Spatial patterns of atrophy, hypometabolism, and amyloid deposition in Alzheimer's disease correspond to dissociable functional brain networks.
Spatial patterns of atrophy, hypometabolism, and amyloid deposition in Alzheimer's disease correspond to dissociable functional brain networks.
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DOI：
10.1002/hbm.23018
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发表时间：
2016-01
影响因子：
4.8
通讯作者：
Alzheimer's Disease Neuroimaging Initiative
中科院分区：
文献类型：
--
作者：
Grothe MJ;Teipel SJ;Alzheimer's Disease Neuroimaging Initiative
最近对阿尔茨海默病 (AD) 的神经影像学研究强调了 AD 相关的大脑变化与称为默认模式网络 (DMN) 的突出皮质关联网络之间的拓扑相似性。然而，与边缘和异模联结皮层的其他内在连接网络（ICN）相比，DMN 的不同成像异常的特异性尚未得到系统检查。我们使用 AV45-PET 评估了区域淀粉样蛋白负荷，使用 FDG-PET 评估了神经元代谢，并使用结构 MRI 评估了灰质体积，对阿尔茨海默病神经影像计划的 473 名参与者进行了评估，包括临床前、痴呆前期和临床表现的 AD 阶段。使用互补的感兴趣区域和基于体素的分析来评估由标准化功能连接图谱定义的人脑七个主要 ICN 内的疾病阶段和模式特定变化。 AD 痴呆中的淀粉样蛋白沉积显示出对 DMN 的偏好，但其他新皮质 ICN 也观察到了高效应大小，最显着的是额顶叶控制网络。萎缩性变化在前边缘网络中最为特异，其次是DMN，而其他新皮质网络则相对较少。代谢减退似乎是淀粉样蛋白和萎缩相关特征的混合。在痴呆前期以及临床前阶段的淀粉样蛋白沉积中也观察到了类似的模态依赖性网络特异性模式。这些定量数据证实了 DMN 对 AD 多模态成像异常的高度脆弱性。然而，成像异常不是对DMN有选择性，而是更普遍地影响高阶认知网络，重要的是，这些网络的脆弱性概况对于AD病理学的不同方面显着不同。
Recent neuroimaging studies of Alzheimer’s disease (AD) have emphasized topographical similarities between AD-related brain changes and a prominent cortical association network called the default-mode network (DMN). However, the specificity of distinct imaging abnormalities for the DMN compared to other intrinsic connectivity networks (ICNs) of the limbic and heteromodal association cortex has not yet been examined systematically. We assessed regional amyloid load using AV45-PET, neuronal metabolism using FDG-PET, and gray matter volume using structural MRI, in 473 participants from the Alzheimer’s Disease Neuroimaging Initiative, including preclinical, predementia and clinically manifest AD stages. Complementary region-of-interest and voxel-based analyses were used to assess disease stage- and modality-specific changes within seven principle ICNs of the human brain as defined by a standardized functional connectivity atlas. Amyloid deposition in AD dementia showed a preference for the DMN, but high effect sizes were also observed for other neocortical ICNs, most notably the frontoparietal-control network. Atrophic changes were most specific for an anterior limbic network, followed by the DMN, whereas other neocortical networks were relatively spared. Hypometabolism appeared to be a mixture of both amyloid- and atrophy-related profiles. Similar patterns of modality-dependent network specificity were also observed in the predementia and, for amyloid deposition, in the preclinical stage. These quantitative data confirm a high vulnerability of the DMN for multimodal imaging abnormalities in AD. However, rather than being selective for the DMN, imaging abnormalities more generally affect higher order cognitive networks and, importantly, the vulnerability profiles of these networks markedly differ for distinct aspects of AD pathology.