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Empirically Derived Trajectories to Dementia Over 15 Years of Follow-up Identified by Using Mixed Membership Models.

TitleEmpirically Derived Trajectories to Dementia Over 15 Years of Follow-up Identified by Using Mixed Membership Models.
Publication TypeJournal Article
Year of Publication2015
AuthorsLecci, F, Junker, B, Kuller, LH, Lopez, OL, Becker, JT
JournalAm J Epidemiol
Volume182
Issue4
Pagination366-74
Date Published2015 Aug 15
ISSN1476-6256
KeywordsAge Distribution, Aged, Aged, 80 and over, Alzheimer Disease, Apolipoprotein E4, Cardiovascular Diseases, Comorbidity, Dementia, Diabetes Mellitus, Disease Progression, Female, Follow-Up Studies, Humans, Magnetic Resonance Imaging, Male, Mild Cognitive Impairment, Neuroimaging, Prevalence, Proportional Hazards Models, Risk Factors, Sex Distribution
Abstract<p>Alzheimer disease is the most common form of dementia in the elderly, and the complex relationships among risk factors produce highly variable natural histories from normal cognition through the prodromal stage of mild cognitive impairment (MCI) to clinical dementia. We used a novel statistical approach, mixed membership trajectory models, to capture the variety of such pathways in 652 participants in the Cardiovascular Health Study Cognition Study over 22 years of follow-up (1992-2014). We identified 3 trajectories: a "healthy" profile with a peak probability of MCI between 95 and 100 years of age and only a 50% probability of dementia by age 100; an "intermediate" profile with a peak probability of MCI between 85 and 90 years of age and progression to dementia between 90 and 95 years; and an "unhealthy" profile with a peak probability of progressing to MCI between ages 75 and 80 years and to dementia between the ages of 80 and 85 years. Hypertension, education, race, and the ϵ4 allele of the apolipoprotein E gene all affected the closeness of an individual to 1 or more of the canonical trajectories. These results provide new insights into the natural history of Alzheimer disease and evidence for a potential difference in the pathophysiology of the development of dementia.</p>
DOI10.1093/aje/kwv051
Alternate JournalAm. J. Epidemiol.
PubMed ID26209524
PubMed Central IDPMC4528953
Grant ListAG-023629 / AG / NIA NIH HHS / United States
AG-027002 / AG / NIA NIH HHS / United States
AG-027058 / AG / NIA NIH HHS / United States
AG-05133 / AG / NIA NIH HHS / United States
AG-15928 / AG / NIA NIH HHS / United States
AG-20098 / AG / NIA NIH HHS / United States
HL080295 / HL / NHLBI NIH HHS / United States
N01-HC-15103 / HC / NHLBI NIH HHS / United States
N01-HC-35129 / HC / NHLBI NIH HHS / United States
N01-HC-45133 / HC / NHLBI NIH HHS / United States
N01-HC-55222 / HC / NHLBI NIH HHS / United States
N01-HC-75150 / HC / NHLBI NIH HHS / United States
N01-HC-85079 / HC / NHLBI NIH HHS / United States
N01-HC-85086 / HC / NHLBI NIH HHS / United States
N01-HC-85239 / HC / NHLBI NIH HHS / United States
P50 AG005133 / AG / NIA NIH HHS / United States