Poor sleep may play a key role in the eventual development of Alzheimer’s disease.
Researchers from the Washington University School of Medicine Center in St. Louis, Radboud University Medical Centre in the Netherlands and Stanford University have found that disrupting just a single night of sleep in a healthy, middle-aged adult can cause an increase in amyloid beta—a brain protein linked with Alzheimer’s disease.
Furthermore, a week of poor sleep is linked to an increase tau—another brain protein linked to brain damage in Alzheimer’s and other neurological diseases.
“We showed that poor sleep is associated with higher levels of two Alzheimer’s-associated proteins,” Dr. David Holtzman, the Andrew B. and Gretchen P. Jones Professor, head of the Department of Neurology and the study’s senior author, said in a statement. “We think that perhaps chronic poor sleep during middle age may increase the risk of Alzheimer’s later in life.”
The brains of Alzheimer’s sufferers are dotted with plaques of amyloid beta protein and tangles of tau protein. The two proteins together cause brain tissue to atrophy and die.
According to Dr. Yo-El Ju, an assistant professor of neurology, a single night or week of poor sleep will not largely increase the risk of the disease because the protein levels likely decrease after the next good sleep.
“The main concern is people who have chronic sleep problems,” Ju said in a statement. “I think that may lead to chronically elevated amyloid levels, which animal studies have shown lead to increased risk of amyloid plaques and Alzheimer’s.
“Many, many Americans are chronically sleep-deprived, and it negatively affects their health in many ways,” she added. “At this point, we can’t say whether improving sleep will reduce your risk of developing Alzheimer’s. All we can really say is that bad sleep increases levels of some proteins that are associated with Alzheimer’s disease. But a good night’s sleep is something you want to be striving for anyway.”
During the study, the researchers examined 17 healthy adults with no sleep problems or cognitive impairments. Each participant wore an activity monitor on their wrist for up to two weeks that measured how much time they spent sleeping each night. After at least five nights of wearing the monitor, each participant spent a night in a specially designed sleep room that is dark, soundproof, climate-controlled and big enough for only one.
The researchers disturbed the sleep of half the participants with a series of beeps through headphones that gradually got louder.
The participants who had been disturbed underwent a spinal tap in the morning so the researchers could measure the levels of amyloid beta and tau in the fluid surrounding the brain and spinal cord.
The researchers repeated this process at least a month later, except they reversed the patients who had their sleep disturbed with those that did not.
This resulted in a 10 percent increase in amyloid beta levels after a single night of interrupted sleep but no corresponding increase in tau levels. However, the participants who slept poorly at home saw a spike in tau levels.
Alzheimer’s disease—which is characterized by gradual memory loss and cognitive decline—impacts more than five million Americans. There are currently no therapies that have been proven to prevent, slow or reverse the course of the disease.
“We were not surprised to find that tau levels didn’t budge after just one night of disrupted sleep while amyloid levels did, because amyloid levels normally change more quickly than tau levels,” Ju said. “But we could see, when the participants had several bad nights in a row at home, that their tau levels had risen.”