NEW YORK (Reuters Health) - Older cognitively normal adults who tend to be sleepy during the day may be more likely to have future beta-amyloid deposition, according to a new study.
As Dr. Adam P. Spira told Reuters Health by email, "We know that poor sleep and sleep-disordered breathing are associated with cognitive decline, and growing evidence indicates that they are associated with increased beta-amyloid deposition. Because EDS (excessive daytime sleepiness) often results from sleep-disordered breathing or other sleep disorders, it makes sense that EDS would be linked to subsequent beta-amyloid deposition."
"What was surprising, however, was that a response to a single yes or no question about EDS - whether participants often become drowsy - was strongly associated with beta-amyloid status many years later," said Dr. Spira of Johns Hopkins Bloomberg School of Public Health and Johns Hopkins University School of Medicine in Baltimore, Maryland.
He presented the findings June 6 at SLEEP 2017, the joint meeting of the American Academy of Sleep Medicine and the Sleep Research Society, in Boston.
Figure: A single yes or no question can predict beta-amyloid status in the elderly
Image credit Marc Lewis / Flickr
Dr. Spira and his colleagues explored the association of baseline self-reported EDS and napping with beta-amyloid deposition measured an average of over 15 years later by positron emission tomography (PET).
The researchers assessed 124 participants in the Baltimore Longitudinal Study of Aging (BLSA) who had EDS with or without napping. They averaged 60.1 years of age and had 16.7 years of education. After almost 16 years of follow-up they had a PET scan.
When the participants were asked about EDS and napping, they were cognitively normal, but by the time they had a PET scan, that was not necessarily true, Dr. Spira noted.
Participants were asked whether they often became drowsy and fell asleep when they would rather be awake, and how frequently they took naps. Those who answered "yes" to the former question were considered to have EDS, and those who napped more often than "never" were considered nappers.
Thirty participants (24.4%) reported EDS, 35 (28.5%) were nappers and 43 (34.7%) had high beta-amyloid levels.
Participants with EDS were significantly more likely to have high beta-amyloid levels (odds ratio, 3.37; p=0.005) than those without EDS. After the researchers adjusted for age, body mass index and education, the odds remained elevated (OR, 2.59; p=0.041). Nappers were roughly twice as likely to have high beta-amyloid but the increase was not statistically significant.
Co-author Dr. Mark N. Wu, also at Johns Hopkins University School of Medicine, told Reuters Health by email, 'What I find really interesting about this study is that daytime sleepiness alone is a fairly strong predictor for beta-amyloid brain deposition in humans."
"While a number of things can induce daytime sleepiness in older adults, such as sleep disordered breathing or reduced sleep amount or quality, this finding really supports the general concept that sleep is important in the pathogenesis of Alzheimer's disease,” he said. “This is important, because sleep disorders are treatable, and thus sleep may be a modifiable risk factor for Alzheimer's disease."
Dr. Spira noted that these results suggest that EDS could be a marker for Alzheimer’s disease.
"Although we need further studies to replicate our findings, asking patients about EDS may be a useful addition to available tools for quantifying Alzheimer’s risk," he said.
"It is unlikely that EDS itself is causing beta-amyloid deposition, but it is likely a marker for sleep disorders that may be modifiable contributors to Alzheimer’s disease. EDS could also be a marker for chronic insufficient sleep caused by work schedules, family demands, or even nighttime social media use or binge watching of TV shows," he added.
Dr. Spira said the study has limitations, including being based on self-reporting and not having objective sleep measures, such as polysomnography.
"Also, we did not have measures of beta-amyloid status at baseline (when we measured EDS and napping), so we are unable to determine whether EDS was associated with an increase in beta-amyloid burden or a change in beta-amyloid status (e.g., from negative to positive)," he explained.
"We are only able to say that EDS was associated with beta-amyloid deposition at the time of imaging and cannot determine whether excessive sleepiness promotes amyloid deposition or whether amyloid deposition results in greater sleepiness," he said.
The research team is now collecting wrist actigraphy and polysomnography data from the BLSA to better understand links between disturbed sleep and later brain changes that are consistent with Alzheimer’s disease.
The study was a collaborative effort between researchers at the National Institute on Aging (NIA) Intramural Research Program, which runs the BLSA, and Johns Hopkins University.
Dr. Spira has agreed to serve as a consultant to Awarables, Inc., which makes devices and software to monitor sleep.