Washington: Turns out, excessive daytime sleepiness is linked with brain protein involved in a memory-robbing disease, a new study reveals.
Analysis of data collected during a long-term study of aging adults showed that those who reported 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 study has revealed 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,” said study author Adam P. Spira.
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, we may be able to treat patients with sleep issues to avoid these negative outcomes,” added Spira.
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.
Daytime sleepiness may be correlated with the deposition of beta-amyloid protein due to two possibilities. 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, 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.
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.
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. Prioritizing sleep may be one way to help prevent or perhaps slow this condition,” added Spira.
The study appeared in the Journal of Sleep.