0219 Sleep Disturbances, Cortisol, and Neuroimaging Correlates Among Memory Clinic Patients

Abstract Introduction Several sleep disturbance parameters as well as abnormal cortisol secretion levels are increasingly acknowledged as risk factors for Alzheimer’s disease (AD). Currently, the mechanisms between sleep disturbances and AD, and the interplay with abnormal cortisol levels, are still not understood. This study examines how self-reported sleep disturbances are associated with structural brain measures and diurnal cortisol dysregulation in a cohort of memory clinic patients. Methods The study was based on a cohort of 146 memory clinic patients diagnosed with either mild cognitive impairment or subjective cognitive impairment. The Karolinska Sleep Questionnaire (KSQ) was used to measure self-reported sleep. Neuroimaging (MRI or CT) was used to quantify structural brain measures using four visual rating scales (Scheltens, Pasquier, Koedam, and Fazekas scales). Salivary cortisol was sampled to measure diurnal cortisol patterns through five computed measures of awakening, bedtime, total, AM/PM cortisol ratio, and cortisol awakening response. Results Some associations were found between sleep, structural brain measures and cortisol. Increased apnea index (based on the KSQ) was associated with greater odds of posterior brain atrophy (OR=1.20, p=0.015) measured by the Koedam visual rating scale. Further, increased apnea index was associated with reduced awakening cortisol (β=-0.03; p=0.045, and an increased daytime sleepiness index (based on the KSQ) was associated with both reduced awakening cortisol (β=-0.03; p=0.025) and a reduced AM/PM cortisol ratio (β=-0.04; p=0.021). Conclusion In a memory clinic cohort, self-reported apnea disturbances are associated with a neuroimaging correlate of increased posterior atrophy and lower awakening cortisol, while daytime sleepiness index is associated with lower awakening cortisol and a reduced AM/PM cortisol ratio. These findings add insights into the early identification of modifiable AD risk factors an¬d their mechanisms. Support (if any)