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A study of 116 adults found that the shape of deep-sleep brain waves changed across groups ranging from cognitively unimpaired people without amyloid abnormalities to people with early Alzheimer’s disease. Some slow-wave power differences were also observed in cognitively unimpaired participants with abnormal amyloid biomarkers, but the study does not show that sleep changes can diagnose Alzheimer’s or predict an individual’s symptoms.
A study of 116 adults found that the shape of brain waves during deep, non-REM sleep differed across groups defined by Alzheimer’s biomarkers and symptoms, with changes also observed among some people who had no cognitive symptoms. Published in Alzheimer’s Research & Therapy, the findings suggest that slow-wave sleep measurements warrant further study as possible indicators of early Alzheimer’s-related changes, but do not establish a diagnostic test.
Researchers compared one night of laboratory sleep monitoring in three groups: 30 cognitively unimpaired adults without abnormal amyloid biomarkers, 45 cognitively unimpaired adults with abnormal amyloid biomarkers, and 41 people with biomarker-confirmed mild cognitive impairment or mild dementia due to Alzheimer’s. The average ages ranged from 63.7 to 68.8 years, and about 57% of participants were women. The study was conducted at Hospital Clinic of Barcelona using overnight polysomnography.
The clearest pattern across the groups was a gradual change in individual slow waves. Their average slope fell from about 370 microvolts per second in the amyloid-negative group to 342 in the amyloid-positive, cognitively unimpaired group and 300 in the early Alzheimer’s group. The report describes the waves as becoming flatter and lower in amplitude across the groups. These are group-level findings; they do not show how accurately an individual’s sleep pattern could identify disease.
Researchers also found lower slow-wave power in the amyloid-positive group in two frequency bands, by about 13% to 15% compared with the amyloid-negative group. In early Alzheimer’s, slow-wave power was about 15% to 21% lower, depending on the frequency band. However, when the researchers limited an analysis to participants who had slept at least six hours, the power difference between the two cognitively unimpaired groups was no longer statistically significant. Early Alzheimer’s participants continued to show lower delta and overall slow-wave activity than the amyloid-negative group.
Broader measures of sleep disruption were most apparent in participants with early Alzheimer’s. They spent about 108 minutes awake after falling asleep, compared with roughly 61 to 64 minutes in the cognitively unimpaired groups, and had lower sleep efficiency and longer delays before REM sleep. The two cognitively unimpaired groups did not significantly differ on these broader measures. Cognitive performance among cognitively healthy participants was tracked over two to four visits spanning about six and a half years.
Deep Sleep as an Early Research Signal
The findings indicate that some measures of sleep differed across groups defined by Alzheimer’s biomarkers and symptoms. Standard measures, such as time awake during the night, differed more clearly in the symptomatic group. Slow-wave shape also varied across the three groups, including among cognitively unimpaired participants with abnormal amyloid biomarkers.
The study examined preclinical Alzheimer’s, the period when biomarkers may be abnormal but a person has no recognized cognitive symptoms. Further studies could assess whether sleep-wave measures are useful for investigating disease progression or selecting participants for additional testing. This study does not establish that sleep recordings can replace established biomarker assessments, predict an individual’s future, or guide treatment.
The authors also examined sex differences as part of the study’s aims. The supplied report does not provide the specific results of those analyses, so it is not possible to determine from this account whether sleep patterns differed between women and men.
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How the Sleep Groups Were Compared
Slow-wave sleep is the deepest stage of non-REM sleep. It has been linked to memory consolidation, and earlier research has associated disruptions in this sleep stage with changes related to Alzheimer’s. The study measured both sleep macroarchitecture—including sleep efficiency and time awake after sleep onset—and microarchitecture, including slow-wave strength and the slope, height, and duration of individual waves.
The groups were classified using cognitive assessments and amyloid biomarkers, rather than sleep patterns alone. The cognitively unimpaired amyloid-positive group represented preclinical Alzheimer’s in the study design; it should not be taken to mean that every person with abnormal amyloid will develop symptoms. Participants with severe sleep apnea were excluded. Nine participants in the early Alzheimer’s group used sleep medication, while cognitively unimpaired participants did not.
The proportion of APOE-ε4 carriers also differed between groups: it was 82.2% among cognitively unimpaired amyloid-positive participants, 40.0% in the amyloid-negative group, and 48.8% in early Alzheimer’s. The report notes that this pattern may reflect a cohort enriched for Alzheimer’s risk factors, which limits how broadly the sample may represent the general population.
“Slow-wave shape changes occur over the Alzheimer’s disease continuum and may represent non-invasive biomarkers for preclinical Alzheimer’s disease.”
— The study authors
Limits of the Sleep Findings
The study measured sleep on one laboratory night in a relatively small group. It identifies differences between groups but does not show whether slow-wave changes appear before amyloid abnormalities, predict later symptoms, or result from other factors. The findings therefore cannot establish that a person with flatter or weaker slow waves has Alzheimer’s disease.
Some results also depended on the analysis. In particular, the difference in slow-wave power between cognitively unimpaired participants with and without abnormal amyloid biomarkers was not statistically significant when the analysis was restricted to people who had slept at least six hours. The report does not supply full numerical results for every slow-wave feature, the sex-specific findings, or the cognitive-trajectory analysis, leaving those details unclear.
It is also not clear from the reported findings how well these sleep measures would perform in larger, more representative populations, or whether they add useful information beyond existing Alzheimer’s biomarkers. No diagnostic accuracy, threshold for identifying risk, or individual-level forecast is established.
Validation in Larger Sleep Studies
The immediate next step is replication in larger groups and across repeated nights, so researchers can determine whether the observed wave-shape differences are consistent and not specific to one night or this selected cohort. Studies that follow cognitively unimpaired participants over time could test whether sleep measurements are associated with later changes in cognition, while accounting for age, medication, sleep duration, and other health factors.
Further reporting and research will also be needed to clarify the study’s sex-specific results and the relationship between slow-wave measures, amyloid and tau biomarkers, and cognitive trajectories. Until those questions are addressed, the findings are best treated as an early research signal, not a screening recommendation or a basis for personal medical decisions.
Key Questions
What did the study find about deep sleep and Alzheimer’s?
It found that slow-wave shape became flatter across groups from cognitively unimpaired adults without abnormal amyloid biomarkers to participants with early Alzheimer’s. Some slow-wave power differences were also seen in cognitively unimpaired adults with abnormal amyloid biomarkers.
Does this mean a sleep test can diagnose Alzheimer’s?
No. The study reports group differences from overnight sleep monitoring; it does not validate a test for diagnosing Alzheimer’s or provide a reliable individual risk prediction.
Did the study show that sleep changes cause Alzheimer’s?
No. The results show associations across study groups and cannot establish whether sleep changes contribute to Alzheimer’s-related processes, result from them, or reflect other influences.
How many people took part?
The study included 116 adults: 30 cognitively unimpaired participants without abnormal amyloid biomarkers, 45 cognitively unimpaired participants with abnormal amyloid biomarkers, and 41 people with biomarker-confirmed early Alzheimer’s.
Source: news-medical.net
