ArticleSleep & breathing = Schlaf & Atmung2026
Instability in sleep architecture and intermittent hypoxia underlie cognitive impairment in patients with obstructive sleep apnea.
Article in Sleep & breathing = Schlaf & Atmung, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeThe association of Obstructive Sleep Apnea (OSA) with cognitive deficits is increasingly recognized. In non-demented OSA patients, this research explored the associations among sleep architecture instability, intermittent hypoxia, and cognitive impairment, along with the potential mediating role of IL-6 and core Alzheimer's disease biomarkers.
methodsA total of 370 participants reporting snoring were enrolled and compledted both polysomnography and cognitive assessment. Ultimately, 299 met inclusion criteria. Sleep stage durations and transitions were extracted from hypnograms using a custom program. Blood samples were collected at ~ 7:00 AM for biochemical assays.Neuronal-derived exosomes (NDEs) were immunocaptured for the quantification of total tau (T-tau), amyloid-β (Aβ42), and phosphorylated tau (P-T181-tau) via ELISA. Mediation analysis was employed to evaluate whether inflammatory and Alzheimer's biomarkers mediate the link between sleep disruption and cognitive performance.
resultsA comparative analysis showed significant differences in OSA patients with mild cognitive impairment, including increased sleep fragmentation, ODI, IL-6 levels, and more N1-to-wake transitions compared to controls and OSA patients without MCI. Spearman correlations revealed negative associations between cognitive scores and both N1-to-wake duration and ODI, as well as IL-6. Linear regression showed N1-to-wake duration was positively correlated with IL-6, while ODI correlated with Aβ42 and IL-6. Mediation analyses indicated IL-6 and P-T181-tau served as a partial mediator in impact of intermittent hypoxia on cognition.
conclusionsSleep instability, along with elevated levels of IL-6, serves as a strong predictor for cognitive impairment observed in OSA. Furthermore, IL-6 and phosphorylated T181-tau in NDEs play a mediating role in the cognitive dysfunction that arises due to intermittent hypoxia.
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