Cell Death Linked to Sleep Deprivation, Age
> 6/30/2008 4:51:03 PM

Past research has indicated that sleep deprivation can contribute to the accumulation of abnormal proteins in brain cells, and a new study from the Journal of Neuroscience furthers our understanding of why the body might be unable to regulate proteins. Using sleep-deprived mice, a group of researchers from the University of Pennsylvania School of Medicine focused on a specific mechanism that allows the body to fix abnormal proteins and keep cells functioning properly. Their findings provide evidence that an individual’s age can affect this process and might contribute to cellular degeneration.

Proteins are naturally able to fold into characteristic shapes, and in doing so they gain a structure that allows them to successfully perform a specific function. But proteins cannot fulfill this purpose when they do not fold or fold incorrectly, and the buildup of these abnormal proteins is thought to boost an individual’s vulnerability to certain neurological conditions associated with aging, including Parkinson’s disease and Alzheimer’s disease. To prevent abnormal proteins from harming cells, the body activates a process known at the unfolded protein response (UPR), which causes proteins to be refolded and promotes the death of cells that cannot be fixed. Sleep deprivation places stress on cells and triggers UPR, but an individual’s age also influences the effectiveness of this process, as the researchers demonstrate in the current study.

They induced sleep deprivation in ten-week old mice and two-year old mice, comparing how the mice reacted to the subsequent cellular stress. In young mice, UPR successfully prevented abnormal proteins from collecting in brain cells, but this process did not work effectively in older mice, and the researchers found that several mechanisms that bring about UPR had been impaired. In particular, these mice had lower levels of proteins that initiate UPR and increased levels of proteins that contribute to cell death, an indication that a diminished UPR can result in higher rates of cellular degeneration.

Age may reduce the body’s ability to regulate the quality of proteins, and when stress caused by sleep-deprivation triggers the UPR, this mechanism may not prevent abnormal proteins from causing harm. Getting enough sleep is crucial to promoting physical and mental health, and older adults should be especially aware of sleep deprivation’s effects, as they are particularly at risk for insomnia and other sleep-related problems. As researchers continue to investigate the UPR, we may find ways to prevent cellular degeneration or slow its progress, but we should also find further evidence of how crucial a good night’s sleep is.

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