Abstract

Study Objectives We firstly studied cognitive performances, polysomnographic sleep, and CSF β-amyloid, tau proteins and lactate levels in patients affected by subjective cognitive impairment (SCI) divided in three groups: obstructive sleep apnea (OSA) patients (showing an Apnea-Hypopnea Index – AHI ≥15/h), subjects not affected by OSA (nonOSA, AHI Methods We compared results among 25 OSA, 10 OSA-CPAP and 15 nonOSA patients, who underwent a protocol counting neuropsychological testing in the morning, 48-hour polysomnography followed by CSF analysis. Results OSA patients showed lower CSF Aβ 42 andhigher CSF lactate levels, together with higher t-tau/Aβ 42 ratio, when compared to nonOSA and OSA-CPAP patients. OSA patients also showed reduced sleep quality and continuity, and lower performances at memory, intelligence and executive tests than nonOSA and OSA-CPAP patients. We found significant relationships among higher CSF tau proteins levels, sleep impairment and increased CSF lactate levels. Moreover, lower CSF Aβ 42 levels correlate with memory impairment and nocturnal oxygen saturation parameters. Conclusions We hypothesize that OSA reducing sleep quality and producing intermittent hypoxia lowers CSF Aβ 42 levels, increases CSF lactate levels, and alters cognitive performances in SCI patients, thus inducing early AD clinico-neuropathological changes. Notably, nonOSA as well as OSA-CPAP SCI patients did not show clinical and biochemical AD markers. Therefore, OSA may induce early but possibly CPAP-modifiable AD biomarkers changes.

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