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The Journal of Neuroscience, February 11, 2009, 29(6):1860-1873; doi:10.1523/JNEUROSCI.5062-08.2009

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Neurobiology of Disease
Cortical Hubs Revealed by Intrinsic Functional Connectivity: Mapping, Assessment of Stability, and Relation to Alzheimer's Disease

Randy L. Buckner,^1,2,3,5,6 Jorge Sepulcre,^1,3,5 Tanveer Talukdar,^3,5 Fenna M. Krienen,^1,5 Hesheng Liu,^3,5 Trey Hedden,^1,3,5 Jessica R. Andrews-Hanna,^1,5 Reisa A. Sperling,^3,5,7 and Keith A. Johnson^3,4,7

¹Department of Psychology and Center for Brain Science, Harvard University, Cambridge, Massachusetts 02138, Departments of ²Psychiatry, ³Radiology, and ⁴Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114, ⁵Athinoula A. Martinos Center for Biomedical Imaging, Charlestown, Massachusetts 02129, ⁶Howard Hughes Medical Institute, Cambridge, Massachusetts 02138, and ⁷Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts 02115

Correspondence should be addressed to Randy L. Buckner, Harvard University, 33 Kirkland Street, William James Hall 2nd Floor, Cambridge, MA 02138. Email: randy_buckner{at}harvard.edu

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 functional magnetic resonance imaging 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) because some models suggest that regions of high activity and metabolism accelerate pathology. Positron emission tomography amyloid imaging in AD (n = 10) compared with older controls (n = 29) showed high amyloid-β deposition in the locations of cortical hubs consistent with the possibility that hubs, while acting as critical way stations for information processing, may also augment the underlying pathological cascade in AD.

Key words: connectivity; cognition; Alzheimer's disease; fMRI; cortex; cingulate

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Received Oct. 12, 2008; revised Nov. 25, 2008; accepted Dec. 3, 2008.

Correspondence should be addressed to Randy L. Buckner, Harvard University, 33 Kirkland Street, William James Hall 2nd Floor, Cambridge, MA 02138. Email: randy_buckner{at}harvard.edu

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