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The Journal of Neuroscience, August 24, 2005, 25(34):7709-7717; doi:10.1523/JNEUROSCI.2177-05.2005
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Neurobiology of Disease
Molecular, Structural, and Functional Characterization of Alzheimer's Disease: Evidence for a Relationship between Default Activity, Amyloid, and Memory
Randy L. Buckner,1,2,3,4,5 Abraham Z. Snyder,3,6 Benjamin J. Shannon,5 Gina LaRossa,3 Rimmon Sachs,3 Anthony F. Fotenos,5 Yvette I. Sheline,3,7 William E. Klunk,9 Chester A. Mathis,9 John C. Morris,6,8 andMark A. Mintun3 1Howard Hughes Medical Institute, 2Department of Psychology, 3Mallinckrodt Institute of Radiology, 4Department of Anatomy and Neurobiology, 5Division of Biology and Biomedical Sciences, and Departments of 6Neurology, 7Psychiatry, and 8Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63105, and 9Department of Neurology, University of Pittsburgh and Western Psychiatric Institute and Clinic, Pittsburgh, Pennsylvania 15312
Alzheimer's disease (AD) and antecedent factors associated with AD were explored using amyloid imaging and unbiased measures of longitudinal atrophy in combination with reanalysis of previous metabolic and functional studies. In total, data from 764 participants were compared across five in vivo imaging methods. Convergence of effects was seen in posterior cortical regions, including posterior cingulate, retrosplenial, and lateral parietal cortex. These regions were active in default states in young adults and also showed amyloid deposition in older adults with AD. At early stages of AD progression, prominent atrophy and metabolic abnormalities emerged in these posterior cortical regions; atrophy in medial temporal regions was also observed. Event-related functional magnetic resonance imaging studies further revealed that these cortical regions are active during successful memory retrieval in young adults. One possibility is that lifetime cerebral metabolism associated with regionally specific default activity predisposes cortical regions to AD-related changes, including amyloid deposition, metabolic disruption, and atrophy. These cortical regions may be part of a network with the medial temporal lobe whose disruption contributes to memory impairment.
Key words: amyloid; PIB; memory; MCI; parietal cortex; FDG-PET; fMRI; human; prefrontal cortex; hippocampus
Received May 29, 2005; revised July 11, 2005; accepted July 11, 2005.
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