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Published online before print October 21, 2009, doi:10.1212/WNL.0b013e3181c33afb)
© 2009 American Academy of Neurology Regional pattern of white matter microstructural changes in normal aging, MCI, and ADFrom the Department of Neurology and Imaging of Dementia and Aging (IDeA) Laboratory, Center for Neuroscience (D.Y.L., E.F., O.M., M.O., N.Z., J.K., J.T., O.C., C.D.), and Department of Radiology (M.B.), University of California at Davis, CA; and the Department of Neuropsychiatry (D.Y.L.), College of Medicine, Seoul National University, Korea. Address correspondence and reprint requests to Dr Lee, Imaging of Dementia and Aging (IDeA) Laboratory, Department of Neurology and Center for Neuroscience, University of California at Davis, 1544 Newton Ct., Davis, CA 95616 selfpsy{at}snu.ac.kr Objective: To cross-sectionally compare the regional white matter fractional anisotropy (FA) of cognitively normal (CN) older individuals and patients with mild cognitive impairment (MCI) and Alzheimer disease (AD), separately focusing on the normal-appearing white matter (NAWM) and white matter hyperintensities (WMH), and to test the independent effects of presumed degenerative and vascular process on FA differences. Methods: Forty-seven patients with AD, 73 patients with MCI, and 95 CN subjects received diffusion tensor imaging and vascular risk evaluation. To properly control normal regional variability of FA, we divided cerebral white matter into 4 strata as measured from a series of young healthy individuals (H1 = highest; H2 = intermediate high; H3 = intermediate low; H4 = lowest anisotropy stratum). Results: For overall cerebral white matter, patients with AD had significantly lower FA than CN individuals or patients with MCI in the regions with higher baseline anisotropy (H1, H2, and H3), corresponding to long corticocortical association fibers, but not in H4, which mostly includes heterogeneously oriented fibers. Vascular risk showed significant independent effects on FA in all strata except H1, which corresponds to the genu and splenium of the corpus callosum. Similar results were found within NAWM. FA in WMH was significantly lower than NAWM across all strata but was not associated with diagnosis or vascular risk. Conclusions: Both vascular and Alzheimer disease degenerative process contribute to microstructural injury of cerebral white matter across the spectrum of cognitive ability and have different region-specific injury patterns.
Abbreviations: AD = Alzheimer disease; ANCOVA = analysis of covariance; ANOVA = analysis of variance; CC = corpus callosum; CN = cognitively normal; DTI = diffusion tensor imaging; FA = fractional anisotropy; MCI = mild cognitive impairment; MDT = minimal deformation template; MMSE = Mini-Mental State Examination; NAWM = normal-appearing white matter; ROI = region of interest; SLF = superior longitudinal fasciculus; UCD = University of California, Davis; WMH = white matter hyperintensities.
Supplemental data at www.neurology.org e-Pub ahead of print on October 21, 2009, at www.neurology.org. Supported by NIH P30 AG 10129, R01 AG010220, and R01 AG021028. Disclosure: Author disclosures are provided at the end of the article. Received June 3, 2009. Accepted in final form September 2, 2009.
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