Abstract
Introduction: ApoE genotype affects cholesterol metabolism, and carriers of the e4 allele have increased risk of heart disease, stroke, Alzheimer’s disease, vascular dementia, Mild Cognitive Impairment, and cognitive decline. Studies have yielded mixed results on the independent and interactive effects of e4 carrier status, demographics, and health variables on risk of cognitive decline. Methods: Drawing from a stratified random subsample of REGARDS study participants, we performed ApoE genotyping on 424 incident cognitive decline cases and 554 cohort members without cognitive decline. Participants with normal baseline cognitive status, no baseline stroke history, and sufficient longitudinal cognitive data were eligible. Incident cognitive decline was defined as a score > 1.5 SD below age-, education-, race- and sex-adjusted expected score on > 2 of 3 cognitive tests (memory, learning, executive function) at most recent assessment. Results: ApoE e4 carrier status interacted with age to determine odds of incident cognitive decline. In sample-weighted and fully adjusted regression models, greater risk for cognitive decline was seen in e4 carriers above but not below age 65 (Table). Stroke Belt residence, lower income, abstaining from alcohol, smoking, diabetes, heart disease, and incident stroke were independent predictors of decline after accounting for e4 carrier status and other model variables (p values < .05) (data not shown). Discussion: Drawing from a national cohort of black and white adults and controlling for key demographics in defining cases of substantive cognitive decline, risk for decline was higher for older ApoE e4 carriers. Risk of decline was also higher for residents of the Stroke Belt and those with low income, smoking, alcohol abstinence, CVD, or incident stroke, even after accounting for e4 and other possible confounders. Results highlight the interplay of genetics and environment in determining cognitive decline risk.
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