by Isabella Colonna
For July, we have selected Nguyen Ho PT, Hoepel SJW, Rodriguez-Ayllon M, Luik AI, Vernooij MW, Neitzel J. Sleep, 24-Hour Activity Rhythms, and Subsequent Amyloid-β Pathology. JAMA Neurol. 2024 Jun 24:e241755. doi: 10.1001/jamaneurol.2024.1755. Epub ahead of print. PMID: 38913396; PMCID: PMC11197458.
Considering the increasing prevalence of Alzheimer disease (AD), it is very important to identify modifiable risk factors in order to develop effective prevention. Recent evidence suggests that disturbances of sleep and of day-night activity rhythms may be risk factors for AD, by increasing neuronal activity and by affecting the amyloid-beta (Aβ) clearance through the glymphatic system, determining a relative excess of soluble Aβ.
Our paper of the month is an observational cohort study exploring the link between sleep measures and AD pathology in 319 participants (mean ± SD age: 61.5 ± 5.4 years; 47% female) from the Rotterdam Study, a prospective population-based study conducted in the Netherlands. All study participants wore an actigraph continuously for one week to track objective sleep metrics (total sleep time; sleep onset latency; sleep efficiency; wake after sleep onset) and 24-hour activity rhythms (inter-daily stability, intra-daily variability and L5 start time). Additionally, seven measures of self-reported sleep were obtained through daily sleep diaries. AD pathology was assessed by AD plasma markers at the baseline, and by 18F-florbetabenamyloid PET imaging at the follow-up (average follow-up time = 7.8 years).
The study found that stronger within-day fragmentation of the 24-hour activity rhythms, indicated by higher intra-daily variability, were related to more severe amyloid-beta pathology at follow-up. This association was stronger in APOE4 carriers and remained statistically significant after excluding participants with AD pathology at baseline, suggesting that these 24-hour activity rhythm disturbances may precede Aβ deposition. No other objective or self-reported measure of sleep was associated with AD pathology.
In conclusion, this study highlights a connection between fragmentation of the 24-hour activity rhythm and increased Aβ accumulation over a 7.8-year follow-up, especially in APOE4 carriers. Further research is needed in order to determine whether reducing the 24 hours activity rhythms fragmentation could help to prevent or delay AD progression.
