Research has indicated a potential association between sleep duration and the risk of Alzheimer’s disease, although previous studies using self-reported sleep data may have been influenced by reverse causation and confounding factors. In this study, conducted using data from the UK Biobank, researchers derived weights for genetic variants linked to sleep duration as measured by wearable devices, analyzing a total of 342,516 white British participants.
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Using the LDpred2-auto method, weights were calculated based on 77,770 participants, contributing to the generation of polygenic scores (PGSs) for an additional 264,746 participants. The study assessed the relationship between genetically determined sleep duration, categorized by fifths, and Alzheimer’s disease risk over a median follow-up period of 12.5 years, during which 1,451 cases of Alzheimer’s disease were recorded.
The PGS explained about 2% of the variation in device-measured sleep duration. Those in the highest fifth of the PGS, indicating roughly 15 minutes more sleep per day compared to the middle fifth, exhibited a lower risk of Alzheimer’s disease with a hazard ratio (HR) of 0.79 (95% CI, 0.67–0.94).
This suggests that a genetic predisposition towards longer sleep duration is linked to a reduced risk of developing Alzheimer’s disease. This study is significant as it employs genetic instruments to mitigate issues associated with observational studies, particularly reverse causation bias.
The research builds on evidence from the 2020 Lancet Commission report, identifying poor sleep as a potentially modifiable risk factor for dementia. Mechanisms underlying this relationship may relate to sleep’s role in clearing metabolic waste from the brain, including beta-amyloid, which has been observed to accumulate following sleep deprivation.
Given the hereditary nature of sleep duration, characterized by heritability estimates around 19%, polygenic scores derive from a broader range of genetic variants compared to previous studies. These findings point towards sleep duration as an important factor in Alzheimer’s disease risk, contrasting with earlier Mendelian randomization studies that found no significant correlations. Additionally, sensitivity analysis indicated a modest association between shorter genetically predicted sleep duration and an increased risk of Alzheimer’s disease when factoring in parental history of the condition.
This research highlights not only the primary association between sleep duration and Alzheimer’s disease risk but also correlations with factors such as educational attainment and depressive symptoms. Future studies may delve deeper into how these interconnected factors contribute to Alzheimer’s disease risk, necessitating a comprehensive understanding of the influence of sleep on cognitive health.