Associations of lifestyle factors with amyloid positivity in cognitively normal individuals at different levels of genetic risk: The amyloid biomarker study.

Background: The role of lifestyle factors in the pathophysiology of Alzheimer's disease is unclear. The aim of this study was to assess the contribution of lifestyle factors to cerebral amyloid pathology in cognitively healthy persons at different levels of genetic risk. Methods: We selected sixteen cohorts from the Amyloid Biomarker Study. Lifestyle data were available for 5542 participants with normal cognition. Amyloid positivity was determined with amyloid‐PET (center‐specific cutoffs) or with aß42 level in CSF (data‐driven cutoffs). Participants were classified as being at low, intermediate or high genetic risk for amyloid positivity according to ApoE e4 copy number (0 vs. 1 vs. 2 e4‐alleles). Participants for whom data was available for >=3 lifestyle factors (n=5046) were classified as having a favorable or unfavorable lifestyle profile on basis of the lifestyle information available for that cohort. A favorable lifestyle was defined as (dichotomized): not smoking (ever), not drinking, normal sleep, physically active, socially active, cognitively active and/or adhering to a Mediterranean diet. Associations of both lifestyle profile and individual lifestyle factors with amyloid positivity, and their dependency on genetic risk, were assessed using generalized estimating equations. Age was included as covariate in all models, Results: Independent of genetic risk level, impaired sleep was associated with lower amyloid positivity (p=0.001) and cognitive inactivity was associated with higher amyloid positivity (p<0.001). Smoking, alcohol use, social activity and diet were not associated with amyloid positivity (table 2). The effects of lifestyle profile and physical activity on amyloid positivity were dependent on genetic risk (p<0.001). Prevalence of amyloid positivity was lower for those with a favorable rather than an unfavorable lifestyle at low (mean difference (md) 3%, p<0.001) and intermediate (md 5%, p<0.001) genetic risk, while this association was reversed for persons at high genetic risk (md 7%, p=0.001, table 3). Amyloid positivity was more common in physically active than inactive participants at high genetic risk only (md 9%, p<0.001). Conclusion: Individual lifestyle factors are limitedly associated with amyloid positivity. However, absence of any unfavorable lifestyle factor is related to lower risk of amyloid positivity in persons at low or intermediate genetic risk. [ABSTRACT FROM AUTHOR]