Associative memory deficits in mild cognitive impairment: The role of hippocampal formation
Associative memory deficits in mild cognitive impairment: The role of hippocampal formation
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DOI：
10.1016/j.neuroimage.2011.05.047
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发表时间：
2011-08-15
期刊：
影响因子：
5.7
通讯作者：
Cantero, J. L.
中科院分区：
文献类型：
--
作者：
Atienza, M.;Atalaia-Silva, K. C.;Cantero, J. L.
阿尔茨海默病（Alzheimer's disease，AD）早期的神经病理学改变主要发生在海马的内嗅皮层（entorhinal cortex，EC）、下托（subiculum，SB）和角氨1（cornu ammonis 1，CA 1），这可能是导致轻度认知障碍（mild cognitive impairment，MCI）的非痴呆患者联想记忆障碍的原因。为了在体内验证这一假设，我们研究了与认知正常（CN）老年受试者相比，MCI中这些区域的体积变化是否与联想记忆失败有关。EC和海马子字段的体积变化进行了测定，通过使用基于变形的形态计量学技术应用于概率cytoarchitectonic地图来自死后人脑。CN受试者区分MCI患者，首先确定EC和海马的局部体积差异，然后评估这些解剖学变化与非故意面部位置关联任务中的表现相关的方式。MCI患者不仅在建立新的关联方面比CN老年人表现更差，而且他们还无法从语义编码中获益以改善情景绑定。根据我们最初的假设，在EC和海马CA的局部体积减少占联想记忆的组间差异，而萎缩CA，但不是在EC，占协会的语义编码。从本研究中可以得出两个主要结论：i）在编码过程中获得语义信息不会减少MCI中的情节缺陷; ii）EC和海马CA，两个早期受AD神经病理学影响的区域，至少部分地负责MCI患者中观察到的联想记忆缺陷。(C)2011 Elsevier Inc. All rights reserved.
Neuropathological events featuring early stages of Alzheimer's disease (AD) appear in the entorhinal cortex (EC), subiculum (SB) and cornu ammonis 1 (CA1) of hippocampus, which may account for associative memory deficits in non-demented people with mild cognitive impairment (MCI). To test this hypothesis in vivo, we investigated whether volume changes in these regions are related to failures in associative memory in MCI as compared to cognitively normal (CN) elderly subjects. Volume changes in EC and hippocampal subfields were determined by using deformation-based morphometry techniques applied to probabilistic cytoarchitectonic maps derived from post mortem human brains. CN subjects were distinguished from MCI patients by firstly identifying local volume differences in EC and hippocampus, and then evaluating the way in which these anatomical changes correlated with performance in a non-intentional face-location association task. MCI patients not only performed worse than CN elders in building new associations, but they were further unable to benefit from semantic encoding to improve episodic binding. According to our initial hypothesis, local volume reductions in both EC and hippocampal CA accounted for group differences in associative memory whereas atrophy in CA, but not in EC, accounted for semantic encoding of associations. Two main conclusions can be drawn from the present study: i) access to semantic information during encoding does not reduce the episodic deficit in MCI; and ii) EC and hippocampal CA, two regions early affected by AD neuropathology, are responsible, at least partially, for associative memory deficits observed in MCI patients. (C) 2011 Elsevier Inc. All rights reserved.