He Yong, Chen Zhang, Evans Alan
McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada H3A 2B4.
J Neurosci. 2008 Apr 30;28(18):4756-66. doi: 10.1523/JNEUROSCI.0141-08.2008.
Recent research on Alzheimer's disease (AD) has shown that cognitive and memory decline in this disease is accompanied by disrupted changes in the coordination of large-scale brain functional networks. However, alterations in coordinated patterns of structural brain networks in AD are still poorly understood. Here, we used cortical thickness measurement from magnetic resonance imaging to investigate large-scale structural brain networks in 92 AD patients and 97 normal controls. Brain networks were constructed by thresholding cortical thickness correlation matrices of 54 regions and analyzed using graph theoretical approaches. Compared with controls, AD patients showed decreased cortical thickness intercorrelations between the bilateral parietal regions and increased intercorrelations in several selective regions involving the lateral temporal and parietal cortex as well as the cingulate and medial frontal cortex regions. Specially, AD patients showed abnormal small-world architecture in the structural cortical networks (increased clustering and shortest paths linking individual regions), implying a less optimal topological organization in AD. Moreover, AD patients were associated with reduced nodal centrality predominantly in the temporal and parietal heteromodal association cortex regions and increased nodal centrality in the occipital cortex regions. Finally, the brain networks of AD were about equally as robust to random failures as those of controls, but more vulnerable against targeted attacks, presumably because of the effects of pathological topological organization. Our findings suggest that the coordinated patterns of cortical morphology are widely altered in AD patients, thus providing structural evidence for disrupted integrity in large-scale brain networks that underlie cognition. This work has implications for our understanding of how functional deficits in patients are associated with their underlying structural (morphological) basis.
近期对阿尔茨海默病(AD)的研究表明,该疾病中的认知和记忆衰退伴随着大规模脑功能网络协调变化的紊乱。然而,AD患者脑结构网络协调模式的改变仍知之甚少。在此,我们利用磁共振成像测量皮质厚度,以研究92名AD患者和97名正常对照者的大规模脑结构网络。通过对54个区域的皮质厚度相关矩阵进行阈值处理构建脑网络,并使用图论方法进行分析。与对照组相比,AD患者双侧顶叶区域之间的皮质厚度相互关联降低,而在涉及颞叶外侧和顶叶皮质以及扣带回和内侧额叶皮质区域的几个选择性区域中相互关联增加。特别地,AD患者在皮质结构网络中表现出异常的小世界架构(聚类增加以及连接各个区域的最短路径增加),这意味着AD中的拓扑组织不太优化。此外,AD患者主要在颞叶和顶叶异模态联合皮质区域的节点中心性降低,而在枕叶皮质区域的节点中心性增加。最后,AD患者的脑网络对随机故障的鲁棒性与对照组大致相同,但更容易受到针对性攻击,这可能是由于病理拓扑组织的影响。我们的研究结果表明,AD患者皮质形态的协调模式广泛改变,从而为认知背后的大规模脑网络完整性破坏提供了结构证据。这项工作对于我们理解患者的功能缺陷如何与其潜在的结构(形态)基础相关具有重要意义。