0284 Disrupted NREM Sleep Physiology Linked to 22q11.2 Deletion Syndrome

Abstract Introduction A 22q11.2 deletion (22qDel), is a recurrent copy number variant with profound impacts on neurodevelopment. Disruptions in non-rapid eye movement (NREM) sleep neurophysiology have been observed across idiopathic psychiatric disorders. However, it is unknown whether NREM disruptions exist in 22qDel carriers, who have elevated risk of developing psychiatric disorders. Here, we test the hypothesis that 22qDel carriers will exhibit disrupted NREM sleep neurophysiology across the power spectrum. Methods 22qDel carriers (n=12, Mage=20.42, 13-28 years, 58.3% males) and TD controls (n=11; Mage=19.18, 13-23 years, 27.3% males) completed multiple nights (89 nights total; 1-6 nights per subject; median=3 nights) of sleep EEG recordings with a wearable headband (Dreem 3). 30-second epochs were excluded for visual artifact or high 20-40Hz power. Relative power in the F7-O2 channel during NREM sleep was calculated using multitaper spectral estimation. Differences in relative power between 22qDel carriers and TD controls were tested across 0.5-20Hz using linear mixed-effects models controlling for age and sex. False Discovery Rate (FDR) was used to correct for multiple comparisons. Results There was increased NREM power in slow delta frequencies (0.76-0.85 Hz; q< 0.05) and theta/alpha frequencies (5.95-9.73 Hz; q< 0.05) in 22qDel carriers, relative to TD controls. There were increases in the alpha/sigma range (9.73-12.63 Hz) in 22qDel carriers, but these results did not survive FDR correction (q< 0.10). Conclusion These findings suggest that neural mechanisms of NREM sleep regulation, particularly homeostatic sleep regulation, may be dysregulated in 22qDel carriers. Next steps will involve examining group differences in specific features of NREM sleep physiology (e.g., slow waves). Support (if any) R01MH085953; UCLA Center for Autism Research Pilot Grant; Autism Speaks Predoctoral Fellowship #13530