Chronic poor sleep may contribute to cognitive decline, according to a study that shows wakeful brain produces more of the Alzheimer’s protein amyloid beta than its waste-disposal system can handle.
Levels of the protein rise, potentially setting off a sequence of changes to the brain that can end with dementia, researchers said.
“This study is the clearest demonstration in humans that sleep disruption leads to an increased risk of Alzheimer’s disease through an amyloid beta mechanism,” said Randall Bateman, from the Washington University School of Medicine, St Louis in the US. “The study showed that it was due to overproduction of amyloid beta during sleep deprivation,” Bateman said.
For the research published in the journal Annals of Neurology, the scientists studied eight people aged between 30 to 60 years with no sleep or cognitive problems. The participants were assigned randomly to one of three scenarios: having a normal night’s sleep without any sleep aids; staying up all night; or sleeping after treatment with sodium oxybate, a prescription medication for sleep disorders.
The scientists studied eight people aged between 30 to 60 years with no sleep or cognitive problems.
Sodium oxybate increases slow-wave sleep – the deep, dreamless phase of sleep that people need to wake up feeling refreshed. Each scenario occurred during 36 hours of monitoring, starting in the morning and continuing through the afternoon of the following day. The researchers took samples of the fluid that surrounds the brain and spinal cord every two hours to monitor how amyloid beta levels change with time of day and tiredness.
All eight participants returned four to six months later to undertake a second scenario, and four people completed all three. Studying the same people under different conditions provides the statistical power to detect changes in amyloid beta levels. Amyloid beta levels in sleep-deprived people were 25 to 30% higher than in those who had slept the night through.
After a sleepless night, amyloid beta levels were on par with the levels seen in people genetically predisposed to develop Alzheimer’s at a young age. “This information could help us figure out how to reduce amyloid beta deposition over time in people whose sleep is chronically disrupted,” said Brendan Lucey, from the Washington University School of Medicine.