O017 Investigating the role of amyloid burden on sleep microarchitecture and associations with cognitive functioning in individuals with OSA

Abstract Background Emerging evidence suggests obstructive sleep apnoea (OSA) is a risk factor for increased amyloid aggregation, a biomarker of Alzheimer’s disease, with disrupted sleep architecture hypothesised as a potential mechanism. Moreover, sleep architecture abnormalities observed in (OSA) may explain impaired cognition. However, the relationships between sleep microarchitecture, amyloid burden and cognition in OSA are unclear. Methods Thirty-four participants with OSA (age=57.7, 19 males), and 12 controls (age=57.1, 6 males) underwent diagnostic polysomnography (PSG), 11C-PiB positron emission tomography (PET) scan to quantify amyloid burden, and a cognitive assessment battery. All-night EEG recordings were processed and spectral power in slow oscillation (SO) and delta frequency ranges were calculated. Results Higher global amyloid burden was associated with lower delta power at O2 during slow wave sleep (SWS) in the OSA group (ß=-0.443, R2=0.142, p=0.048, controlled for age and non-REM AHI) and in the entire sample (ß=-.497, R2=.161, p=.019). Delta power and SO power in the OSA group was in turn associated with verbal memory (frontal regions - delta: ß=-0.811, p<0.001 and SO: ß=-0.661, p=0.008; central - delta: ß=0.537, p=0.026; occipital - delta: ß=0.586, p=0.014 and SO: ß=0.526, p =0.043). Discussion Greater amyloid burden was associated with slow wave deficits in older people with and without OSA. Worse memory performance was associated with lower slow frequency activity in central and occipital brain regions but higher activity in frontal regions. It is possible that pathological EEG slowing in some brain regions may explain the differential associations between sleep neurophysiological measures and memory.