homozygotes have less sleep fragmentation in late adulthood.

STUDY OBJECTIVES

, a genetic risk factor for Alzheimer's Disease (AD), is associated with reduced functional connectivity of brain regions that regulate sleep, which may predispose persons to AD via altered sleep architecture. However, little is known about differences in sleep architecture by genotype, and whether they vary by age and sex.

METHODS

This cross-sectional study examined the association between genotype and sleep architecture, using in-home polysomnography (Sleep Heart Health Study, N=3,107). genotype included: heterozygotes, homozygotes, carriers, and homozygotes (reference). Sleep architecture was quantified using the percentage of time spent in rapid eye movement sleep (%REM), N1 (N1%), N2 (%N2), N3 (%N3), and arousal index. Linear regression was employed, adjusting for age, sex, marital status, race, education, and parent cohort. Interactions with age and sex-stratified analyses examined variations by age and sex, respectively.

RESULTS

The median age was 67 years, 27.4% carried at least one , and 52.9% were females. Without age by genotype interaction, %REM, %N1, %N2, %N3, and arousal index were comparable across genotypes in the full sample, males, and females. When an age by genotype interaction was introduced, homozygotes showed fewer arousals with each year of age (β=-0.33 arousals, p=0.04), leading to significantly less arousals at age ≥70 (marginal difference=-2.98, p=0.04).

CONCLUSIONS

homozygotes showed comparable proportions of REM, N1, N2, and N3, but exhibited fewer arousals in old age. homozygotes may have an elevated arousal threshold.