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轻度阿尔茨海默病中相对保留的海马葡萄糖代谢。

Relatively preserved hippocampal glucose metabolism in mild Alzheimer's disease.

作者信息

Ishii K, Sasaki M, Yamaji S, Sakamoto S, Kitagaki H, Mori E

机构信息

Division of Imaging Research, Hyogo Institute for Aging Brain and Cognitive Disorders (HI-ABCD), Himeji, Japan.

出版信息

Dement Geriatr Cogn Disord. 1998 Nov-Dec;9(6):317-22. doi: 10.1159/000017083.

DOI:10.1159/000017083
PMID:9769444
Abstract

The purpose of this study was to clarify the changes in hippocampal glucose metabolism in mild Alzheimer's disease (AD) using positron emission tomography (PET) and 2-(18F)fluoro-2-deoxy-D-glucose (FDG). Forty-one patients with probable mild AD (age: 69.0 +/- 8.0 years; MMSE: 22.6 +/- 2.1) and 22 normal volunteers (age: 67.7 +/- 7.1 years) were studied. The regional cerebral metabolic rate for glucose (CMRglc) was measured using FDG and PET. Although the mean CMRglc in the parietal region was significantly lower in the AD group (right: 6.35 +/- 1.26 mg/100 g/min; left: 6.37 +/- 1.21 mg/100 g/min) than in the control group (right: 7.73 +/- 1.02 mg/100 g/min; left: 7.63 +/- 0.95 mg/100 g/min), the mean CMRglc in the hippocampus did not show a significant difference between the AD group (right: 4.58 +/- 0.70 mg/100 g/min; left: 4.63 +/- 0.67 mg/100 g/min) and the control group (right: 5.22 +/- 0.65 mg/100 g/min; left: 5.22 +/- 0.67 mg/100 g/min) by analysis of variance and post-hoc Tukey's test. The magnitude of the hippocampal CMRglc reduction was not as large as that of parietal CMRglc reduction. Statistical parametric maps (SPM) analysis also did not significantly demonstrate reduced hippocampal CMRglc in AD patients, although it did show a significant reduction in parietal CMRglc in AD patients. Hippocampal CMRglc was not significantly decreased in mild AD. This was unexpected in view of previous studies that have shown atrophy and clinical dysfunction concerning hippocampus in AD, and suggests that the pathophysiology of the hippocampus in AD may be more complex than was previously thought.

摘要

本研究的目的是使用正电子发射断层扫描(PET)和2-(18F)氟-2-脱氧-D-葡萄糖(FDG)来阐明轻度阿尔茨海默病(AD)患者海马葡萄糖代谢的变化。对41例可能患有轻度AD的患者(年龄:69.0±8.0岁;简易精神状态检查表(MMSE)评分:22.6±2.1)和22名正常志愿者(年龄:67.7±7.1岁)进行了研究。使用FDG和PET测量局部脑葡萄糖代谢率(CMRglc)。尽管AD组顶叶区域的平均CMRglc(右侧:6.35±1.26mg/100g/分钟;左侧:6.37±1.21mg/100g/分钟)显著低于对照组(右侧:7.73±1.02mg/100g/分钟;左侧:7.63±0.95mg/100g/分钟),但通过方差分析和事后Tukey检验,AD组(右侧:4.58±0.70mg/100g/分钟;左侧:4.63±0.67mg/100g/分钟)和对照组(右侧:5.22±0.65mg/100g/分钟;左侧:5.22±0.67mg/100g/分钟)海马的平均CMRglc未显示出显著差异。海马CMRglc降低的幅度不如顶叶CMRglc降低的幅度大。统计参数映射(SPM)分析也未显著显示AD患者海马CMRglc降低,尽管该分析确实显示AD患者顶叶CMRglc显著降低。轻度AD患者的海马CMRglc未显著降低。鉴于先前的研究表明AD患者海马存在萎缩和临床功能障碍,这一结果出人意料,表明AD中海马的病理生理学可能比之前认为的更为复杂。

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