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Body Mass Index, Weight Change, and Clinical Progression in Mild Cognitive Impairment and Alzheimer Disease

Besser, Lilah M. MSPH*; Gill, Dawn P. PhD*,†,‡; Monsell, Sarah E. MS*; Brenowitz, Willa MPH*; Meranus, Dana H. MPH*; Kukull, Walter PhD*; Gustafson, Deborah R. PhD§,∥,¶

Alzheimer Disease & Associated Disorders:
doi: 10.1097/WAD.0000000000000005
Original Articles
Abstract

The speed and severity of clinical progression after Alzheimer disease (AD) diagnosis varies and depends on multiple factors, most not well elucidated. We assessed whether body mass index (BMI) and 1-year weight change (WC) are associated with clinical progression in amnestic mild cognitive impairment (aMCI) and early-stage AD. Longitudinal data comprising 2268 aMCI and 1506 AD participants in the National Alzheimer’s Coordinating Center’s Uniform Data Set were used to examine nuances of clinical progression by BMI and WC, as well as potential variations in associations by age, sex, BMI (WC model), or apolipoprotein E genotype. In aMCI, high BMI (vs. moderate BMI) was associated with slower progression; weight loss (vs. no WC) was associated with faster progression. In AD, no significant differences were observed in clinical progression by BMI or WC. The association between BMI and clinical progression varied significantly by apolipoprotein E genotype in AD, and the association between WC and clinical progression varied significantly by sex and BMI in aMCI. Baseline BMI and 1-year WC in late life may serve as early prognostic indicators in aMCI and early-stage AD. If replicated, these results may help in counseling patients on anticipated clinical progression and suggest windows of opportunity for intervention.

Author Information

*Department of Epidemiology, National Alzheimer’s Coordinating Center, University of Washington, Seattle, WA

§Aging, Rehabilitation & Geriatric Care Research Centre

Department of Neurology, State University of New York - Downstate Medical Center, Brooklyn, NY

Lawson Health Research Institute

School of Health Studies, Western University, London, ON, Canada

Neuropsychiatric Epidemiology Unit, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden

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The National Alzheimer’s Coordinating Center is funded by NIH U01 AG016976. D.R.G. receives support from NIH/NIAID U01-AI-31834, the Swedish Research Council Diarienummer: 523-2005-8460, and the SUNY Research Foundation.

The authors declare no conflicts of interest.

Reprints: Lilah M. Besser, MSPH, National Alzheimer’s Coordinating Center, 4311 11th Ave NE, Suite 300, Seattle, WA 98105 (e-mail: lmbesser@uw.edu).

Received January 9, 2013

Accepted August 13, 2013

© 2014 by Lippincott Williams & Wilkins.