CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。一些观察结果有助于推测阿尔茨海默病（AD）中脑葡萄糖代谢的改变，这些包括：葡萄糖转运蛋白的数量和功能减少[1；[2]、淀粉样蛋白？抑制葡萄糖转运[3]；4]，星形细胞葡萄糖代谢[5]的神经元谷氨酸信号缺陷，糖酵解酶缺陷[6]，以及外周葡萄糖调节功能的改变[7-9]。在ApoE基因未受损的携带者中，静息时脑葡萄糖代谢减少的观察结果进一步证实了这一推测。4个等位基因，在没有结构性萎缩变化的情况下。该研究将直接验证AD患者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.