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Trajectory of Mobility Decline by Type of Dementia

Tolea, Magdalena I. PhD; Morris, John C. MD; Galvin, James E. MD, MPH

Alzheimer Disease & Associated Disorders: January–March 2016 - Volume 30 - Issue 1 - p 60–66
doi: 10.1097/WAD.0000000000000091
Original Articles

Cognitive and physical aspects of functionality are closely related. However, whether physical decline differs by dementia type and progression rate is debatable. To address these issues, we conducted a longitudinal study of 766 older adults whose physical performance and cognitive status were assessed annually with standard assessment tools [eg, Physical Performance Test, Clinical Dementia Rate (CDR)] for 8 years. Compared with participants who remained cognitively normal, those progressing to later-stage dementia (CDR=1) declined in their mobility by a factor of 2.82 (P<0.001), followed by those who maintained a later-stage diagnosis (slope=−1.84, P<0.001), those progressing from early-stage to later-stage (CDR=0.5 to CDR=1) dementia (slope=−1.20, P<0.001), and those who progressed to early-stage dementia (slope=−0.39, P=0.038) suggesting a steeper physical decline with dementia progression, particularly in those with the fastest disease progression. Although all types of dementia experienced mobility decline, those progressing to non-Alzheimer disease (AD) dementias, especially vascular dementia declined faster than those who remained normal (slope=−2.70, P<0.001) or progressed to AD (slope=−2.18, P<0.001). These associations were better captured by the gait/balance component of physical functionality. Our findings suggest that rapidly progressing dementia patients particularly those with non-AD subtypes should be targeted for interventions to maintain or improve gait/balance and prevent functional decline and disability although AD patients may also benefit.

*Departments of Neurology, Psychiatry, and Population Health, Alzheimer’s Disease Center, Center for Cognitive Neurology, New York University School of Medicine, New York, NY

Charles F. and Joanne Knight Alzheimer’s Disease Research Center, Washington University, St Louis, MO

Data collection was supported by Grants from NIH (P01 AG03991 and P50 AG05681) to J.C.M. Data analysis was supported by Grants from the NIH (R01 AG040211 and P30 AG008051), Morris and Alma Schapiro Fund, and the New York State Department of Health (DOH-2011-1004010353) to J.E.G.

M.I.T.: study concept and design, analysis and interpretation of data, drafting of manuscript, critical revision of manuscript for important intellectual content. J.C.M.: data acquisition, critical revision of manuscript for important intellectual content, obtained funding. J.E.G.: data acquisition, study concept and design, analysis and interpretation of data, critical revision of the manuscript for important intellectual content, obtained funding, provided study supervision.

The authors declare no conflicts of interest.

Reprints: Magdalena I. Tolea, PhD, 145 E 32nd Street, 8th Floor, Room 830, New York, NY 10016 (e-mail:

Received July 18, 2014

Accepted January 26, 2015

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