Sleep Problems Linked To Onset of Alzheimer’s

The problems while sleeping may be early sign of Alzheimer's disease.

A study by a team of researchers from the Washington University School of Medicine in St. Louis was published in the journal Science Translation Medicine. It suggests that when the first signs of Alzheimer's plaques appear in the brain, it disrupts the normal sleep cycle.

"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," says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University's Department of Neurology.

"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."

Holtzman's laboratory was the first study to link sleep problems with Alzheimer's through study on mice. In a study in 2009, he had projected how the brain levels of plaques rise when healthy young mice are awake and drops when they go to sleep. Depriving the mice of sleep disrupted this cycle and accelerated the development of brain plaques.

The co-author Randall Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology at Washington University has conducted a study in which they showed the similar rise and fall of the plaque component, amyloid beta that is present in the cerebrospinal fluid of healthy humans.

According to the research that is carried out by Jee Hoon Roh, MD, PhD, a neurologist and postdoctoral fellow in Holtzman's laboratory, when the first indicators of brain plaques pop up, the natural fluctuations in amyloid beta levels stop in both mice and humans.

"We suspect that the plaques are pulling in amyloid beta, removing it from the processes that would normally clear it from the brain," Holtzman says.

Mice, an octurnal animal showed a change in the sleep pattern,
their normal sleep of 40 minutes was reduced to 30 minutes when Alzheimer's plaques began forming in their brains.

They also tested a link between amyloid beta and sleep pattern by injecting a vaccine against amyloid beta to a new group of mice with the same genetic modifications. They noticed that over the period of time these mice did not develop brain plaques. Their sleeping pattern did not alter and amyloid beta levels in the brain continued to rise and fall regularly.

"If sleep abnormalities begin this early in the course of human Alzheimer's disease, those changes could provide us with an easily detecable sign of pathology," Dr. Holtzman was quoted in EmaxHealth, " 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."