More daytime sleepiness, more Alzheimer's risk?
Excessive daytime sleepiness linked with brain protein involved in memory-robbing disease
September 6, 2018
Science Daily/Johns Hopkins University Bloomberg School of Public Health
Analysis of data captured during a long-term study of aging adults shows that those 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, reported 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 P. Spira, PhD, associate professor in the Department of Mental Health at the Johns Hopkins Bloomberg School of Public Health. Spira led the study with collaborators from the National Institute on Aging (NIA), the Bloomberg School and Johns Hopkins Medicine.
"If disturbed sleep contributes to Alzheimer's disease," he adds, "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), a long-term study started by the NIA in 1958 that followed the health of thousands of volunteers as they age. As part of the study's periodic exams, 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. These plaques 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. They then analyzed this data to see if there was a correlation between participants who reported daytime sleepiness or napping and whether they scored positive for beta-amyloid deposition in their brains.
Before adjusting for demographic factors that could influence daytime sleepiness, such as age, sex, education, and body-mass index, their 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 these factors, the risk was still 2.75 times higher in those with daytime sleepiness.
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 -- due to obstructive sleep apnea, for example -- 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.
Animal studies in Alzheimer's disease models have shown that restricting nighttime sleep can lead to more beta-amyloid protein in the brain and spinal fluid. A handful of human studies have linked poor sleep with greater measures of beta-amyloid in neuronal tissue.
Researchers have long known that sleep disturbances are common in patients diagnosed with Alzheimer's disease -- caregiver stress from being up with patients at night is a leading reason for Alzheimer's disease patients to be placed in long-term care, Spira explains. Growing beta-amyloid plaques and related brain changes are thought to negatively affect sleep.
But this new study adds to growing evidence that poor sleep might actually contribute to Alzheimer's disease development, Spira adds. This 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. "Prioritizing sleep may be one way to help prevent or perhaps slow this condition."
https://www.sciencedaily.com/releases/2018/09/180906141501.htm
Sleep problems may be early sign of Alzheimer's
July 5, 2017
Science Daily/American Academy of Neurology
Poor sleep may be a sign that people who are otherwise healthy may be more at risk of developing Alzheimer's disease later in life than people who do not have sleep problems, according to a study. Researchers have found a link between sleep disturbances and biological markers for Alzheimer's disease found in the spinal fluid.
"Previous evidence has shown that sleep may influence the development or progression of Alzheimer's disease in various ways," said study author Barbara B. Bendlin, PhD, of the University of Wisconsin-Madison. "For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain's clearance system kicks into action during sleep. Our study looked not only for amyloid but for other biological markers in the spinal fluid as well."
Amyloid is a protein that can fold and form into plaques. Tau is a protein that forms into tangles. These plaques and tangles are found in the brains of people with Alzheimer's disease.
For the study, researchers recruited 101 people with an average age of 63 who had normal thinking and memory skills but who were considered at risk of developing Alzheimer's, either having a parent with the disease or being a carrier of a gene that increases the risk for Alzheimer's disease called apolipoprotein E or APOE. Participants were surveyed about sleep quality. They also provided spinal fluid samples that were tested for biological markers of Alzheimer's disease.
Researchers found that people who reported worse sleep quality, more sleep problems and daytime sleepiness had more biological markers for Alzheimer's disease in their spinal fluid than people who did not have sleep problems. Those biological markers included signs of amyloid, tau and brain cell damage and inflammation.
"It's important to identify modifiable risk factors for Alzheimer's given that estimates suggest that delaying the onset of Alzheimer's disease in people by a mere five years could reduce the number of cases we see in the next 30 years by 5.7 million and save $367 billion in health care spending," said Bendlin.
While some of these relationships were strong when looking at everyone as a group, not everyone with sleep problems has abnormalities in their spinal fluid. For example, there was no link between biological markers in the spinal fluid and obstructive sleep apnea.
The results remained the same when researchers adjusted for other factors such as use of medications for sleep problems, amount of education, depression symptoms or body mass index.
"It's still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep," said Bendlin. "More research is needed to further define the relationship between sleep and these biomarkers."
Bendlin added, "There are already many effective ways to improve sleep. It may be possible that early intervention for people at risk of Alzheimer's disease may prevent or delay the onset of the disease."
One limitation of the study was that sleep problems were self-reported. Monitoring of sleep patterns by health professionals may be beneficial in future studies.
https://www.sciencedaily.com/releases/2017/07/170705164548.htm