CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN NORMAL AGING

正常衰老过程中纵向 PET 变化的临床相关性

• 批准号: 7607905
• 负责人: MONY J. de LEON
• 金额: $ 1.55万
• 依托单位: STATE UNIVERSITY NEW YORK STONY BROOK
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-03-23 至 2007-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7607905
• 关键词: Alzheimer' s Disease; Brain; Clinical; Computer Retrieval of Information on Scientific Projects Database; Defect; Funding; Glucose; Grant; Hippocampal Formation; Hyperglycemia; Institution; Positron-Emission Tomography; Research; Research Personnel; Resources; Source; System; Testing; United States National Institutes of Health; glucose metabolism; glucose transport; normal aging; theories

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Several observations have contributed to speculation that brain glucose metabolism is altered in Alzheimer's disease (AD). One of the contributing factors appears to be a defect in the glucose transport system in AD subjects. This study will test the theory that defects in hippocampal formation glucose mark the earliest features of regional vulnerability. This will be done by observing glucose activity via Positron Emission Tomography after a mild hyperglycemic challenge.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 几种观察结果导致人们猜测，阿尔茨海默氏病（AD）改变了大脑葡萄糖代谢。促成因素之一似乎是AD受试者中葡萄糖传输系统中的缺陷。 这项研究将测试以海马形成葡萄糖缺陷的理论，标志着区域脆弱性的最早特征。这将通过在轻度高血糖挑战后通过正电子发射断层扫描观察葡萄糖活性来完成。