David M. Holtzman with the Washington University in St. Louis is head of the Department of Neurology, an Andrew B. and Gretchen P. Jones Professor, and over the years has conducted several studies on the correlation between sleep deprivation and neurological diseases such as Alzheimer’s. Alzheimer’s afflicts more than 5 million Americans today. The disease is responsible for memory loss most commonly and cognitive decline. While Holtzman, the study’s senior author, and his co-first author Yo-El Ju, an assistant professor of neurology, do not claim that their study indicates that more or better sleep can reduce the risk of developing Alzheimer’s, they are fairly confident that their results indicate there is a relationship between the increased presence of the proteins tau and amyloid beta in the brain. Both tau and amyloid beta are proteins found in “plaques” and in significantly greater amounts in the brains of those with Alzheimer’s. These proteins are responsible for the brain tissue atrophy and death of those afflicted with the disease.
Their study published in the July 2017 issue of the Journal Brain, detailed how results showed an increased presence for those afflicted with irregular or poor sleeping patterns. Previous studies by these researchers showed how cognitive impairments were likely to develop 10 years earlier in individuals suffering from sleep apnea; a symptom of Alzheimer’s developing. How poor sleep caused this damaged needed to be addressed so Holtzman, Ju, along with Sharon Ooams (a graduate of Radbound), Jurgen Claassen and MD and PhD of Radbound and Emmanuel Mignot an MD and PhD of Standford contributed with colleagues to create a sleep study of 17 healthy adults ages 35-65 with no sleep problems or cognitive impairments.
Each participant was given a wrist monitor that would record their sleeping patterns for five or more consecutive nights and reported to the School of Medicine wherein they would spend the night in a room aptly designed for sleep. These participants wore headphones and electrodes on their scalp to monitor their brain waves. Half were randomly selected to receive a series of beeps increasing in volume until their deep sleep was interrupted. They accomplished this by monitoring their slow-wave patterns characteristic of deep, dreamless sleep and bringing the participants into more shallow sleep. The participants reported hardly recalling waking up or being disturbed, but felt tired just the same. Afterwards, they received a spinal tap to measure the levels of amyloid beta and tau in their brain and spinal cord fluid. One month later the exercise was repeated using the other half of participants who were not disturbed the first time and letting the previous group sleep through the night.
Results showed that after one night of disrupted sleep that participants had a 10 percent increase in amyloid beta levels but no changes in tau protein levels. Though, monitor data indicating a week of poor sleep in participants did correspond with a “spike” in tau protein levels. Ju notes that this is a reasonable outcome, because amyloid levels respond more quickly to change.
They concluded that the number of hours of sleep did not impact their results; rather the quality of sleep marked these changes. Though one week of poor sleep increased tau and amyloid levels is not likely to increase the risk of Alzheimer’s in these participants, researchers did establish that poor sleep over a long period of time has credible consequences of increased likelihood for the development of Alzheimer’s. It is in deep sleep that our brains clean away the byproducts of brain activities when we are alert and thinking, with chronic poor sleep these byproducts accumulate to an extent.
More information: Washington University in St. Louis. “Sleep, Alzheimer’s link explained.” ScienceDaily. ScienceDaily, 10 July 2017. https://www.sciencedaily.com/releases /2017/07/170710161442.html>