Sleep disruption with aging in senescence-accelerated mice-prone 8 (SAMP8) mice and analysis of factors associated with age-related sleep fragmentation using RNA sequencing of the hypothalamus

📖 Top 30% JournalJan 19, 2026Neurobiology of sleep and circadian rhythms

Sleep problems with aging in fast-aging mice and related brain changes in the sleep control area

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

Average sleep episode duration decreased with age in both SAMR1 and SAMP8 mice, indicating accelerated sleep fragmentation in SAMP8.

Sleep fragmentation was evaluated at 4, 36, and 56 weeks of age using a PiezoSleep® system.
Both SAMR1 and SAMP8 exhibited a decrease in average sleep episode duration as they aged.
Significant differences in sleep parameters between SAMR1 and SAMP8 emerged at 36 and 56 weeks of age, not at 4 weeks.
RNA sequencing of hypothalamic specimens from 49-week-old mice showed upregulation of type I interferon-responsive genes in SAMP8.
Higher serum levels of IFN-α were observed in SAMP8 compared to SAMR1 at 49 weeks, suggesting a potential link to sleep fragmentation.

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Aging is a risk factor for various disorders, and age-dependent changes in sleep parameters are involved in the pathogenesis of many diseases. Senescence-accelerated mice-prone 8 (SAMP8) have a short lifespan and show a disrupted circadian rhythm. However, little is known about how sleep parameters change with age in SAMP8. In this study, we evaluated changes in sleep parameters with aging in SAMP8 compared with those in senescence-accelerated mouse resistant 1 (SAMR1) as the control. Sleep quantity and fragmentation of sleep were evaluated at 4, 36, and 56 weeks of age using a PiezoSleep® system. The average duration of sleep episodes, reflected as the sleep fragmentation, decreased in an age-dependent manner in both SAMR1 and SAMP8, especially under light phase conditions. Interestingly, while the difference between SAMR1 and SAMP8 was not evident at 4 weeks of age, it was significantly reduced in SAMP8 at 36 and 56 weeks of age. These results suggest that the reduction of average sleep episode duration associated with the aging process was accelerated in SAMP8. To explore the mechanisms underlying the accelerated sleep fragmentation in SAMP8, we performed RNA sequencing on hypothalamic specimens obtained from SAMR1 and SAMP8 at 49 weeks of age, which revealed upregulation of type I interferon (IFN)-responsive genes in the SAMP8 hypothalamus. Furthermore, serum IFN-α levels at 49 weeks of age were higher in SAMP8 compared with those in SAMR1, suggesting that elevated IFN-α production in SAMP8 could be associated with the sleep fragmentation.

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