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From the Department of Anatomy and Neurobiology (R.S.D., T.L.K., R.J.K.) and Center for Biomedical Imaging (R.J.K.), Boston University School of Medicine; Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology (B.F.), Department of Psychiatry (D.B., R.J.K.), and Department of Neurology (B.T.H.), Massachusetts General Hospital; Computer Science and Artificial Intelligence Laboratory (B.F.), Massachusetts Institute of Technology; Departments of Biostatistics (H.J.C.) and Environmental Health (R.J.K.), Boston University School of Public Health; Department of Radiology (C.R.G.G., R.J.K.), Brigham and Women’s Hospital, Boston, MA; and Department of Neurology (M.S.A.), Johns Hopkins University School of Medicine, Baltimore, MD.
Address correspondence and reprint requests to Dr. Ronald J. Killiany, Dept. of Anatomy and Neurobiology, Center for Biomedical Imaging, Boston University School of Medicine, Boston, MA 02118 killiany{at}bu.edu
Background: MRI studies have demonstrated differential rates of atrophy in the entorhinal cortex and hippocampus during the prodromal phase of Alzheimer disease (AD). The current study was designed to determine whether a broader set of temporoparietal regions show differential rates of atrophy during the evolution of AD.
Methods: Sixteen regions of interest (ROIs) were analyzed on MRI scans obtained at baseline and follow-up in 66 subjects comprising three groups: controls = individuals who were cognitively normal at both baseline and follow-up; nonconverters = subjects with mild cognitive impairment (MCI) at both baseline and follow-up; converters had MCI at baseline but had progressed to AD at follow-up.
Results: Annualized percent change was analyzed with multivariate analysis of variance (MANOVA), covaried for age. The MANOVA demonstrated an effect of group (p = 0.004). Post hoc comparisons demonstrated greater rates of atrophy for converters vs nonconverters for six ROIs: hippocampus, entorhinal cortex, temporal pole, middle temporal gyrus, fusiform gyrus, and inferior temporal gyrus. Converters showed differentially greater rates of atrophy than controls in five of the same ROIs (and inferior parietal lobule). Rates of change in clinical status were correlated with the atrophy rates in these regions. Comparisons between controls and nonconverters demonstrated no differences.
Conclusion: These results demonstrate that temporoparietal regions show differential rates of atrophy on MRI during prodromal Alzheimer disease (AD). MRI data correlate with measures of clinical severity and cognitive decline, suggesting the potential of these regions of interest as antemortem markers of prodromal AD.
Abbreviations: AD = Alzheimer disease; APC = annualized percent change; CDR-SB = Clinical Dementia Rating Sum of Boxes; CVLT = California Verbal Learning Test; MANOVA = multivariate analysis of variance; MCI = mild cognitive impairment; ROI = region of interest; SRT = Selective Reminding Test.
e-Pub ahead of print on July 30, 2008, at www.neurology.org.
Supported by grants from the National Institute on Aging (P01-AG04953), the National Center for Research Resources (P41-RR14075, R01-RR16594, U24-RR021382), the National Institute for Biomedical Imaging and Bioengineering (R01-EB001550), the National Institute for Neurological Diseases and Stroke (R01 NS052585), the BIRN Mophometric Project, and the Mental Illness and Neuroscience Discovery (MIND) Institute.
Disclosure: The authors report no disclosures.
Received October 30, 2007. Accepted in final form May 5, 2008.
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