A prospective population-based cohort study in the Netherlands suggests that sleep rhythm disturbances can precede amyloid-β (Aβ) deposition and may be a modifiable risk factor for Alzheimer disease (AD). From September 2018 to November 2021, 319 participants without dementia who underwent Aβ positron emission tomography (PET) were included with the mean follow-up of 7.8 years. The mean (range) age was 61.5 (48-80) years at baseline and 69.2 (60-88) years at follow-up; 47% were women. Higher intradaily variability (the ratio of the mean squares of the differences between all successive hours and the mean squares around the grand mean) at baseline by 7 days and nights of actigraphy, an indicator of fragmented 24-hour activity rhythms, was associated with higher Aβ PET burden at follow-up. The association was even stronger in APOE4 carriers. The associations remained after excluding participants with AD pathology at baseline, suggesting that a fragmented 24-hour activity rhythm may have preceded Aβ deposition and be a risk factor, rather than a result of AD pathology. The findings are consistent with previous studies indicating higher soluble Aβ during wake than sleep and add to the growing evidence that circadian disruption may increase dementia risk. The relationship between AD and sleep may be bidirectional. Dementia may be prevented or delayed by modifying key risk factors. Source: https://jamanetwork.com/
