Abstract
Background
Sleep disturbances are common maladies associated with human age. Sleep duration is decreased, sleep fragmentation is increased, and the timing of sleep onset and sleep offset is earlier. These disturbances have been associated with several neurodegenerative diseases. Mouse models for human sleep disturbances can be powerful due to the accessibility to neuroscientific and genetic approaches, but these are hampered by the fact that most mouse models employed in sleep research have spontaneous mutations in the biosynthetic pathway(s) regulating the rhythmic production of the pineal hormone melatonin, which has been implicated in human sleep.
Purpose and method
The present study employed a non-invasive piezoelectric measure of sleep wake cycles in young, middle-aged and old CBA mice, a strain capable of melatonin biosynthesis, to investigate naturally-occurring changes in sleep and circadian parameters as the result of aging.
Results
The results indicate that young mice sleep less than do middle-aged or aged mice, especially during the night, while the timing of activity onset and acrophase is delayed in aged mice compared to younger mice.
Conclusion
These data point to an effect of aging on the quality and timing of sleep in these mice but also that there are fundamental differences between control of sleep in humans and in laboratory mice.
Ethical disclosure
BFO is a co-founder and co-owner of Signal Solutions, LLC (Lexington, KY) that manufactures and sells the PiezoSleep system used in this study.
Disclosure
Dr Bruce F O’Hara is a co-founder and co-owner of Signal Solutions LLC, that manufatures the PiezoSleep technology used in this study. However, his role in this study was as a Professor of Biology, and nothing in this work has significant financial ramifications for Signal Solutions LLC, and thus the conflict of interest is very low to non-existent in this case. The other authors report no conflicts of interest in this work.