Impaired sleep quality is associated with smaller volumes of a part of the brain that is vulnerable to Alzheimer’s disease, new research shows.
In the new study, Yale School of Medicine (YSM) researchers investigated if individuals’ sleep patterns were linked to brain regions that undergo neurodegeneration in the early stages of Alzheimer’s disease.
They found that less time in slow-wave sleep and rapid-eye movement (REM) sleep were correlated with smaller volumes of the inferior parietal region—the part of the brain that helps integrate sensory information—more than a decade later.
The finding could help doctors identify at-risk patients earlier and intervene before the disease arises.
“Our population is aging, and more and more people are living with Alzheimer’s disease,” says Gawon Cho, postdoctoral associate in the laboratory of Brienne Miner, and the study’s first author.
“Our findings suggest that a person’s overnight sleep architecture could be used as a potential marker for identifying people who may have an increased risk of Alzheimer’s disease-related brain atrophy.”
Epidemiological research has shown that abnormal sleep quality and duration are associated with a greater risk of Alzheimer’s disease. Research has also linked sleep disturbances to increased accumulation of amyloid-beta and tau proteins—hallmark pathological features of the disease. Cho is interested in the underlying pathways that connect sleep deficiency to Alzheimer’s disease.
Sleep is organized into different stages. Sleep architecture refers to how a person progresses through the different stages of sleep throughout the night. In Cho’s latest study, she explored how a person’s sleep architecture was associated with volumes of vulnerable regions in their brains.
Non-REM sleep accounts for about 75% to 80% of a person’s total sleep. It can be divided into stage N1, N2, and N3, in which stage N1 is lightest and stage N3—also called slow-wave sleep—is deepest. REM sleep is the stage during which most dreaming occurs and is crucial for memory consolidation, emotional processing, and more.
For the study, Cho’s team analyzed data from the Atherosclerosis Risk in the Communities Study, an ongoing, decades-long study funded by the National Institutes of Health. The data included polysomnographies—which measure an individual’s sleep architecture overnight—of 270 participants with a median age of 61, as well as high-resolution brain imaging of the individuals collected 13 to 17 years after the sleep measures.
The finding that less slow-wave and REM sleep was associated with smaller volumes of the inferior parietal region more than a decade later is intriguing, says Cho, because visuospatial impairment—in which the brain struggles to interpret what we see—can be a sign of early Alzheimer’s disease.
“This brain region synthesizes various pieces of sensory information, including visuospatial information,” she explains. “And when you ask people who are in early Alzheimer’s disease to do a clock-drawing test, or to draw a cube, they often find that difficult.”
There is currently no cure for Alzheimer’s disease. The study suggests that a person’s overnight sleep architecture could help doctors screen for at-risk patients. It has also inspired Cho to begin investigating the glymphatic system, which helps clear waste from the brain and is most active during slow-wave sleep.
“I’m digging into the glymphatic system to see if there are any potential targets of intervention,” she says.
The research appears in the Journal of Clinical Sleep Medicine.
This research used data from the National Heart, Lung, and Blood Institute and received support from Yale University.
The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Source: Yale
