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.

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 一些观察结果支持了人们的猜测，即阿尔茨海默病(AD)患者的大脑葡萄糖代谢发生了变化。阿尔茨海默病患者葡萄糖转运系统的缺陷似乎是其中一个致病因素。 这项研究将检验这一理论，即海马体结构葡萄糖缺陷标志着局部脆弱性的最早特征。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血糖活动来完成。