A new study from University of Pennsylvania School of Medicine suggests that lack sleep can exacerbate cellular aging cells in elderly.
Researchers have found that stress induced by sleep deprivation could exacerbate an already-impaired protective response to protein misfolding that happens in aging cells.
"Protein misfolding and aggregation is associated with many diseases like Alzheimer's and Parkinson's," said first author Nirinjini Naidoo, PhD, Assistant Professor in the Division of Sleep Medicine.
The unfolded protein response (UPR) is one part of the quality control system for monitoring protein synthesis in the endoplasmic reticulum, the cellular compartment where some proteins are made.
In this study conducted using a mouse model, the team found that the UPR was activated in 10-week old, sleep-deprived mice, so that misfolded proteins did not accumulate in the endoplasmic reticulum of brain cells in the cerebral cortex.
However, in two-year-old, sleep-deprived mice, the UPR failed to do its job and misfolded proteins clogged the endoplasmic reticulum. Old mice that were not stressed by sleep deprivation were shown to already have an impaired UPR.
We could speculate that sleep disturbance in older humans places an additional burden on an already-stressed protein folding and degradation system," said Naidoo.
The study appears in the June issue of the Journal of Neuroscience.