Gonzalez R G, Guimaraes A R, Moore G J, Crawley A, Cupples L A, Growdon J H
Massachusetts General Hospital NMR Center, Charlestown, Massachusetts, USA.
Alzheimer Dis Assoc Disord. 1996 Spring;10(1):46-52.
The purpose of this study was to determine whether, in Alzheimer disease (AD) patients, abnormalities in energy charge or phospholipid metabolism could be detected during life with quantitative phosphorus magnetic resonance spectroscopy (31P MRS). We performed in vivo 31P MRS in 16 patients with a clinical diagnosis of probable AD with mild to moderate dementia severity (mean Blessed Dementia Score = 17.5, range = 7-37) and in 8 healthy, nondemented, age-matched, control subjects. MR studies were performed on a commercial 1.5 T MR imager using a volume head coil. We acquired brain spectra by sampling a 6-cm-thick axial slice through the cerebrum (a region that includes approximately 900 ml of brain tissue); we measured beta-nucleoside triphosphate (beta-NTP), phosphocreatine (PCr), phosphomonoesters (PME), phosphodiesters (PDE), and inorganic phosphate (Pi) concentrations, then calculated ratios of these resonances. The beta-NTP, PCr, and Pi resonances in AD and control subjects were not significantly different. These data indicate that brain energy stores are not depleted in AD. No significant differences were detected in the absolute measurements of PME and PDE between the AD and control groups. However, among the calculated ratios, an increase in the PME/PDE ratio of approximately 50%, mostly due to a decrease in the PDE signal, was statistically significant (AD PME/PDE mean = 0.35, range 0.13-0.71; normal PME/PDE mean = 0.22, range 0.16-0.34). We speculate that the difference in PDE reflects changes in the biophysical state of membrane phospholipids in AD.
本研究的目的是确定能否在阿尔茨海默病(AD)患者生前通过定量磷磁共振波谱(31P MRS)检测到能量电荷或磷脂代谢异常。我们对16例临床诊断为可能患有AD且痴呆严重程度为轻度至中度(平均Blessed痴呆评分 = 17.5,范围 = 7 - 37)的患者以及8名年龄匹配、健康且无痴呆的对照者进行了活体31P MRS检查。磁共振研究在一台商用1.5 T磁共振成像仪上使用容积头部线圈进行。我们通过对穿过大脑的一个6厘米厚的轴向切片(该区域包含约900毫升脑组织)进行采样来获取脑波谱;我们测量了β - 核苷三磷酸(β - NTP)、磷酸肌酸(PCr)、磷酸单酯(PME)、磷酸二酯(PDE)和无机磷酸盐(Pi)的浓度,然后计算这些共振的比率。AD患者和对照者的β - NTP、PCr和Pi共振无显著差异。这些数据表明AD患者脑内能量储备未耗尽。AD组和对照组之间PME和PDE的绝对测量值未检测到显著差异。然而,在计算出的比率中,PME/PDE比率增加了约50%,主要是由于PDE信号降低,具有统计学意义(AD组PME/PDE平均值 = 0.35,范围0.13 - 0.71;正常组PME/PDE平均值 = 0.22,范围0.16 - 0.34)。我们推测PDE的差异反映了AD患者膜磷脂生物物理状态的变化。