CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE

阿尔茨海默病纵向 PET 变化的临床相关性

• 批准号: 7607903
• 负责人: MONY J. de LEON
• 金额: $ 0.02万
• 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/7607903
• 关键词: Alleles; Alzheimer' s Disease; Amyloid; Atrophic; Brain; Clinical; Computer Retrieval of Information on Scientific Projects Database; Defect; Funding; Glucose Transport Inhibition; Glucose Transporter; Glutamates; Grant; Institution; Neurons; Numbers; Peripheral; Research; Research Personnel; Resources; Rest; Signal Transduction; Source; Testing; United States National Institutes of Health; apolipoprotein E-4; glucose metabolism; glucose transport

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), these include: reduced numbers and function of glucose transporters [1;2], amyloid ? inhibition of glucose transport [3;4], defective neuronal glutamate signaling of astrocytic glucose metabolism [5], glycolytic enzymatic defects [6], and altered peripheral glucoregulatory function [7-9]. Further contributing to such speculation have been observations that resting brain glucose metabolism is reduced among unimpaired carriers of the ApoE ? 4 allele, in the absence of structural atrophic changes. The proposed study will directly test the hypothesis that brain glucose transport is altered in AD.

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，其中包括：葡萄糖转运蛋白的数量和功能减少和功能[1; 2]，淀粉样蛋白？葡萄糖转运的抑制[3; 4]，星形细胞葡萄糖代谢的缺陷神经元谷氨酸信号传导[5]，糖酵解酶促缺陷[6]和周围外周糖调节功能的改变[7-9]。进一步促进这种猜测的是，观察到静息脑葡萄糖代谢在未损坏的APOE载体中减少了？ 4等位基因，在没有结构性萎缩的情况下。 拟议的研究将直接检验以下假设：AD中脑葡萄糖转运发生了改变。