Daytime sleepiness may be a new risk factor for Alzheimer’s disease.
It affects around 5.7 million people in the United States — and this number is predicted to rise.
Some estimate that, by 2050, 13.8 million U.S. adults might be affected.
Despite its growing prevalence, treatment options are lacking and there is no cure.
The exact causes are not yet known, so a great deal of research goes into understanding what factors increase the risk of developing Alzheimer’s. By recognizing the risk factors, it may be possible to significantly reduce the chances of getting Alzheimer’s.
To date, a number of these risk factors have been discovered. The most well-known is age; most people who develop Alzheimer’s are 65 or older. After the age of 85, the risk of developing Alzheimer’s is almost one third.
Genetic factors also play a role; a person’s risk increases if a family member has had the disease, and certain genes have been identified that are strongly linked to Alzheimer’s risk.
Sleep as a risk factor
Published in the journal SLEEP, the new study was led by Adam P. Spira, Ph.D., who is an associate professor at the Johns Hopkins Bloomberg School of Public Health in Baltimore, MD.
“Factors like diet, exercise, and cognitive activity,” he states, “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.”
Specifically, the researchers looked for a relationship between excessive daytime sleepiness and napping and the buildup of beta-amyloid plaques in the brain, which is a hallmark of Alzheimer’s disease.
Understanding the links between sleepiness and Alzheimer’s here could be important. “If disturbed sleep contributes to Alzheimer’s disease,” Spira explains, “we may be able to treat patients with sleep issues to avoid these negative outcomes.”
To investigate, they took data from the Baltimore Longitudinal Study of Aging, which has followed the health of thousands of participants since 1958. Of particular interest was a questionnaire that was completed in 1991–2000. Two questions were relevant to this study:
- “Do you often become drowsy or fall asleep during the daytime when you wish to be awake?” This was a simple yes or no question.
- “Do you nap?” The multiple choice answers were: “daily,” “one to two times each week,” “three to five times each week,” and “rarely or never.”
Also, as part of the Baltimore study, some participants received brain scans that could detect beta-amyloid plaques in the brain.
Analyzing the impact of sleep
In all, there were 123 participants who had both answered the questionnaire and had a brain scan. The scans occurred an average of 16 years after the questionnaires.
Next, the scientists looked for correlations between daytime sleepiness, napping, and Alzheimer’s plaques. After adjusting for factors that might account for sleepiness, such as sex, age, level of education, and body mass index (BMI), the relationship was still significant.
They found that individuals who reported excessive daytime sleepiness had 2.75 times the risk of beta-amyloid buildup.
When they analyzed daytime napping, the relationship was in a similar direction but the results did not reach statistical significance.
The next question is why does daytime sleepiness correlate with the buildup of Alzheimer’s plaques? This will take much more work to unravel; it might be that daytime sleepiness is due to factors that decrease sleep quality at night, such as sleep apnea, which occurs when an individual stops breathing for short amounts of time throughout the night.
If this is the case, plaque buildup is encouraged by interrupted sleep during the night, rather than it being daytime sleepiness, directly.
Many questions remain
Assessing cause and effect will be challenging, as ever. As the study authors explain, “we cannot rule out that amyloid plaques that were present at the time of sleep assessment caused the sleepiness.”
Do beta-amyloid plaques make a person tired, or does a lack of sleep enhance plaque formation?
Previous animal studies concluded that a reduction in night-time sleep appears to increase beta-amyloid buildup. Also, a handful of human studies have drawn lines between poor sleep and amyloid buildup.
Though the recent study cannot provide conclusive evidence that a lack of sleep influences the development of Alzheimer’s, it adds to a growing body of evidence.
Soon, sleep may be considered another modifiable risk factor for Alzheimer’s disease, which would be an important finding.
“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.
“Prioritizing sleep may be one way to help prevent or perhaps slow this condition.”