People who spend less time in deep sleep or rapid eye movement (REM) sleep may be at greater risk for brain changes linked to Alzheimer’s disease. A new study published in the Journal of Clinical Sleep Medicine found that lower proportions of slow wave and REM sleep were associated with smaller volumes in certain brain regions that tend to show early signs of atrophy in Alzheimer’s. These findings suggest that sleep quality may play an important role in brain aging and could be a modifiable risk factor for dementia.
Alzheimer’s disease is a progressive neurodegenerative condition that slowly erodes memory and thinking skills. It affects more than 6 million older adults in the United States. One of the main features of the disease is brain atrophy, or the gradual loss of brain volume, particularly in areas like the hippocampus and parietal lobe. These structural changes typically begin years before symptoms appear. Researchers have long been interested in understanding what contributes to this atrophy and whether any lifestyle factors might influence it.
Sleep has emerged as one of the potential contributors. Poor sleep is common among older adults, and evidence has shown that disruptions in sleep can increase the risk of cognitive decline and dementia. Most earlier studies have relied on self-reported sleep habits, which can be inaccurate. Others have focused more on general sleep duration rather than the specific stages of sleep. The current study aimed to fill this gap by using objective, clinical-grade sleep measurements and by focusing on specific sleep stages—slow wave sleep and REM sleep—which are thought to be particularly important for brain health.
“On a personal level, three of my grandparents had dementia, which led me to study the broader topic of Alzheimer’s disease. I investigated this specific topic because there is not a lot of evidence on sleep architecture and region-specific atrophy,” said lead author Gawon Cho, a postdoctoral associate at Yale School of Medicine.
The research team analyzed data from a long-running study called the Atherosclerosis Risk in Communities (ARIC) Study, which has been following the health of U.S. adults for several decades. Between 1996 and 1998, a subset of participants underwent overnight sleep monitoring in their homes using a technique called polysomnography. This method records brain waves, heart rate, breathing, and muscle activity to determine what stage of sleep a person is in throughout the night. Over a decade later, between 2011 and 2013, some of the participants underwent brain imaging as part of a follow-up study.
For this study, researchers focused on 270 individuals who had both sleep and brain imaging data available and who had no signs of stroke or dementia at the time of the sleep assessment. The team used high-resolution magnetic resonance imaging (MRI) scans to measure the volume of specific brain regions known to be vulnerable to Alzheimer’s disease. These included the inferior parietal lobe, cuneus, precuneus, hippocampus, and entorhinal cortex. They also looked for small areas of brain bleeding called cerebral microbleeds, which are linked to vascular damage and may signal an increased risk of cognitive impairment.
The researchers then looked at whether the amount of time people spent in each sleep stage was related to the size of these brain regions years later. They accounted for many other factors that could influence brain health, such as age, sex, education, medical conditions, alcohol use, smoking history, and genetic risk for Alzheimer’s.
The results showed a clear pattern: people who spent less time in slow wave sleep and REM sleep tended to have smaller volumes in certain brain areas. Specifically, lower amounts of slow wave sleep were linked to reduced size in the inferior parietal and cuneus regions. Less REM sleep was associated with smaller volumes in the inferior parietal and precuneus areas. These findings remained statistically significant even after adjusting for other health and lifestyle factors.
Among the regions analyzed, the inferior parietal lobe showed the strongest association with both reduced slow wave and REM sleep. This part of the brain plays a role in memory, spatial reasoning, and attention—and it tends to shrink early in the course of Alzheimer’s disease. The researchers did not find any significant links between sleep quality and the presence of cerebral microbleeds, suggesting that the effects of poor sleep on brain structure may be independent of small vessel disease.
“The results were in the direction I expected,” Cho told PsyPost. “It was interesting that I found an association in the inferior parietal region, which plays a role in the synthesis of sensory information, given that visuospatial deficits can be observed in early Alzheimer’s disease.”
One of the interesting aspects of this study is that it also examined whether the association between sleep and brain atrophy differed depending on whether someone carried the APOE4 gene, a well-known genetic risk factor for Alzheimer’s. Although prior studies in animals and humans have found that APOE4 carriers may be more sensitive to the effects of poor sleep, this study did not find significant differences based on APOE genotype. However, the authors noted that their sample consisted entirely of white participants, which may have influenced the results. Other research has shown that racial and ethnic background can affect how sleep and genetic risk factors interact.
The study also considered the possibility that smaller brain volumes might cause changes in sleep architecture, rather than the other way around. While this kind of reverse relationship is possible, the researchers argued that it is more likely that sleep patterns influence brain structure in this case. They point to other studies showing that sleep deprivation can reduce activity in the parietal lobe and that persistent poor sleep may contribute to longer-term structural decline in this area.
These findings support the idea that deep, restorative sleep may help protect the brain against aging and disease. Slow wave sleep and REM sleep are thought to play key roles in memory consolidation and brain repair. Both stages also help clear waste products from the brain, including amyloid-beta, a protein that builds up in Alzheimer’s disease. If sleep disruptions reduce the brain’s ability to carry out these cleaning and maintenance processes, that could contribute to the gradual shrinkage seen in key brain regions.
While the study has many strengths—including the use of objective sleep measurements, long follow-up period, and detailed brain imaging—it also has several limitations. The participants were all white and generally healthier than the broader population, which may limit how generalizable the findings are. The number of participants with microbleeds was relatively small, reducing the ability to detect subtle associations.
Importantly, because the study is observational, it cannot prove that poor sleep causes brain atrophy—only that there is a connection. “The study does not demonstrate causality,” Cho said.
Future studies will be needed to confirm these findings in larger and more diverse populations, and to test whether improving sleep can actually slow or prevent the brain changes associated with dementia. Cho said she is also “looking to examine mechanisms underlying the observed association, focusing on brain waste clearance.”
The study, “Lower slow wave sleep and rapid eye movement sleep are associated with brain atrophy of AD-vulnerable regions,” was authored by Gawon Cho, Adam P. Mecca, Orfeu M. Buxton, Xiao Liu, and Brienne Miner.
