Researchers at the University of Pennsylvania School of Medicine say that inadequate sleep in the elderly, who normally experience sleep disturbances, 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," researcher Nirinjini Naidoo, told the Journal of Neuroscience. The unfolded protein response (UPR) is one part of the quality control system for monitoring protein synthesis in the cellular compartment where some proteins are made. In this study, researchers found that the UPR was activated in 10-week old, sleep-deprived mice, so that misfolded proteins did not accumulate 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 also had less of the proteins that refold abnormal proteins than young mice, and old mice had more of the proteins that cause cell death than young mice. Thus, several processes are upset in old mouse brains by sleep deprivation, and the overall result is a further accumulation of misfolded proteins.
"We could speculate that sleep disturbance in older humans places an additional burden on an already-stressed protein folding and degradation system," says Naidoo, who plans future studies to examine whether augmenting key protective proteins delays the effects of aging and reduces sleep disturbances.
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Source: University of Pennsylvania School of Medicine
