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The Journal of Neuroscience, October 7, 2009, 29(40):12686-12694; doi:10.1523/JNEUROSCI.3189-09.2009
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Neurobiology of Disease
Disruption of Functional Connectivity in Clinically Normal Older Adults Harboring Amyloid Burden
Trey Hedden,1,2,5 Koene R. A. Van Dijk,1,5 J. Alex Becker,2 Angel Mehta,1,5 Reisa A. Sperling,1,3,7 Keith A. Johnson,2,3,7 andRandy L. Buckner1,2,4,6 1Athinoula A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Charlestown, Massachusetts 02129, 2Departments of Radiology, 3Neurology, and 4Psychiatry, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts 02114, 5Department of Psychology and Center for Brain Science, Harvard University and 6Howard Hughes Medical Institute at Harvard University, Cambridge, Massachusetts 02138, and 7Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115
Correspondence should be addressed to Dr. Trey Hedden, Athinoula A. Martinos Center for Biomedical Imaging, 149 13th Street, Suite 2301, Charlestown, MA 02129. Email: hedden{at}nmr.mgh.harvard.edu
Amyloid deposition is present in 20–50% of nondemented older adults yet the functional consequences remain unclear. The current study found that amyloid accumulation is correlated with functional disruption of the default network as measured by intrinsic activity correlations. Clinically normal participants (n = 38, aged 60–88 years) were characterized using 11C-labeled Pittsburgh Compound B positron emission tomography imaging to estimate fibrillar amyloid burden and, separately, underwent functional magnetic resonance imaging (fMRI). The integrity of the default network was estimated by correlating rest-state fMRI time courses extracted from a priori regions including the posterior cingulate, lateral parietal, and medial prefrontal cortices. Clinically normal participants with high amyloid burden displayed significantly reduced functional correlations within the default network relative to participants with low amyloid burden. These reductions were also observed when amyloid burden was treated as a continuous, rather than a dichotomous, measure and when controlling for age and structural atrophy. Whole-brain analyses initiated by seeding the posterior cingulate cortex, a region of high amyloid burden in Alzheimer's disease, revealed significant disruption in the default network including functional disconnection of the hippocampal formation.
Received July 4, 2009; revised Aug. 25, 2009; accepted Aug. 26, 2009.
Correspondence should be addressed to Dr. Trey Hedden, Athinoula A. Martinos Center for Biomedical Imaging, 149 13th Street, Suite 2301, Charlestown, MA 02129. Email: hedden{at}nmr.mgh.harvard.edu
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