Cortical hubs revealed by intrinsic functional connectivity: mapping, assessment of stability, and relation to Alzheimer's disease.
Cortical hubs revealed by intrinsic functional connectivity: mapping, assessment of stability, and relation to Alzheimer's disease.
复制标题
通过内在功能连接揭示的皮质中枢:绘图、稳定性评估以及与阿尔茨海默病的关系。
DOI:
10.1523/jneurosci.5062-08.2009
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发表时间:
2009-02-11
影响因子:
5.3
通讯作者:
Johnson, Keith A.
中科院分区:
文献类型:
--
作者:
Buckner, Randy L.;Sepulcre, Jorge;Talukdar, Tanveer;Krienen, Fenna M.;Liu, Hesheng;Hedden, Trey;Andrews-Hanna, Jessica R.;Sperling, Reisa A.;Johnson, Keith A.
Recent evidence suggests that some brain areas act as hubs interconnecting distinct, functionally-specialized systems. These nexuses are intriguing because of their potential role in integration and also because they may augment metabolic cascades relevant to brain disease. To identify regions of high connectivity in the human cerebral cortex, we applied a computationally-efficient approach to map the degree of intrinsic functional connectivity across the brain. Analysis of two separate fMRI datasets (each n=24) demonstrated hubs throughout heteromodal areas of association cortex. Prominent hubs were located within posterior cingulate, lateral temporal, lateral parietal, and medial/lateral prefrontal cortices. Network analysis revealed that many, but not all, hubs were located within regions previously implicated as components of the default network. A third dataset (n=12) demonstrated that the locations of hubs were present across passive and active task states suggesting that they reflect a stable property of cortical network architecture. To obtain an accurate reference map, data were combined across 127 participants to yield a consensus estimate of cortical hubs. Using this consensus estimate, we explored whether the topography of hubs could explain the pattern of vulnerability in Alzheimer’s disease (AD) as some models suggest that regions of high activity and metabolism accelerate pathology. PET amyloid imaging in AD (n=10) as compared to older controls (n=29) showed high Aβ deposition in the locations of cortical hubs consistent with the possibility that hubs, while acting as critical waystations for information processing, may also augment the underlying pathological cascade in AD.