Study Suggests Link Between Sleep Deprivation, Alzheimer’s Risk

WEDNESDAY, Sept. 28 (HealthDay News) — A new study shows that levels of amyloid beta, a byproduct of brain activity that is considered a marker for Alzheimer’s disease, normally rise during the day and decrease at night.

While the finding is preliminary, it could suggest a possible link between sleep deprivation and people’s risk for developing the brain-robbing disease, researchers say.

“We’ve known for some time that significant sleep deprivation has negative effects on cognitive [brain] function comparable to that of alcohol intoxication,” Dr. Stephen Duntley, professor of neurology and director of Washington University’s Sleep Medicine Center, said in a university news release. “But it’s recently become apparent that prolonged sleep disruption and deprivation can actually play an important role in pathological processes that underlie diseases. This connection to Alzheimer’s disease isn’t confirmed yet in humans, but it could be very important.”

The findings were released online in advance of publication in an upcoming print issue of Archives of Neurology.

According to the researchers, levels of the amyloid beta protein do seem to ebb and flow.

“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,” Dr. Randall Bateman, associate professor of neurology at Washington University School of Medicine in St. Louis, explained in the news release.

“We looked at many different behaviors, and the transitions between sleep and wakefulness were the only phenomena that strongly correlated with the rise and fall of amyloid beta in the spinal fluid,” he added.

Bateman and colleagues also found this pattern was most prevalent in healthy, young people and less pronounced in older adults who suffer from shorter or more disrupted periods of sleep.

They suggested the reason for this may be that the brain’s low activity during sleep allows the body to clear amyloid beta through the spinal fluid.

Levels of amyloid beta in older adults with Alzheimer’s appear to be constant, suggesting a possible link between lack of sleep and people’s odds for developing the disease, the team said.

In conducting the study, the researchers divided study participants into three groups:

• People aged 60 and older who tested positive for the presence of amyloid beta plaques in the brain.
• People aged 60 and older who did not have amyloid beta plaques.
• Healthy people ranging in age from 18 to 60 years.

Using a spinal tap, researchers monitored amyloid beta levels in the participants’ spinal fluid every hour for up to 36 hours. During this time, they also videotaped the patients’ activities and monitored their brain activity.

In the group with brain plaques, amyloid beta levels remained virtually constant. In the other two groups, however, the levels regularly rose and fell in snake-like waves. The highs and lows of this pattern were much more obvious in younger participants, and flatter in older people.

Although the participants’ activities did not have an impact on changes in amyloid beta levels, peaks in their sleep and wakefulness consistently occurred before peaks and drops in amyloid beta levels.

The study authors said that more research is needed to explore how disrupted sleep in young people disrupts the normal ebb and flow of spinal amyloid beta, and how sleep aids may help maintain this wave-like pattern.

“It’s still speculation, but there are tantalizing hints that better sleep may be helpful in reducing Alzheimer’s disease risk,” concluded 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.”

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about Alzheimer’s disease.

– Mary Elizabeth Dallas

SOURCE: Washington University School of Medicine, news release, Sept. 26, 2011

Last Updated: Sept. 28, 2011