Deficits in episodic memory retrieval reveal impaired default mode network connectivity in amnestic mild cognitive impairment
Deficits in episodic memory retrieval reveal impaired default mode network connectivity in amnestic mild cognitive impairment
复制标题
DOI：
10.1016/j.nicl.2014.02.010
复制
发表时间：
2014-01-01
影响因子：
4.2
通讯作者：
Shine, James M.
中科院分区：
文献类型：
--
作者：
Dunn, Cameron J.;Duffy, Shantel L.;Shine, James M.
遗忘型轻度认知障碍（aMCI）被认为是正常健康老龄化和痴呆症发展之间的过渡阶段。特别是，aMCI患者已被证明比没有认知障碍的个体具有更高的阿尔茨海默病（AD）的年转化率。尽管越来越多的兴趣调查这种转变的神经解剖学基础，仍然存在一些问题的病理生理过程的基础aMCI本身。最近对aMCI的一些研究表明，默认模式网络（DMN）内的连接存在特定损伤，DMN是一组与情景记忆能力密切相关的区域。然而，迄今为止，还没有研究调查了aMCI患者和具有非遗忘型MCI（naMCI）的患者之间的DMN的完整性，所述非遗忘型MCI具有认知障碍，但记忆存储系统完整。在这项研究中，我们对比了24 aMCI和33 naMCI患者使用种子为基础的静息态fMRI的DMN连接。两组的DMN内连接无统计学差异。然而，当根据情景记忆提取指标的表现分析连接性时，两组是可分离的，aMCI患者表现出海马结构和后扣带皮层之间的功能连接受损。我们提供的证据表明，这种连接的缺乏是由后扣带回枢纽的通信受损驱动的，并不简单地代表海马萎缩，这表明后扣带回变性是aMCI中DMN连接受损的驱动力。(C)2014作者爱思唯尔公司出版
Amnestic mild cognitive impairment (aMCI) is believed to represent a transitional stage between normal healthy ageing and the development of dementia. In particular, aMCI patients have been shown to have higher annual transition rates to Alzheimer's Disease (AD) than individuals without cognitive impairment. Despite intensifying interest investigating the neuroanatomical basis of this transition, there remain a number of questions regarding the pathophysiological process underlying aMCI itself. A number of recent studies in aMCI have shown specific impairments in connectivity within the default mode network (DMN), which is a group of regions strongly related to episodic memory capacities. However to date, no study has investigated the integrity of the DMN between patients with aMCI and those with a non-amnestic pattern of MCI (naMCI), who have cognitive impairment, but intact memory storage systems. In this study, we contrasted the DMN connectivity in 24 aMCI and 33 naMCI patients using seed-based resting state fMRI. The two groups showed no statistical difference in their DMN intra-connectivity. However when connectivity was analysed according to performance on measures of episodic memory retrieval, the two groups were separable, with aMCI patients demonstrating impaired functional connectivity between the hippocampal formation and the posterior cingulate cortex. We provide evidence that this lack of connectivity is driven by impaired communication from the posterior cingulate hub and does not simply represent hippocampal atrophy, suggesting that posterior cingulate degeneration is the driving force behind impaired DMN connectivity in aMCI. (C) 2014 The Authors. Published by Elsevier Inc.