SPECTROSCOPY OF ALZHEIMER'S DISEASE & VASCULAR DEMENTIA

这个项目的总体目标是确定，使用31-磷(31P) 和质子(1H)核磁共振(核磁共振)谱，如果大脑 代谢标记物存在，可以区分阿尔茨海默病和 与多部位皮质下缺血相关的痴呆。A五 一年的纵向研究将调查临床、成像(磁学 磁共振成像)、代谢(体内31P和1H核磁共振)和 部分皮质下多发性疾病患者的神经病理学资料 缺血性痴呆(MSID)、阿尔茨海默病(AD)或混合AD和 血管疾病。而在非痴呆症老年人对照组中。这项研究旨在 描述大脑能量磷酸盐，磷脂代谢， PH、游离镁、N-乙酰天冬氨酸和可能 准确预测AD、MSID和混合性疾病的临床和病理诊断 MSID/AD。此外，还将检验两种假设来解释这种转变 朝向磷光谱的高能磷酸盐一端 在MSID中报告。一种假设将这种转变归因于 分子能量在大脑浅层不相连区域的利用 来自皮质下损伤的神经元输入。其他假设属性 大脑皮质区域向星形细胞反应性增强的转变 受到轻度缺血的影响。第一种假说预言 高能磷酸盐转移的程度应该与 皮质下白质的范围和位置 MRI上可见高信号。第二种假设预测MSID 向高能磷酸盐末端转移的患者 磷光谱将有微空洞和增加的神经胶质 获得光谱的皮质区域的免疫反应性，甚至 尽管这些区域在核磁共振上看起来是正常的。

The overall aim of this project is to determine, using 31-Phosphorous (31P) and proton (1H) nuclear magnetic resonance (NMR) spectroscopy, if brain metabolic markers exist that will distinguish Alzheimer's disease from dementia associated with multiple sites of subcortical ischemia. A five year longitudinal study will investigate clinical, imaging (magnetic resonance imaging, MRI), metabolic (in vivo 31P and 1H NMR) and neuropathologic data in selected patients with multiple subcortical ischemic dementia (MSID), Alzheimer's disease (AD), or mixed AD and vascular disease. and in nondemented elderly controls. The study aims to characterize changes in brain energy phosphate, phospholipid metabolism, pH, free magnesium, N-acetyl aspartate, and cholinated compounds that might accurately predict clinical and pathologic diagnoses of AD, MSID, and mixed MSID/AD. Further, two hypotheses will be tested to explain the shift towards the high energy phosphate end of the phosphorus spectrum previously reported in MSID. One hypothesis attributes the shift to a decreased utilization of molecular energy in superficial brain regions disconnected from neuronal input by subcortical lesions. The other hypothesis attributes the shift to increased astrocytic reactivity in cortical regions that have been subjected to mild levels of ischemia. The first hypothesis predicts that the extent of the high energy phosphate shift should be correlated with the extent and location of the subcortical white matter hyperintensities observed on MRI. The second hypothesis predicts that MSID patients with a shift towards the high energy phosphate end of the phosphorus spectrum will have microcavities and increased glial immunoreactivity in cortical regions where spectra are obtained, even though these areas appeared to be normal on MRI.