Brain Damage On The Cards For Sleep-deprived Shift Workers
Sleep is for the weak, goes the adage, but followers of that philosophy might want to rethink their night owl tendencies. A recent study ...
Sleep is for the weak, goes the adage, but followers of that philosophy might want to rethink their night owl tendencies. A recent study has shown that night shift workers who suffer from interrupted sleeping patterns are at a higher risk of brain damage, with prolonged lack of sleep factoring into the permanent loss of brain cells.
The study looked at the brains of mice who were kept awake in order to accurately mimic the neurological conditions of humans who participate in shift work. Contrary to the assumption that added sleep on weekends and days off repairs any damage incurred from a lack of sleep throughout the week, the research found that the mice lost around 25 percent of crucial locus coeruleus (LC) neurons. It's the first study of its kind to find that excessive wakefulness contributes to permanent loss of neurons.
"In general, we've always assumed full recovery of cognition following short- and long-term sleep loss," said lead author Sigrid Veasey, associate professor of Medicine and a member of the Center for Sleep and Circadian Neurobiology at the University of Pennsylvania's Perelman School of Medicine. "But some of the research in humans has shown that attention span and several other aspects of cognition may not normalize even with three days of recovery sleep, raising the question of lasting injury in the brain. We wanted to figure out exactly whether chronic sleep loss injures neurons, whether the injury is reversible, and which neurons are involved."
Of course, more research will need to be conducted in order to confirm that the findings are the same with human subjects. Nevertheless, the study paves the way for further exploration of ideas, with scientists encouraged by the results - and particularly the potential for targeting circadian rhythms and LC neurons to develop medication that could prevent irreparable damage. Such medication would largely be dependent on introducing or stimulating production of the SirT3 protein, which typically disappears as cells die. "We can now overexpress SirT3 in LC neurons," said Veasey. "If we can show that we can protect the cells and wakefulness, then we're launched in the direction of a promising therapeutic target for millions of shift workers."
The study appeared in the Journal of Neuroscience.
By Tabitha Laffernis, Tech Times