MONDAY, Oct. 21, 2013 (HealthDay News) -- Older people who get less sleep or poor sleep may have more of the plaque that is suggestive of Alzheimer's disease in their brains, a new study indicates.
"There is a link between sleep and the amount of [beta] amyloid in the brain," said lead researcher Adam Spira, an assistant professor in the department of mental health at the Johns Hopkins Bloomberg School of Public Health.
The unanswered question is whether poor sleep is a result of plaque build-up or if poor sleep leads to more plaque and eventually Alzheimer's disease. Also, although the study showed an association between the two, it did not prove any cause-and-effect links.
"We can't say that sleep disturbance preceded the amyloid deposits," Spira said. "One possibility is that changes in the brain are leading to disturbed sleep."
It is known that people with Alzheimer's disease have disturbed sleep, Spira said. "But that we found this in people without Alzheimer's disease leads us to think that there might be a connection between sleep disturbance and developing amyloid plaque and Alzheimer's disease, but we can't tell that yet," he said.
Still, Spira suggested it might be possible that improving sleep could help prevent Alzheimer's disease. "We live in a sleep-deprived society," he said. "It may be that changing sleep habits has significant implications for mental health and specifically the prevention of Alzheimer's disease, but that remains to be seen."
The report was published online Oct. 21 in the journal JAMA Neurology.
Spira said a study published Oct. 17 in the journal Science showed that during sleep there are changes in the brains of mice that help flush out toxins such as beta amyloid.
The lead researcher of the Science study, Dr. Maiken Nedergaard, co-director of the University of Rochester Medical Center for Translational Neuromedicine, said this latest study "fits perfectly with our recent analysis."
Another expert agreed that sleeping well might help prevent Alzheimer's disease.
"Since researchers know that more amyloid protein is produced by neurons in active circuits, the results could mean that quieting them down and getting a good night's sleep might help to prevent Alzheimer's," said Greg Cole, a neuroscientist at the Greater Los Angeles VA Healthcare System.
Or it might just mean that Alzheimer's disease causes sleep disturbances, he added.
"So far, there is no evidence that sleeping pills reduce Alzheimer's disease risk," said Cole, who also is associate director of the Alzheimer's Disease Research Center at the University of California, Los Angeles, David Geffen School of Medicine. "Like problems with sleep, people treating the sleep loss with sleeping pills still have increased Alzheimer's disease risk. You wouldn't want to lose too much sleep worrying about sleep loss as a cause or consequence of Alzheimer's disease until we learn more."
Dr. Sam Gandy, director of the Mount Sinai Center for Cognitive Health, in New York City, said sleep appears to be necessary to clear the brain of toxins like beta amyloid.
"There is accumulating evidence that beta amyloid and other metabolites are cleared during sleep, so there is probably at least an effect of sleep dysfunction on beta amyloid accumulation," Gandy said.
"That does not exclude the possibility that amyloid regulates sleep," he said. "That should be testable, by transferring cerebrospinal fluid from sleep-deprived animals into non-sleep-deprived animals to see whether that causes sleep dysfunction in the recipient."
For this study, Spira's team used data from 70 adults who took part in the Baltimore Longitudinal Study of Aging. Those in the study, who had an average age of 76, reported how well they slept, while the amount of beta amyloid in their brains was measured with brain scans.
The researchers found that those who said they slept less -- around five hours a night -- and those whose quality of sleep was poor had more plaque build-up than those who slept longer and better.
Visit the Alzheimer's Association for more on this memory-robbing disease.
SOURCES: Adam Spira, Ph.D., assistant professor, department of mental health, Johns Hopkins Bloomberg School of Public Health, Baltimore; Greg Cole, Ph.D., neuroscientist, Greater Los Angeles VA Healthcare System, and associate director, Alzheimer's Disease Research Center, University of California, Los Angeles, David Geffen School of Medicine; Sam Gandy, M.D., Ph.D., director, Mount Sinai Center for Cognitive Health, New York City; Maiken Nedergaard, M.D., co-director, University of Rochester Medical Center for Translational Neuromedicine, New York; Oct. 21, 2013, JAMA Neurology, online
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