According to a team of researchers at Washington University School of Medicine, one of the first signs of Alzheimer’s disease is sleep disruptions.

The finding came from a mouse experiment which showed that the regular sleep-wake cycle is seriously disrupted when the earliest indicators of Alzheimer’s plaques become visible in the brain.

David M. Holtzman, M.D., head researcher, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology, explained:

“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. 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.”

Problems sleeping was first linked to Alzheimer’s in Holtzman’s laboratory where sleeping mice were genetically changed to develop Alzheimer’s plaques when they grew older.

When healthy young mice are awake, brain levels of a key element of the plaques naturally rise, but drop after they fall asleep, according to Holtzman’s research in 2009. The speed of development of the plaques increased when the mice were deprived of sleep because it disrupted this cycle.

Randall Bateman, M.D., co-author and the Charles F. and Joanne Knight Distinguished Professor of Neurology at Washington University, studied similar fluctuation levels of the plaque component, a protein called amyloid beta, that was identified in the cerebrospinal fluid of healthy individuals.

The current study, led by Jee Hoon Roh, M.D., Ph.D., a neurologist and postdoctoral fellow in Holtzman’s laboratory, has evidence that the natural rising and falling in amyloid beta levels stop in both mice and humans when the initial signs of brain plaques come into sight.

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

Research showed that when Alzheimer’s plaques start appearing in the nocturnal animals’ brains, their normal sleep time of 40 minutes during every hour of daylight is reduced to 30 minutes per hour.

A vaccine against amyloid beta was given to a new group of mice with the same genetic alterations in other to prove there was a direct link between changes in sleep and the protein.

Brain plaques were never seen in these mice as they aged, their sleeping behaviors stayed the same, and the amyloid beta levels in the brain continued with its regular fluctuations.

Scientists believe it may be possible that patients who have not yet developed any problems with memory, but have plaques in the brain, or other indicators of the disease, are experiencing sleep problems. They are currently conducting research to determine if their theory is correct.

Holtzman concluded: “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. But we’re working to find out.”

Written by Sarah Glynn