September 6, 2012
Sleep Problems May Be Early Sign Of Alzheimer’s
Connie K. Ho for redOrbit.com — Your Universe Online
Getting the right amount of sleep is more important than ever, as sleep is thought to have important health effects for individuals. In particular, a study by researchers at Washington University School of Medicine in St. Louis involving laboratory mice found that sleep disruption could be an early sign of Alzheimer´s disease.In the project, the scientists worked with a mouse model and discovered that the first indicators of Alzheimer´s plaques were seen in the brain due to significant disruptions to the normal sleep-wake cycle. The findings were recently published in Science Translational Medicine.
"If sleep abnormalities begin this early in the course of human Alzheimer's disease, those changes could provide us with an easily detectable sign of pathology," explained senior author Dr. David M. Holtzman, head of Washington University's Department of Neurology, in a prepared statement. "As we start to treat Alzheimer's patients before the onset of dementia, the presence or absence of sleep problems may be a rapid indicator of whether the new treatments are succeeding."
A previous research project completed by one of the investigators was utilized as it was one of the first studies to connect sleep problems to Alzheimer´s disease in sleep studies done on mice. In 2009, Holtzman published a study on how the ingredient of the brain plaques of Alzheimer´s will raise naturally when mice are awake and drop when they are asleep. The findings showed that depriving mice of sleep can cause disruptions in the sleep cycle and quicken the formation of brain plaques. The protein amyloid beta, which is a falling and rising plaque component, was also found in the cerebrospinal fluid of healthy humans during a study completed by Dr. Randall Bateman of Washington University.
The new research was conducted with a neurologist and postdoctoral fellow in Holtzman´s laboratory, Dr. Jee Hoon Roh; Roh demonstrated that the early signs of brain plaques corresponded to the end of natural fluctuations in amyloid beat levels in humans and mice.
"We suspect that the plaques are pulling in amyloid beta, removing it from the processes that would normally clear it from the brain," commented Holtzman in a statement.
In the project, the researchers injected a vaccine against amyloid beta to a group of mice who had the same genetic modifications. They wanted to confirm that amyloid beta was directly connected to differences in the sleep cycle of the mice. When the mice aged, they didn´t develop brain plaques. As well, their sleeping patterns stayed normal and amyloid beta levels in the brain still rose and fell regularly. When the Alzheimer´s plaques began to develop in the brain of the mice, the average sleep time lowered to 30 minutes per hour instead of the normal 40 minutes of sleep for every hour of daylight.
In moving forward with the research, the investigators are planning to look at whether sleep problems could be found in patients who didn´t have signs of Alzheimer´s disease, like the development of brain plaques, but who hadn´t shown any memory or cognitive problems.
"If these sleep problems exist, we don't yet know exactly what form they take–reduced sleep overall or trouble staying asleep or something else entirely," concluded Holtzman in the statement. "But we're working to find out."