Chronic poor sleep has been linked to cognitive decline, and a new study from Washington University School of Medicine in St. Louis explains why: As a wakeful brain churns away through the night, it 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.
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, the study showed that it was due to overproduction of amyloid beta during sleep deprivation. Sleeping poorly increases levels of brain proteins such as amyloid beta that are linked to Alzheimer’s disease. But it wasn’t clear why amyloid beta levels rise in a tired brain.
Neurologist studied eight people ages 30 to 60 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. 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 percent 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. brain changes. The brains of people with Alzheimer’s disease are dotted with such plaques. Amyloid beta is a byproduct of normal brain activity.
The researchers found that when people stay awake, their brains continue to produce amyloid beta through the night. A sleeping brain produces much less. Asleep or awake, however, the brain clears the protein away at the same rate, so the increased production during sleep deprivation leads to higher levels of the damaging protein.
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