CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE

这个子项目是利用由NIH/NCRR资助的中心拨款提供的资源的许多研究子项目之一。子项目和调查员(PI)可能从另一个NIH来源获得了主要资金，因此可能会出现在其他CRISE条目中。列出的机构是针对中心的，而不一定是针对调查员的机构。一些观察结果支持了阿尔茨海默病(AD)患者大脑葡萄糖代谢改变的推测，其中包括：葡萄糖转运蛋白[1；2]的数量和功能减少，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神经元谷氨酸信号缺陷[5]，糖酵解酶缺陷[6]，以及外周糖调节功能改变[7-9]。进一步促成这种推测的是观察到，在没有结构性萎缩性改变的情况下，ApoE？4等位基因的未受损携带者的静息脑葡萄糖代谢降低。这项拟议的研究将直接检验阿尔茨海默病患者大脑葡萄糖转运发生改变的假设。

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 gluco-regulatory 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.