ArticleThe clinical respiratory journal2026
Exploring the Role of Nocturnal Hypoxemia and Sleep Fragmentation in Memory Decline: Insights From Explainable Machine Learning Models.
Article in The clinical respiratory journal, 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
introductionSleep-disordered breathing (SDB) is linked to memory decline, but the exact relationship between sleep fragmentation, nocturnal hypoxemia, and cognitive impairment remains unclear.
objectivesThis study aimed to investigate the associations between micro-arousal burden, nocturnal oxygen desaturation, and memory decline in patients with moderate-to-severe OSA.
methodsData were retrieved from the clinical and overnight polysomnographic (PSG) records of adult patients evaluated for suspected SDB. The primary clinical endpoint was the presence and severity of memory decline, ascertained via a standardized Subjective Cognitive Decline (SCD) instrument. A multidimensional array of variables was systematically extracted, encompassing baseline demographic characteristics, cardiometabolic comorbidities, and high-resolution sleep architecture metrics, with a distinct emphasis on stage-specific micro-arousal burdens and the morphological profiles of nocturnal oxygen desaturation. Then, independent t tests and
resultsThe final analytical sample comprised 884 participants with complete primary outcome data (memory-normal: N = 408; memory-decline: N = 476). Initial comparative analyses revealed the memory-decline group was older (50.24 vs. 45.95 years, p < 0.001) with a significantly higher prevalence of cardiometabolic comorbidities, including hypertension (47.3% vs. 40.2%, p = 0.035) and diabetes (24.4% vs. 8.8%, p < 0.001). Polysomnographically, this group exhibited a distinct hypopnea-predominant phenotype: despite a comparable overall AHI (45.82 vs. 48.64 events/h, p = 0.099) and global arousal index (26.98 vs. 28.85 events/h, p = 0.172), they demonstrated a significantly higher hypopnea count (122.25 vs. 110.40, p = 0.047) and prolonged awake time with SpO
conclusionsMemory decline in SDB is more robustly associated with the morphological profile of oxygen exposure rather than absolute event frequencies. A hypopnea-dominant profile with mild, persistent low oxygen levels offers an associative framework for understanding cognitive decline. Future research and clinical interventions should prioritize hypoxic burden as a key factor in phenotype identification and memory decline treatment.
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