Limbic hypometabolism in Alzheimer's disease and mild cognitive impairment
Limbic hypometabolism in Alzheimer's disease and mild cognitive impairment
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DOI：
10.1002/ana.10669
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发表时间：
2003-09-01
影响因子：
11.2
通讯作者：
Hodges, JR
中科院分区：
文献类型：
--
作者：
Nestor, PJ;Fryer, TD;Hodges, JR
早期阿尔茨海默病（AD）的特征性遗忘症的神经基础仍然不确定。死后病理学研究表明，早期参与内侧颞叶，而在体内代谢研究表明，代谢减退的后扣带回皮质。使用的技术相结合的解剖精度的磁共振成像与正电子发射断层扫描，我们发现严重减少代谢的边缘结构（海马复合体，内侧丘脑，乳头体，后扣带回）在轻度AD患者的网络。然后，我们研究了一个轻度认知障碍的队列，其中健忘症是唯一的认知异常，并通过相同的网络发现了可比的代谢低下。AD和轻度认知功能障碍组的区别，但是，在这个网络之外的变化，前者表现出显着的代谢减退，杏仁核和颞顶和额叶联合皮层，而后者没有。早期AD的遗忘症反映了严重但局部的边缘系统功能障碍。
The neural basis of the amnesia characterizing early Alzheimer's disease (AD) remains uncertain. Postmortem pathological studies have suggested early involvement of the mesial temporal lobe, whereas in vivo metabolic studies have shown hypometabolism of the posterior cingulate cortex. Using a technique that combined the anatomic precision of magnetic resonance imaging with positron emission tomography, we found severe reductions of metabolism throughout a network of limbic structures (the hippocampal complex, medial thalamus, mamillary bodies, and posterior cingulate) in patients with mild AD. We then studied a cohort with mild cognitive impairment in whom amnesia was the only cognitive abnormality and found comparable hypometabolism through the same network. The AD and mild cognitive impairment groups were differentiated, however, by changes outside this network, the former showing significant hypometabolism in amygdala and temporoparietal and frontal association cortex, whereas the latter did not. The amnesia of very early AD reflects severe but localized limbic dysfunction.