TOPOGRAPHY OF CROSS-SECTIONAL AND LONGITUDINAL GLUCOSE METABOLIC DEFICITS IN ALZHEIMERS-DISEASE - PATHOPHYSIOLOGIC IMPLICATIONS
TOPOGRAPHY OF CROSS-SECTIONAL AND LONGITUDINAL GLUCOSE METABOLIC DEFICITS IN ALZHEIMERS-DISEASE - PATHOPHYSIOLOGIC IMPLICATIONS
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DOI：
10.1001/archneur.1992.00530350056020
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发表时间：
1992-11-01
影响因子：
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通讯作者：
LAREGINA, ME
中科院分区：
文献类型：
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作者：
SMITH, GS;DELEON, MJ;LAREGINA, ME
脑葡萄糖代谢的正电子发射断层扫描研究在区分退行性痴呆和阿尔茨海默病(AD)与正常衰老方面显示出很高的诊断特异性。本研究采用横断面和纵向研究设计，对AD患者的局部糖代谢缺陷进行了研究。所有受试者均符合美国国家神经与沟通障碍与卒中-阿尔茨海默病及相关障碍协会关于AD的标准(n=45)或正常(n=20)，并根据全球病情恶化程度将AD受试者细分为早期和轻度AD以及中度和中度重度AD亚组。受试者接受了非对比CT扫描和正电子发射断层扫描(PETT VI)。AD受试者(n=14)和正常对照组受试者(n=15)在基线研究2-3年后接受评估。在不同阶段显示糖代谢缺陷的大脑区域(颞叶和顶叶联合区域，皮质下灰质结构缺陷程度较轻)，在相同的AD受试者中，纵向上也显示出进一步的缺陷。从大脑萎缩的程度来看，葡萄糖代谢的减少比预期的要大。葡萄糖代谢缺陷在AD的神经病理发现和神经递质缺陷的背景下进行了讨论。
Positron emission tomographic studies of cerebral glucose metabolism have shown high diagnostic specificity in distinguishing among the degenerative dementias and differentiating between Alzheimer's disease (AD) and normal aging. The current investigation was undertaken to characterize the regional glucose metabolic deficits in AD, using cross-sectional and longitudinal study designs. All subjects met the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorders Association criteria for AD (n=45) or were normal (n=20), and the AD subjects were subdivided into incipient and mild AD and moderate plus moderately severe subgroups based on the Global Deterioration Scale. The subjects underwent a non-contrast computed tomographic scan and a positron emission tomographic (PETT VI) scan. The AD subjects (n=14) and normal control subjects (n=15) received evaluations 2 to 3 years after baseline study. The brain regions that show glucose metabolic deficits cross-sectionally (temporal and parietal association areas, with lesser degrees of deficit in subcortical gray matter structures), over the stages of AD, also show further deficits longitudinally within the same AD subjects. The reduction in glucose metabolism is greater than would be expected from the degree of brain atrophy. The glucose metabolic deficits are discussed in the context of neuropathologic findings and neurotransmitter deficits in AD.