiology of schizophrenia, and the NINDS Center Core for Brain Imaging to add "extra value" to this proposal. The increasing complexity and cost of the technologies required to characterize biological phenomenon are often beyond the expertise and resources of an individual laboratory. This makes it very difficult to establish and validate key new discoveries in a cohesive, timely, and cost-efficient manner without access to facilities specializing in these enabling technologies. The proposed Core infrastructure, situated within the collaborative environment that exists between the basic neurosciences and the neurobiology of disease community at Washington University, will help catalyze a strong translational effort to convert basic discoveries into diagnostic and therapeutic advances. This will be manifested as: 1) greater efficiency in utilizing enabling technologies by individual investigators; 2) greater collaboration aimed at pre-clinical development of potential therapeutic strategies; and, 3) faster translation of initial discoveries into useful treatments for disorders of the nervous system.

该基金的主要目标是支持华盛顿大学神经科学研究人员共享的集中资源、设施和专业知识，以促进发现神经系统疾病的基本机制，并将这一认识转化为治疗和治愈。核心A(行政)将组织和促进其他6个核心之间的互动：核心B(生物显微镜和临床数据采集)、核心C(分子分析)、核心D(病毒载体)、核心E(光学成像)、核心F(功能评估)和核心G(信息学)。通过汇集和组织资源和专业知识，华盛顿大学神经科学界的巨大广度和协作精神几乎横跨每个部门，可以利用规模经济，应对对单个调查人员来说太大的挑战，并开发一个将服务于120多名调查人员用户群体的基础设施。WUCTN将利用华盛顿大学三项新计划的发展和资源：BioMed 21，Hope Center for Neurotics Disorder，和Neurotics临床研究单位，以及利用长期建立的McDonnell神经科学中心的支持和专业知识，以协助支持本提案所要求的人员和基础设施。此外，我们将与华盛顿大学由NIH资助的几个正在进行的中心合作，包括阿尔茨海默病研究中心、康特精神分裂症神经生物学研究中心和NINDS脑成像中心核心，为这项提议增加“额外价值”。描述生物现象所需技术的日益复杂和成本往往超出了单个实验室的专门知识和资源。这使得在没有专门从事这些使能技术的设施的情况下，很难以连贯、及时和经济高效的方式建立和验证关键的新发现。拟议的核心基础设施位于华盛顿大学疾病的基础神经科学和神经生物学之间存在的合作环境中，将有助于促进将基本发现转化为诊断和治疗进展的强大转化努力。这将表现为：1)个人研究人员利用使能技术的效率更高；2)旨在临床前开发潜在治疗策略的更大合作；以及3)将最初的发现更快地转化为神经系统疾病的有用治疗方法。

项目成果

期刊论文数量（61）

专著数量（0）

科研奖励数量（0）

会议论文数量（0）

专利数量（0）

Dopamine deficiency underlies learning deficits in neurofibromatosis-1 mice.

DOI：
10.1002/ana.23793
发表时间：
2013-02
期刊：
ANNALS OF NEUROLOGY
影响因子：
11.2
作者：
Diggs-Andrews, Kelly A.;Tokuda, Kazuhiro;Izumi, Yukitoshi;Zorumski, Charles F.;Wozniak, David F.;Gutmann, David H.
通讯作者：
Gutmann, David H.

Increased human leukocyte antigen-G expression at the maternal-fetal interface is associated with preterm birth.