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Abstract
One of the most significant problems facing older individuals is difficulty staying asleep at night and awake during the day. Understanding the mechanisms by which the regulation of sleep/wake goes awry with age is a critical step in identifying novel therapeutic strategies to improve quality of life for the elderly. We measured wake, non-rapid eye movement (NREM) and rapid-eye movement (REM) sleep in young (2–4 months-old) and aged (22–24 months-old) C57BL6/NIA mice. We used both conventional measures (i.e., bout number and bout duration) and an innovative spike-and-slab statistical approach to characterize age-related fragmentation of sleep/wake. The short (spike) and long (slab) components of the spike-and-slab mixture model capture the distribution of bouts for each behavioral state in mice. Using this novel analytical approach, we found that aged animals are less able to sustain long episodes of wakefulness or NREM sleep. Additionally, spectral analysis of EEG recordings revealed that aging slows theta peak frequency, a correlate of arousal. These combined analyses provide a window into the mechanisms underlying the destabilization of long periods of sleep and wake and reduced vigilance that develop with aging.
Highlights
Life expectancy is on the rise worldwide
We found that aged mice have reduced wakefulness and did not sustain long periods of wake during the active phase
Decreased wake with aging was accompanied by increased non-rapid eye movement (NREM) sleep and aged mice did not sustain long periods of NREM sleep compared to young adult animals
Summary
Life expectancy is on the rise worldwide. Within the US alone, it is estimated that 20% of the population will be over the age of 65 years by 2030 (U.S Census Estimate). Previous studies suggest that alterations in neurotransmitter and receptor levels in brain regions that regulate sleep/wake underlie these age-induced disruptions in sleep. Orexinergic and noradrenergic neurons in aged mice show reduced activity during the active phase [13]. These agerelated disruptions in signaling may underlie the inability to maintain wakefulness and sleep, as well as the alterations of EEG spectral profile that accompany normal aging. These two hallmarks of aging have been well characterized in humans [3,6]
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