Researchers found that mice that were chronically deprived of sleep had more plaques and developed them earlier compared with mice that slept normally. Plaques, a hallmark of Alzheimer's disease, are made up of amyloid beta protein. The study also showed that the protein orexin, which helps regulate sleep cycles, appears to be involved in the process.
The research team, led by Dr. David M. Holtzman of Barnes Jewish Hospital and Washington University in St. Louis, monitored levels of beta amyloid in mice that were genetically engineered to model Alzheimer's disease. Investigators found that the amount of brain amyloid beta rose and fell in association with sleep and wakefulness (with lower levels during sleep). They then used electroencephalograph scans to show that mice who stayed awake longer had higher amyloid beta levels. Depriving mice of sleep caused a 25% increase in levels.
Finally, when the scientists injected orexin into the brains of mice, they stayed awake longer and amyloid beta levels increased.
The results suggest that sleep loss may play a role in development of Alzheimer's disease, which affects 39 million Americans, and that treatments to promote sleep may be helpful.
"Orexin or compounds it interacts with may become new drug targets for treatment of Alzheimer's disease," Holtzman said in a news release. "The results also suggest that we may need to prioritize treating sleep disorders not only for their many acute effects but also for potential long-term impacts on brain health."
The study was published Thursday in the journal Science Express.
-- Shari Roan
Photo: Advanced Cell Technology Inc.