Functional connectivity tracks clinical deterioration in Alzheimer's disease

被引:417
作者
Damoiseaux, Jessica S. [1 ]
Prater, Katherine E. [2 ]
Miller, Bruce L. [3 ]
Greicius, Michael D. [1 ]
机构
[1] Stanford Univ, Funct Imaging Neuropsychiat Disorders Lab, Dept Neurol & Neurol Sci, Sch Med, Palo Alto, CA 94304 USA
[2] Univ Michigan, Neurosci Grad Program, Ann Arbor, MI 48109 USA
[3] Univ Calif San Francisco, Dept Neurol, Memory & Aging Ctr, San Francisco, CA USA
关键词
Alzheimer's disease; Functional connectivity; Resting state fMRI; Disease progression; Default mode network; Fractionation; POSTERIOR CINGULATE CORTEX; RESTING-STATE NETWORKS; DEFAULT-MODE; BRAIN ACTIVITY; FMRI; IMPAIRMENT; CARRIERS; ATROPHY; ALLELE; ROBUST;
D O I
10.1016/j.neurobiolaging.2011.06.024
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
While resting state functional connectivity has been shown to decrease in patients with mild and/or moderate Alzheimer's disease, it is not yet known how functional connectivity changes in patients as the disease progresses. Furthermore, it has been noted that the default mode network is not as homogenous as previously assumed and several fractionations of the network have been proposed. Here, we separately investigated the modulation of 3 default mode subnetworks, as identified with group independent component analysis, by comparing Alzheimer's disease patients to healthy controls and by assessing connectivity changes over time. Our results showed decreased connectivity at baseline in patients versus controls in the posterior default mode network, and increased connectivity in the anterior and ventral default mode networks. At follow-up, functional connectivity decreased across all default mode systems in patients. Our results suggest that earlier in the disease, regions of the posterior default mode network start to disengage whereas regions within the anterior and ventral networks enhance their connectivity. However, as the disease progresses, connectivity within all systems eventually deteriorates. (C) 2012 Elsevier Inc. All rights reserved.
引用
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页数:12
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