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Alzheimer Disease-associated Cortical Atrophy Does not Differ Between Chinese and Whites

Fan, Jia MD, PhD*,†; Tse, Marian BA*; Carr, Jessie S. PhD*; Miller, Bruce L. MD*; Kramer, Joel H. PsyD*; Rosen, Howard J. MD*; Bonham, Luke W. BSc*,‡; Yokoyama, Jennifer S. PhD*

Alzheimer Disease & Associated Disorders: July–September 2019 - Volume 33 - Issue 3 - p 186–193
doi: 10.1097/WAD.0000000000000315
Original Articles
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Purpose: To assess whether there are differences in Alzheimer disease (AD)-associated atrophy regions in Chinese and white patients with AD versus cognitively normal older adults, and to test whether associations between clinical severity and gray matter volume are similar or different across these ethnic groups in a cross-sectional analysis.

Materials and Methods: Chinese and white patients with AD, individuals with mild cognitive impairment, and cognitively normal controls (46 white and 48 Chinese) were clinically evaluated at an academic center within 1 year of magnetic resonance imaging acquisition. Clinical severity was assessed using the Clinical Dementia Rating Sum of Boxes and cortical atrophy was measured using voxel-based morphometry as well as Freesurfer. Chinese and white cohorts were demographically matched for age, sex, and education.

Results: Clinical severity by diagnosis was similar across ethnicities. Chinese and white patient groups showed similar amounts of atrophy in the regions most affected in AD after accounting for demographic variables and head size. There was no significant difference between ethnic groups when compared by atrophy and clinical severity.

Conclusions: Our study suggests that Chinese and white patients with AD, when matched demographically, are clinically and neuroanatomically similar on normalized measures of cortical atrophy and clinical severity.

Departments of *Neurology, Memory and Aging Center

Radiology and Biomedical Imaging, University of California, San Francisco, San Francisco, CA

Department of Neurology, Second Hospital, Jilin University, Changchun, Jilin, China

L.W.B. and J.S.Y. contributed equally.

Primary support for data analysis was provided by the NIA K01 AG049152 (J.S.Y.), Larry L. Hillblom Foundation 2016-A-005-SUP (J.S.Y.), Tau Consortium (J.S.Y.), Bluefield Project to Cure FTD (J.S.Y.), John Douglas French Alzheimer’s Foundation (J.S.Y.), and Radiological Society of North America (RSNA) RMS1741 (L.W.B.). Additional support was provided by NIH grants P50-AG023501 and P01-AG1972403 (B.L.M.), the Larry L. Hillblom Foundation (J.H.K.), and the National Center for Advancing Translational Sciences of the NIH under Award Number TL1 TR001871 (J.S.C.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

The authors declare no conflicts of interest.

Reprints: Jennifer S. Yokoyama, PhD, Department of Neurology, Memory and Aging Center, University of California, San Francisco, 675 Nelson Rising Lane, Suite 190, San Francisco, CA 94158 (e-mail: jennifer.yokoyama@ucsf.edu).

Received September 17, 2018

Accepted February 24, 2019

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