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Brain Advance Access originally published online on May 12, 2009
Brain 2009 132(9):2579-2592; doi:10.1093/brain/awp071
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© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

White matter damage in frontotemporal dementia and Alzheimer's disease measured by diffusion MRI

Yu Zhang1,2, Norbert Schuff1,2, An-Tao Du1, Howard J. Rosen3, Joel H. Kramer3, Maria Luisa Gorno-Tempini3, Bruce L. Miller3 and Michael W. Weiner1,2,3

1 Center for Imaging of Neurodegenerative Diseases, Department of Veterans Affairs Medical Center, San Francisco, CA, USA 2 Department of Radiology, University of California, San Francisco, CA, USA 3 Department of Neurology, University of California, San Francisco, CA, USA

Correspondence to: Yu Zhang, Center for Imaging of Neurodegenerative Diseases, VA Medical Center, 4150, Clement Street, San Francisco, CA 94121, USA. E-mail: Yu.Zhang{at}ucsf.edu

Frontotemporal dementia (FTD) and Alzheimer's disease are sometimes difficult to differentiate clinically because of overlapping symptoms. Using diffusion tensor imaging (DTI) measurements of fractional anisotropy (FA) can be useful in distinguishing the different patterns of white matter degradation between the two dementias. In this study, we performed MRI scans in a 4 Tesla MRI machine including T1-weighted structural images and diffusion tensor images in 18 patients with FTD, 18 patients with Alzheimer's disease and 19 cognitively normal (CN) controls. FA was measured selectively in specific fibre tracts (including corpus callosum, cingulum, uncinate and corticospinal tracts) as well as globally in a voxel-by-voxel analysis. Patients with FTD were associated with reductions of FA in frontal and temporal regions including the anterior corpus callosum (P < 0.001), bilateral anterior (left P < 0.001; right P = 0.005), descending (left P < 0.001; right P = 0.003) cingulum tracts, and uncinate tracts (left P < 0.001; right P = 0.005), compared to controls. Patients with Alzheimer's disease were associated with reductions of FA in parietal, temporal and frontal regions including the left anterior (P = 0.003) and posterior (P = 0.002) cingulum tracts, bilateral descending cingulum tracts (P < 0.001) and left uncinate tracts (P < 0.001) compared to controls. When compared with Alzheimer's disease, FTD was associated with greater reductions of FA in frontal brain regions, whereas no region in Alzheimer's disease showed greater reductions of FA when compared to FTD. In conclusion, the regional patterns of anisotropy reduction in FTD and Alzheimer's disease compared to controls suggest a characteristic distribution of white matter degradation in each disease. Moreover, the white matter degradation seems to be more prominent in FTD than in Alzheimer's disease. Taken together, the results suggest that white matter degradation measured with DTI may improve the diagnostic differentiation between FTD and Alzheimer's disease.

Key Words: Alzheimer's disease; frontotemporal dementia; diffusion tensor imaging; diffusion tensor fibre tracking

Abbreviations: CN, cognitively normal; Dax, axial diffusivity; Dra, radial diffusivity; DTI, diffusion tensor imaging; FA, fractional anisotropy; FDR, false discovery rate; FTD, frontotemporal dementia; ICC, intraclass correlation coefficients; MMSE, Mini-Mental State Examination; ROI, regions of interest; TOI, tracts of interest; WMSH, white matter signal hyperintensities

Received October 1, 2008. Revised February 13, 2009. Accepted February 18, 2009.


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