期刊
INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY
卷 30, 期 8, 页码 824-832出版社
WILEY
DOI: 10.1002/gps.4221
关键词
Alzheimer; growth mixture model; trajectory; disease course
资金
- NIH [R01AG21136, R01AG11380, R01AG18712]
- NATIONAL INSTITUTE ON AGING [R01AG021136, R01AG011380, P50AG005146, R01AG018712, T32AG027668] Funding Source: NIH RePORTER
ObjectiveSeveral longitudinal studies of Alzheimer's disease (AD) report heterogeneity in progression. We sought to identify groups (classes) of progression trajectories in the population-based Cache County Dementia Progression Study (N=328) and to identify baseline predictors of membership for each group. MethodsWe used parallel-process growth mixture models to identify latent classes of trajectories on the basis of Mini-Mental State Exam (MMSE) and Clinical Dementia Rating sum of boxes scores over time. We then used bias-corrected multinomial logistic regression to model baseline predictors of latent class membership. We constructed receiver operating characteristic curves to demonstrate relative predictive utility of successive sets of predictors. ResultsWe fit four latent classes; class 1 was the largest (72%) and had the slowest progression. Classes 2 (8%), 3 (11%), and 4 (8%) had more rapid worsening. In univariate analyses, longer dementia duration, presence of psychosis, and worse baseline MMSE and Clinical Dementia Rating sum of boxes were associated with membership in class 2, relative to class 1. Lower education was associated with membership in class 3. In the multivariate model, only MMSE remained a statistically significant predictor of class membership. Receiver operating characteristic areas under the curve were 0.98, 0.88, and 0.67, for classes 2, 3, and 4 relative to class 1. ConclusionsHeterogeneity in AD course can be usefully characterized using growth mixture models. The majority belonged to a class characterized by slower decline than is typically reported in clinical samples. Class membership could be predicted using baseline covariates. Further study may advance our prediction of AD course at the population level and in turn shed light on the pathophysiology of progression. Copyright (c) 2014 John Wiley & Sons, Ltd.
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