scholarly journals The Preventative Benefit of Group Diversification on Group Performance Decline: An Investigation with Latent Growth Models

2020 ◽  
Author(s):  
Jia Li ◽  
Meir Shemla ◽  
Jürgen Wegge
Keyword(s):  
Group Performance ◽  
Growth Models ◽  
Latent Growth ◽  
Latent Growth Models ◽  
Performance Decline

Nuances in Alzheimer’s Genetic Risk Reveal Differential Predictions of Non-demented Memory Aging Trajectories: Selective Patterns by APOE Genotype and Sex

2019 ◽  
Vol 16 (4) ◽  
pp. 302-315 ◽  
Author(s):  
G. Peggy McFall ◽  
Lars Bäckman ◽  
Roger A. Dixon
Keyword(s):  
Genetic Risk ◽  
Growth Models ◽  
Memory Performance ◽  
Apoe Genotype ◽  
Cognitively Impaired ◽  
Latent Growth ◽  
Latent Growth Models ◽  
Selective Protection ◽  
Underlying Mechanisms ◽  
Apoe Genotypes

Background: Apolipoprotein E (APOE) is a prominent genetic risk factor for Alzheimer’s disease (AD) and a frequent target for associations with non-demented and cognitively impaired aging. APOE offers a unique opportunity to evaluate two dichotomous comparisons and selected gradations of APOE risk. Some evidence suggests that APOE effects may differ by sex and emerge especially in interaction with other AD-related biomarkers (e.g., vascular health). Methods: Longitudinal trajectories of non-demented adults (n = 632, 67% female, Mage = 68.9) populated a 40-year band of aging. Focusing on memory performance and individualized memory trajectories, a sequence of latent growth models was tested for predictions of (moderation between) APOE and pulse pressure (PP) as stratified by sex. The analyses (1) established robust benchmark PP effects on memory trajectories, (2) compared predictions of alternative dichotomous groupings (ε4- vs ε4+, ε2- vs ε2+), and (3) examined precision-based predictions by disaggregated APOE genotypes. Results: Healthier (lower) PP was associated with better memory performance and less decline. Therefore, all subsequent analyses were conducted in the interactive context of PP effects and sex stratification. The ε4-based dichotomization produced no differential genetic predictions. The ε2-based analyses showed sex differences, including selective protection for ε2-positive females. Exploratory follow-up disaggregated APOE genotype analyses suggested selective ε2 protection effects for both homozygotic and heterozygotic females. Conclusion: Precision analyses of AD genetic risk will advance the understanding of underlying mechanisms and improve personalized implementation of interventions.

Sign in / Sign up

Export Citation Format

Share Document