Animal Study Suggests Inadequate Sleep May Increase Pace of Cellular Aging in Older Adults

By Richard Shank

Researchers at the University of Pennsylvania have shown that the protein reaction to stress caused by sleep deprivation was impaired in the brains of older mice. These findings suggest that inadequate sleep can aggravate an age-related impairment of a protective cellular process. This impaired process is known as protein misfolding and is associated with ailments such as Alzheimer’s Disease and Parkinson’s Disease. Insomnia

The unfolded protein response (UPR) is a part of a process that monitors protein synthesis in the cellular compartment where proteins are made (i.e., the endoplasmic reticulum). This study utilized mice in order to examine how this process works within the context of aging. They compared 10-week-old and 2-year-old mice and found that the younger mice did not experience misfolding of proteins during the UPR process while the older mice did. The endoplasmic reticulum in the older mice was found to be clogged—this impairment was worsened by introducing the mice to sleep deprivation experiments.

Sleep in mice is characterized by short periods of rest throughout the day and night; typically, mice sleep one hour for every two hours they are awake. In order to deprive the mice of sleep, the researchers constantly monitored and gently stroked them with a brush in order to disturb their periods of inactivity.

At three, six, nine, or twelve hours of sleep deprivation, proteins were examined from the mice’s brains. By six hours of sleep deprivation, older mice were unable to maintain a normal UPR process while younger mice were able to balance this process. Furthermore, older mice were less likely to handle abnormal proteins and had more presence of cellular death than younger mice.

Because of these findings, Nirinjini Naidoo, lead author of the study, was quoted as saying, “we could speculate that sleep disturbances in older humans places an additional burden on an already-stressed protein folding and degradation system.” This suggests that sleep deprivation can lead to the types of abnormal cellular functioning that are known to be associated with various diseases and can even lead to cellular death, leading to the breakdown of bodily systems and organs.

Future studies should examine whether strengthening these protein systems delays the impact of aging in a way that can reduce sleep disturbances.

Source: Nirinjini Naidoo, Megan Ferber, Monali Master, Yan Zhu, and Allan Pack. 2008. Aging impairs the unfolded protein response to sleep deprivation and leads to proapoptotic signaling. Journal of Neuroscience 28(26): 6539-6548

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