Sleep Disruption Link to Alzheimers Disease Found Using Spinal Fluid Marker
Scientists have known for some time that sleep deprivation and chronic sleep loss can contribute to the risk of Alzheimer’s disease in animals. For the first time, using a spinal fluid marker, researchers have found a pattern that reinforces the theory that the risk factor also applies in humans.
Sleep Disruption and Deprivation Plays Role in Pathological Processes Leading to Disease
One of the key characteristics of Alzheimer’s disease is the presence of accumulated amounts of amyloid beta protein in the brain. This biomarker can also be found circulating in the blood and in the spinal fluid. Normally, the body clears amyloid beta from the brain, but in those with Alzheimer’s disease, the protein builds up and interrupts communication between neurons.
Researchers at the Washington University School of Medicine in St. Louis studied amyloid beta in the spinal fluid of three sets of subjects. The first was a group of participants aged 60 and older who tested positive for the presence of amyloid beta plaques in the brain. A second group of participants fell into the same age range but did not have brain plaques. The third group consisted of healthy persons aged 18 to 60. The patients’ activities and brain activity was monitored and spinal fluid tested hourly for 24 to 36 hours.
Although there were no significant changes in spinal fluid amyloid beta during waking activities such as eating or watching television, there were peaks during sleep and wakefulness that correlated with peaks and valleys of amyloid beta levels. The pattern was strongest in the healthy young people, which appears to reinforce the link found in animal studies that inadequate sleep is linked to a greater risk for Alzheimer’s disease.
“In healthy people, levels of amyloid beta drop to their lowest point about six hours after sleep, and return to their highest point six hours after maximum wakefulness,” says Randall Bateman, MD, associate professor of neurology.
The team also noted that the highs and lows of amyloid beta levels were “flattened” in the older adults, whose sleep periods are often shorter and more prone to disruption.
The researchers suspect that during sleep, while the brain is relatively inactive, the body finishes clearing away amyloid beta through the spinal fluid so that it doesn’t have time to accumulate in the brain.
“We’ve known for some time that significant sleep deprivation has negative effects on cognitive function comparable to that of alcohol intoxication,” says Stephen Duntley, MD, professor of neurology and director of the center. “But it’s recently become apparent that prolonged sleep disruption and deprivation can actually play an important role in pathological processes that underlie diseases.”
“It’s still speculation, but there are tantalizing hints that better sleep may be helpful in reducing Alzheimer’s disease risk,” says Duntley. “We know from a number of studies that exercise enhances sleep, and research also has shown that exercise is associated with decreased risk of Alzheimer’s. Sleep might be one link through which that effect occurs.”
Y. Huang, R. Potter, W. Sigurdson, A. Santacruz, S. Shih, Y.-E. Ju, T. Kasten, J. C. Morris, M. Mintun, S. Duntley, R. J. Bateman. Effects of Age and Amyloid Deposition on A Dynamics in the Human Central Nervous System.Archives of Neurology, 2011; DOI:10.1001/archneurol.2011.235