Investigation of the effective connectivity of resting state networks in Alzheimer's disease: a functional MRI study combining independent components analysis and multivariate Granger causality analysis

默认模式网络 静息状态功能磁共振成像 格兰杰因果关系 神经科学 心理学 功能磁共振成像 认知 神经影像学 疾病 因果关系(物理学) 功能连接 神经生理学 医学 计算机科学 内科学 机器学习 物理 量子力学
作者
Zhenyu Liu,Yumei Zhang,Lijun Bai,Hao Yan,Ruwei Dai,Chongguang Zhong,Hu Wang,Wen‐Juan Wei,Ting Xue,Yuanyuan Feng,Youbo You,Jie Tian
出处
期刊:NMR in Biomedicine [Wiley]
卷期号:25 (12): 1311-1320 被引量:57
标识
DOI:10.1002/nbm.2803
摘要

Recent neuroimaging studies have shown that the cognitive and memory decline in patients with Alzheimer's disease (AD) is coupled with abnormal functions of focal brain regions and disrupted functional connectivity between distinct brain regions, as well as losses in small‐world attributes. However, the causal interactions among the spatially isolated, but functionally related, resting state networks (RSNs) are still largely unexplored. In this study, we first identified eight RSNs by independent components analysis from resting state functional MRI data of 18 patients with AD and 18 age‐matched healthy subjects. We then performed a multivariate Granger causality analysis (mGCA) to evaluate the effective connectivity among the RSNs. We found that patients with AD exhibited decreased causal interactions among the RSNs in both intensity and quantity relative to normal controls. Results from mGCA indicated that the causal interactions involving the default mode network and auditory network were weaker in patients with AD, whereas stronger causal connectivity emerged in relation to the memory network and executive control network. Our findings suggest that the default mode network plays a less important role in patients with AD. Increased causal connectivity of the memory network and self‐referential network may elucidate the dysfunctional and compensatory processes in the brain networks of patients with AD. These preliminary findings may provide a new pathway towards the determination of the neurophysiological mechanisms of AD. Copyright © 2012 John Wiley & Sons, Ltd.
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