CLINICAL CORRELATES OF LONGITUDINAL PET CHANGES IN ALZHEIMER'S DISEASE

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目及 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 一些观察结果有助于推测阿尔茨海默病（AD）的脑葡萄糖代谢发生改变，这些观察结果包括：葡萄糖转运蛋白的数量和功能减少[1;2]，淀粉样蛋白？葡萄糖转运抑制[3;4]、星形胶质细胞葡萄糖代谢的神经元谷氨酸信号传导缺陷[5]、糖酵解酶缺陷[6]和外周葡萄糖调节功能改变[7-9]。进一步促进这种猜测已经观察到，静息脑葡萄糖代谢减少之间未受损的载脂蛋白E？4等位基因，在没有结构萎缩性改变。 拟议的研究将直接检验AD患者脑葡萄糖转运改变的假设。

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 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.