P4‐057: Prevalence of Prodromal Alzheimer's Disease Across Late Life: Results from the Cache County Study

With the advances in clinical detection of mild cognitive impairment (MCI), it is increasingly possible to diagnose Alzheimer's disease (AD) prior to the full expression of dementia symptoms. The prevalence of this prodromal stage of AD (prAD) remains unknown, as does the influence of age and other factors on its expression and duration. In an exceptionally long-lived population, we investigated the prevalence of prAD and the relationship of early AD symptom expression to age, gender, and APOE genotype. The sample included all surviving members of the Cache County Study population cohort at the commencement of the Study's third wave of case detection in 2002 (n=3396; mean age/sd = 81.0 (5.9) years). Using a multi-stage screening process, we determined the prevalence of prAD and dementia at this time point. Corrections for non-response were made using polytomous logistic regression, allowing imputation of diagnostic status based on six variables (age, education, gender, APOE, score on the 3MS, and memory performance on a verbal learning test). Prevalence of prAD among participants without dementia was 10.1%. Dementia was present in another 20.6%. The average age of cases in each group were 83 years (5.2 sd) and 85 years (6.3 sd) for prAD and dementia, respectively. Advancing age was associated with increased prevalence of both dementia and prAD, such that more than 60% of the population over age 90 had one of these conditions. There was no appreciable difference in prevalence of prAD between men and women at any age;however, dementia was more prevalent in women than in men after age 85. APOE ϵ4 genotype was associated with higher prevalence of dementia, but not of prAD. Without an effective means of prevention, AD dementia and related cognitive disorders are extremely common consequences of survival to advanced age. Although strongly associated with dementia prevalence, APOE ϵ4 is not associated with prevalence of prAD, perhaps reflecting an offsetting influence of this genetic polymorphism on rates of transition to dementia.