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P3‐020: THE EFFECTS OF SUBJECTIVE COGNITIVE DECLINE ON APOE GENOTYPE DISCLOSURE IN THE BUTLER ALZHEIMER'S PREVENTION REGISTRY
Author(s) -
Lee Athene K.W.,
Thompson Louisa I.,
Collier Meghan K.,
Goldfarb Danielle,
Dawson Brittany,
Salloway Stephen,
Alber Jessica
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.06.1375
Subject(s) - apolipoprotein e , mood , montreal cognitive assessment , dementia , clinical psychology , psychology , anxiety , cognition , medicine , cognitive decline , psychiatry , disease
Background:Alzheimer’s disease (AD) prevention trial recruitment targets healthy older adults at high risk for AD. Common risk measures include the presence of subjective cognitive decline (SCD) or the apolipoprotein (APOE) 34 allele. Understanding the relationship between SCD and the impact of APOE disclosure has implications for the psychological well-being and health behaviors of trial volunteers. This study investigates how SCD associates with other participant characteristics and whether SCD interacts with APOE genotype to effect emotional impact of APOE disclosure over time.Methods:67 healthy adults (aged 59-77) from the Butler Hospital Alzheimer’s Prevention Registry completed a pre-APOE genotyping assessment (psychological interview, Montreal Cognitive Assessment (MoCA)), genetic disclosure, and two follow-ups (3 days, 6 weeks). Baseline variables of interest included education, first-degree family dementia history, psychiatric history, and perceived risk of AD. Mood measures included self-reported depression, anxiety, and impact of events scales (IES). All variables were compared across 3 groups at baseline: no SCD (no cognitive concerns, n1⁄430), SCD (cognitive concerns, MoCA 26, n1⁄422), and mildly impaired (MoCA<26, n1⁄415). The interaction effect between SCD (no SCD, SCD, mildly impaired) and APOE genotype ( 34-carriers, non-carriers) on mood measures and perceived risk of AD over time were computed using a mixed model RMANOVA design. Results:The three groups showed no difference in baseline characteristics or mood measures, with the exception of relatively lower education in the mildly impaired group (p<0.05), which was controlled for in subsequent analyses. Following APOE disclosure, there was a significant SCD by APOE genotype interaction on IES (p<0.05), such that ε4-carriers with SCD and non-carriers with mild impairment scored higher on IES than other groups. However, this difference dissipated with all groups reporting low IES at both follow-ups. There were no significant interaction effects on other measures. Conclusions: These findings suggest that baseline SCD heightened the acute emotional impact of APOE disclosure for 34-carriers. Interestingly, individuals with mild impairment on cognitive screening showed stronger emotional reaction to the disclosure of non34 vs. 34 status, possibly due to a dissonant effect. As good clinical practice, the presence of SCD should be taken into consideration when disclosing APOE risk to prevention trial candidates.