Abstract

Recent research suggests that subjective cognitive decline (SCD) may be a harbinger of mild cognitive impairment (MCI) and Alzheimer's disease (AD). However, its prognostic significance remains unclear. To date, no studies have examined independent predictors of SCD in individuals concerned about incipient dementia enrolled in an AD prevention registry. This cross-sectional study characterized prevalence of SCD, APOE status, baseline cognitive screening performance and aspects of family and personal health history in the Rhode Island Alzheimer Prevention Registry. We also assessed which factors independently predicted SCD. Participants were 100 registry members with undisclosed APOE test results (78% female, 97% Caucasian, mean age=64±7.5 years, mean education=16±2.5 years). Multivariate linear regression predicted SCD (0=no memory decline, 1=decline without concern, 2=decline with concern) based on APOE status (ε4+ or not), reported AD family history, baseline Minnesota Cognitive Acuity Screen (MCAS) performance, and personal histories of mild psychiatric conditions (e.g., depression, anxiety) and neurological events without persisting cognitive sequelae (e.g., migraine, concussion, TIA). Most participants reported AD family history (87%). APOE ε4+ status was highly prevalent (41%). Nearly a quarter of the sample reported mild psychiatric (23%) and neurological histories (22%). MCAS scores were in the non-impaired range in 84% of individuals, and in the MCI range in 16%. Of the 65% endorsing SCD, 63% expressed concern about perceived memory changes. Results of the regression analysis (R2=.14, p=.02) revealed that AD family history (β=.53, p=.04) and personal history of mild psychiatric (β=.41, p=.05) and neurological conditions (β=.48, p=.02) independently and significantly predicted SCD whereas APOE status (β=-.04. p=.88) and MCAS performance (β=-.00, p=.88) did not. In this cross-sectional study, SCD was common among AD prevention registry members. However, SCD was not significantly associated with cognitive screening performance or APOE status. Rather, SCD varied as a function of reported AD family history, which could plausibly be mediated by health anxiety. SCD was also associated with personal history of mild psychiatric and neurological conditions, which raises the question of whether perceived declines were misattributed to such symptoms. Future research should examine these relationships longitudinally in AD prevention registries and other healthy aging cohorts.

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