Aging adults who report being very sleepy during the day were nearly three times more likely than those who didn’t to have brain deposits of beta amyloid, a protein that’s a hallmark for Alzheimer’s disease, years later.
The finding, published on Sept. 5 in the journal SLEEP, adds to a growing body of evidence that poor quality sleep could encourage this form of dementia to develop, suggesting that getting adequate nighttime sleep could be a way to help prevent Alzheimer’s disease.
“Factors like diet, exercise and cognitive activity have been widely recognized as important potential targets for Alzheimer’s disease prevention, but sleep hasn’t quite risen to that status–although that may well be changing,” says Adam Spira, associate professor at the Johns Hopkins Bloomberg School of Public Health.
“If disturbed sleep contributes to Alzheimer’s disease,” he said. “We may be able to treat patients with sleep issues to avoid these negative outcomes.”
The study used data from the Baltimore Longitudinal Study of Aging (BLSA) that was started way back in 1958 to follow the health of thousands of volunteers as they age. Volunteers filled a questionnaire between 1991 and 2000 that asked a simple yes/no question: “Do you often become drowsy or fall asleep during the daytime when you wish to be awake?” They were also asked, “Do you nap?” with response options of “daily,” “1-2 times/week,” “3-5 times/week,” and “rarely or never.”
A subgroup of BLSA volunteers also began receiving neuroimaging assessments in 1994. Starting in 2005, some of these participants received positron emission tomography (PET) scans using Pittsburgh compound B (PiB), a radioactive compound that can help identify beta-amyloid plaques in neuronal tissue, which are a hallmark of Alzheimer’s disease.
The researchers identified 123 volunteers who both answered the earlier questions and had a PET scan with PiB an average of nearly 16 years later and then analyzed it to see if there was a correlation between participants who reported daytime sleepiness and whether they scored positive for beta-amyloid deposition in the brain.
The results showed that those who reported daytime sleepiness were about three times more likely to have beta-amyloid deposition than those who didn’t report daytime fatigue. After adjusting for other health factors, the risk was still 2.75 times higher among them.
The unadjusted risk for amyloid-beta deposition was about twice as high in volunteers who reported napping, but this did not reach statistical significance.
It’s currently unclear why daytime sleepiness would be correlated with the deposition of beta-amyloid protein, Spira says. One possibility is that daytime sleepiness itself might somehow cause this protein to form in the brain.
Based on previous research, a more likely explanation is that disturbed sleep or insufficient sleep due to other factors, causes beta-amyloid plaques to form through a currently unknown mechanism, and that these sleep disturbances also cause excessive daytime sleepiness.
“However, we cannot rule out that amyloid plaques that were present at the time of sleep assessment caused the sleepiness,” he added.
This new study adds to growing evidence that poor sleep might actually contribute to Alzheimer’s disease development. Spira suggests that sleep quality could be a risk factor that’s modifiable by targeting disorders that affect sleep, such as obstructive sleep apnea and insomnia, as well as social- and individual-level factors, such as sleep loss due to work or binge-watching TV shows.
“There is no cure yet for Alzheimer’s disease, so we have to do our best to prevent it. Even if a cure is developed, prevention strategies should be emphasized,” Spira says.