Disrupted circadian rhythms in cognitively normal adults have been found to be associated with higher subsequent amyloid-beta levels. This relationship is particularly strong in APOE4 carriers and remains consistent even after excluding participants with baseline Alzheimer’s pathology. The findings from a recent study shed light on the potential impact of fragmented 24-hour activity rhythms on amyloid burden and ultimately on dementia risk.
Exploring the Relationship
Julia Neitzel, PhD, and her team from Erasmus University Medical Center in Rotterdam conducted a prospective study that revealed a significant association between higher daily variability at baseline, indicative of fragmented activity rhythms, and increased PET amyloid burden 8 years later. This relationship was particularly pronounced in APOE4 carriers, suggesting a genetic susceptibility component. The fact that the findings remained similar even after accounting for baseline Alzheimer’s pathology highlights the independent effect of circadian disruption on amyloid levels.
The Role of Sleep in Alzheimer’s Disease
While previous research has yielded inconsistent results regarding the link between sleep and Alzheimer’s disease pathology, Neitzel’s study brings a fresh perspective by controlling for baseline Alzheimer’s pathology. By excluding participants with positive Alzheimer’s blood tests at baseline, the researchers were able to isolate the impact of 24-hour rest-activity rhythm fragmentation on Alzheimer’s PET burden at follow-up. This finding suggests that circadian disruption may serve as a risk factor for Alzheimer’s disease rather than a consequence.
According to the Lancet Commission, modifying key risk factors could prevent or delay up to 40% of dementia cases. While sleep is not currently included in these risk factors, there is growing interest in understanding the role of sleep dysfunction in dementia development. Matthew Pase, PhD, from Monash University, emphasizes that improving sleep quality could potentially lower dementia risk if poor sleep contributes to the disease. Neitzel’s study adds to the evidence indicating that circadian disruption may indeed increase the risk of developing dementia.
The study involved 319 participants from the Rotterdam study who were dementia-free at baseline. Through actigraphy and self-reporting, the researchers assessed sleep and 24-hour activity rhythms, correlating them with amyloid burden measured on PET scans 8 years later. While higher fragmentation of activity rhythms was linked to more severe amyloid pathology, no other sleep measures showed a strong relationship with amyloid levels. Contrary to some previous research, sleep duration did not significantly impact amyloid pathology in this study.
The study’s limitations include the use of a single PET scan per participant, which limited longitudinal analyses. Additionally, actigraphy studies may have smaller sample sizes due to their demanding nature compared to self-report studies. The researchers acknowledge that polysomnography is the gold standard for sleep measurement, and the assessment of possible sleep apnea through self-reports may have influenced the results.
Disrupted circadian rhythms in cognitively normal adults appear to be associated with higher subsequent amyloid-beta levels, highlighting a potential risk factor for Alzheimer’s disease. Further research focusing on larger sample sizes and longitudinal data may provide a deeper understanding of the link between circadian disruption, sleep, and dementia risk. Improved sleep quality and the maintenance of healthy circadian rhythms could offer promising strategies for dementia prevention and management.
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