Education as a Moderator of the Relationship Between Episodic Memory and Amyloid Load in Normal Aging.

The current study explored whether education, a proxy of cognitive reserve, modifies the association between episodic memory (EM) performance and ßeta-amyloid load (Aß), a biomarker of Alzheimer's disease, in a cohort of cognitively normal older adults. One hundred and four participants (mean age 73.3 years) evenly spread out in three bands of education were recruited. Participants underwent neuropsychological assessment, structural MRI as well as PET imaging to quantify Aß load. Moderation analyses and the Johnson-Neyman technique were carried out to examine the interaction of education with Aß load to predict EM performance. Linear regressions were then performed within each group of education to better illustrate the interaction effect (all analyses were controlled for age and sex). The interaction between education and Aß load was significant (p < .05) for years of education, reaching a cutoff point of 13.5 years, above which the relationship between Aß load and EM was no longer significant. Similarly, significant associations were found between Aß and EM among participants with secondary (p < .01) and pre-university education (p < .01), but not with a university degree (p = .253). EM performance is associated with Aß load in cognitively normal older individuals, and this relationship is moderated by educational attainment.

Amyloid burden and white matter hyperintensities mediate age-related cognitive differences.

This study examined the additive versus synergistic contribution of beta-amyloid (Aß) and white matter hyperintensities (WMHs) across 7 cognitive domains in 104 cognitively normal older adults. It also measured the extent to which age-related differences in cognition are driven by measurable brain pathology. All participants underwent neuropsychological assessment along with magnetic resonance imaging and Pittsburg compound B-positron emission tomography imaging for Aß quantification. WMH severity was quantified using the age-related white matter changes scale. Stepwise regressions, moderation, and mediation modeling were performed. Our findings show that Aß deposition single-handedly predicts poorer episodic memory performance and that Aß and WMHs contribute additively to poorer performance in working memory and language while carrying synergistic associations with executive functions and attention. Through mediation modeling, we demonstrated that the influence of age over episodic memory, working memory, executive functions, and language is fully mediated by brain pathology. This study permits to conclude that, in healthy older adults, (1) Aß burden and WMHs have synergistic associations with some cognitive domains and (2) age-related differences in most cognitive domains are driven by brain pathology associated with dementia.