NEW YORK (Reuters Health) - After a night of no sleep, even a healthy brain has higher than normal levels of the protein that forms the signature tangles in Alzheimer’s disease, according to a new study from the Netherlands.
“We think normal healthy sleep helps reduce the amount of (amyloid) beta in the brain and if your sleep is disturbed this decrease is prevented,” said the study’s senior author Dr. Jurgen Claassen, from Radboud University Medical Center in Nijmegen.
In people who repeatedly fail to get a good night’s sleep, the amyloid-beta concentration may build up and could be one factor in the development of Alzheimer’s disease, he said.
Alzheimer’s is the most common form of dementia and the sixth leading cause of death for older Americans, according to the Centers for Disease Control and Prevention. Up to 5 million Americans have the condition.
Distinct from other forms of dementia, Alzheimer’s is partly defined by accumulations in the brain of the amyloid-beta protein. The cause of Alzheimer’s disease is not known, but the amyloid-beta plaques have long been thought to play an important role.
Claassen and his colleagues point out in JAMA Neurology that studies on mice have found decreases in the amount of amyloid-beta in healthy animals’ brains after a good night’s sleep. That suggests sleep plays a role in cleaning out the protein overnight.
To see if the same is true in people, the researchers recruited 26 middle-aged men with normal sleep habits to have their protein levels measured before and after sleep, or a lack of it.
The men were brought into the clinic, where a catheter was put into their spine to take fluid samples before they went to bed and after they woke up. Half of the men were randomly assigned to get a good night’s sleep while the other half were kept awake.
The researchers found that the men who got a good night’s sleep had amyloid-beta levels in their spinal fluid about 6 percent lower in the morning than when they had gone to bed. The men who were kept awake all night had no change in their amyloid-beta levels.
The quality of sleep men got was also linked to how much of a decrease in amyloid-beta was measured, which suggests more of the amino acid is cleared out with better sleep, the team writes.
“We think the beta is cleared from the brain or less produced during sleep,” Claassen told Reuters Health, adding that it could be both.
While most people may not stay up all night for weeks at a time, Claassen also said that even partly-sleepless nights can add up.
“We did a complete night of sleep deprivation which is kind of extreme, but it’s similar to a week of partial sleep deprivation,” he said.
“Based on this and other studies, it would be good to have people look at their sleep behaviors, but not be frightened themselves if they miss a good night’s sleep,” he added.
Dr. Michael Shelanski, co-director of Columbia University Medical Center’s Taub Institute for Research on Alzheimer’s Disease and the Aging Brain in New York City, cautioned that the new study can’t prove the amyloid-beta proteins have anything to do with Alzheimer’s risk.
“We really don’t have any evidence from this paper that that’s the case,” said Shelanski, who was not involved in the new study.
“This is an interesting study,” he said. “It’s a good study, but it doesn’t really say anything about Alzheimer’s disease other than you should look further and see if the sleep patterns are related to these things.”
Claassen acknowledges that his team’s results do not prove that getting ample sleep will prevent Alzheimer’s disease, or that an amyloid-beta build-up causes the condition. Sleep may be just one of many risk factors for the illness, he said. Others include genetics, high blood pressure and obesity.
“We think it’s a disease that has several causes not just one, but we don’t know which ones,” he added.
SOURCE: bit.ly/1osTpc3 JAMA Neurology, online June 2, 2014.
This story replaces “amino acid” in paragraph 10 with “protein” and clarifies affiliation in paragraph 15.
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