Telomere dynamics are influenced by sleep, sleep variability and circadian rhythms in older adults with or without alzheimer’s risk

Dec 5, 2025Alzheimer's research & therapy

Sleep patterns and body clock rhythms affect chromosome aging in older adults with or without Alzheimer's risk

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Longevity & Aging on OpenScience ↗PubMed ↗DOI ↗OA ↗

Abstract

Poor sleep quality and variability may increase the percentage of critically short telomeres (%CST) in healthy older adults.

Lower sleep efficiency and higher wake after sleep onset are linked to increased %CST.
Greater variability in sleep efficiency is associated with an increase in %CST.
More regular sleep/wake patterns may lead to a decrease in 50th and 20th percentile telomere length (TL) and an increase in %CST.
In individuals with amyloid positivity, longer latency of rapid eye movement sleep is associated with a reduction in 20th percentile TL and an increase in %CST.
These findings suggest a connection between sleep disturbances and cellular ageing processes in older adults.

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INTRODUCTION: Sleep and circadian rhythm disturbances have been related to cognitive decline and increased risk of Alzheimer's disease (AD). These disruptions are also closely associated with biological ageing processes. , a key marker of cellular ageing, has been implicated in various age-related diseases, including AD. Although sleep disturbances have been linked to shorter telomere length (TL), the effects of sleep, its variability, and circadian rhythms on telomere dynamics (over 18 months) remain unknown. Furthermore, the interplay between these factors and AD risk has yet to be investigated in healthy older adults. Therefore, the objective of this study was to explore how sleep, sleep variability, and circadian rhythms affect telomere dynamics in healthy older adults and the influence of AD risk on these relationships.

METHODS: Data from 124 healthy older adults (mean age ± SD: 69.27 ± 3.73y) from the Age-Well interventional trial (NCT02977819) were analyzed. Blood samples were collected to determine three TL metrics (50th and 20th percentile TL, and percentage of critically short telomeres (%CST) at baseline and after 18-month follow-up). Sleep and its variability were assessed using the Somno-Artdevice over 5 nights (n = 77), and circadian rhythms using actigraphy for 1 week (n = 123). Multiple linear regressions examined whether baseline sleep and circadian rhythm measures predicted TL changes over time. Interaction analyses assessed the modulatory effects of amyloid (Aβ) status, assessed using Forbetapir-PET imaging, and APOE4 status on these relationships. Age, sex, education, BMI, and intervention group were included as covariates. ®

RESULTS: Poor sleep quality (characterized by lower sleep efficiency and higher wake after sleep onset) and greater variability in sleep efficiency predicted an increase in %CST. Greater regularity in sleep/wake patterns was associated with a decrease in 50th and 20th percentile TL and an increase in %CST. In Aβ-positive individuals, longer latency of rapid eye movement sleep predicted a reduction in 20th percentile TL and an increase in %CST.

CONCLUSIONS: This study suggests that poor sleep quality, sleep variability and circadian rhythm disturbances may accelerate cellular ageing through telomere shortening in older adults. Our results highlight the potential value of sleep interventions in mitigating biological ageing and reducing vulnerability to age-related diseases.

Key numbers

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Increase in %CST

Association between poor sleep quality and telomere dynamics.

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Increase in %CST

Link between sleep variability and cellular aging.

−0.272

Shorter telomeres with higher regularity

Unexpected association between sleep regularity and telomere length.

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Telomere dynamics are influenced by sleep, sleep variability and circadian rhythms in older adults with or without alzheimer’s risk

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