Biomarker Core

生物标志物核心

• 批准号: 8287317
• 负责人: Anne Fagan
• 金额: $ 28.45万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-09-30 至 2016-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8287317
• 关键词: Address; Adult Children; Affect; Age; Aging; Alzheimer' s Disease; Amyloid; Biological; Biological Assay; Biological Markers; Brain; Cataloging; Catalogs; Cell Death; Clinical; Clinical Pathology; Clinical Trials; Clinical Trials Design; Collaborations; Collection; Communities; Correlative Study; Data; Data Base Management; Databases; Dementia; Diagnosis; Diagnostic; Disease; Drops; Epidemic; Equipment and supply inventories; Event; Fasting; Functional disorder; Funding; Future; Grant; Impaired cognition; Individual; Informatics; Instruction; Journals; Late Onset Alzheimer Disease; Left; Lewy Bodies; Link; Liquid substance; Measurement; Mission; Monitor; Neurobehavioral Manifestations; Neurons; Paper; Participant; Pathology; Peer Review; Physicians; Pittsburgh Compound-B; Plasma; Positron-Emission Tomography; Probability; Process; Productivity; Proteomics; Public Health; Publishing; Qualifying; Research; Research Infrastructure; Research Personnel; Sampling; Senile Plaques; Specimen; Staging; Symptoms; Synapses; System; Testing; Therapeutic; Therapeutic Intervention; Universities; Washington; amyloid imaging; base; brain volume; cohort; data management; data sharing; disease diagnosis; disorder risk; drug candidate; effective therapy; high risk; medical schools; neuron loss; novel; outcome forecast; pre-clinical; prevent; prognostic; quality assurance; repository; success; tau Proteins; therapy development; tool

Alzheimer's disease (AD) will become a public health crisis within the next 2-3 decades if left unchecked. There are no proven treatments that delay the onset or prevent the progression of AD, although several promising candidates are being developed. During the development of these therapies, it will be very important to have biomarkers that can identify individuals at high risk for AD in eariiest clinical stages in order to target them for clinical trials of disease-modifying therapies and to monitor therapy success. Clinicopathologic evidence suggests that AD pathology (particularly the buildup of amyloid plaques) begins 10-20 years before the onset of cognitive symptoms. The earliest clinical symptoms of AD are accompanied by, and likely due to, neuronal and synaptic dysfunction and/or cell death. Thus, it will be critical to identify individuals with "preclinical" and very early stage symptomatic AD, prior to marked clinical symptoms and neuron loss, so new therapies will have the greatest chance to preserve normal brain function. The Adult Children Study (ACS) Biomarker Core was initially funded as a competitive supplement to the ACS PPG in April 2008. The Core's mission is to facilitate and support antecedent AD biomarkers research by providing the necessary infrastructure for the collection, storage, and dissemination of fluid (CSF and plasma) samples (and associated data) for our own research at Washington University and that of the greater AD scientific community. Since inception of the Core, our productivity has roughly doubled (as defined by the number of CSF and plasma samples collected, the number of samples disseminated to investigators, and the number of papers using our samples that have been published in peer-reviewed journals). Thus, in the present renewal application, we propose to build upon our success and propose the following aims: Aim 1: Maintain and grow a repository of fasted CSF and plasma samples for present and future aging and AD biomarker studies. Aim 2: Coordinate the distribution of CSF and plasma samples to qualified investigators. Aim 3: Compare the values obtained for CSF Ap42, tau and ptauiei in Project 2 as a function of assay (Innotest vs. xMAP) and plasma Ap species (APi^o, APx-40, APi.42. APx^2) as a function of fasting state.

如果不加以控制，阿尔茨海默病（AD）将在未来20 - 30年内成为公共卫生危机。 没有经过证实的治疗方法可以延迟AD的发作或预防AD的进展，尽管有几种治疗方法可以延缓AD的发作或预防AD的进展。 正在培养有前途的候选人。在这些治疗方法的发展过程中， 重要的是具有可以在最早的临床阶段识别处于AD高风险的个体的生物标志物， 将他们作为疾病缓解疗法的临床试验的目标，并监测治疗的成功率。 临床病理学证据表明，AD病理学（特别是淀粉样斑块的积累）开始于 在认知症状出现前10-20年。AD的最早临床症状伴随着 由或可能由神经元和突触功能障碍和/或细胞死亡引起。因此，关键是要确定 患有“临床前”和极早期症状性AD的个体，在出现明显的临床症状之前， 因此，新的治疗方法将有最大的机会保持正常的大脑功能。 成人儿童研究（ACS）生物标志物核心最初是作为一个竞争性的补充， ACS PPG，2008年4月。核心的使命是促进和支持AD生物标志物的研究 通过提供必要的基础设施来收集、储存和散布流体（CSF和 血浆）样本（和相关数据），用于我们自己在华盛顿大学的研究和 更大的AD科学界。自从核心开始以来，我们的生产力大约翻了一番（ 由采集的CSF和血浆样本数量、分发至 研究人员，以及使用我们的样本发表在同行评审中的论文数量 期刊）。因此，在目前的续期申请中，我们建议在我们成功的基础上， 以下目标： 目的1：维持和培养空腹CSF和血浆样本库，以备当前和未来衰老之需 和AD生物标志物研究。 目的2：协调将CSF和血浆样本分发给合格的研究者。 目的3：比较项目2中获得的CSF Ap 42、tau和ptauiei的值作为测定的函数 （Innotest对xMAP）和血浆Ap种类（API-40、APx-40、AP 1 - 42）。APx ^2）作为空腹状态的函数。