Abstract TP076: Sleep Alterations and Cognitive Function in Cerebral Amyloid Angiopathy

Introduction: Irregular sleep and reduced slow-wave sleep (SWS) have been linked to cognitive decline in aging and Alzheimer’s disease, partly through impaired glymphatic clearance of neurotoxic proteins. Cerebral amyloid angiopathy (CAA), characterized by vascular amyloid deposition, may share this mechanism, yet the impact of sleep alterations on cognition in CAA remains unclear. We investigated whether sleep duration, instability in nightly sleep duration and reductions in SWS are associated with cognitive performance in CAA. Methods: Twenty-four participants with probable CAA were enrolled in a prospective study that included detailed cognitive and sleep assessments as well as advanced neuroimaging. Sleep-duration variability (SDV) was calculated as the standard deviation divided by the mean sleep duration of all nights (%). From PSG, SWS was expressed as a percentage of total sleep time. Separate multivariable linear regression models tested associations of SDV and SWS with z scores of memory, processing speed, and executive function, adjusting for age, sex, education, intracerebral hemorrhage, white matter hyperintensity volume, and total brain volume. Results: CAA patients without cognitive impairment (mean age 71.7±6.7 years; 52.2% male) completed 7-day electronic sleep diaries and a neuropsychological battery. A subset (n=12) underwent in-laboratory polysomnography (PSG). Greater SDV was associated with lower memory scores in unadjusted (p=0.034) and adjusted models (β =−0.67, 95% CI −3.8 to −0.4, p=0.017). Mean sleep duration was not associated with memory scores in univariate or multivariate models (p>0.2). In the PSG subset, lower SWS was associated with lower memory scores in unadjusted (p=0.014) and adjusted models (β = 1.1, 95% CI 0.02–0.15, p=0.019). Lower SWS also correlated with greater SDV (p=0.049), but not with sleep duration (p=0.612). Neither SDV nor SWS was related to executive function or processing speed (p>0.2). Conclusion: In CAA, instability in nightly sleep duration and reductions in deep, restorative sleep might be associated with poorer memory performance. These findings identify sleep–wake stability and SWS as potentially modifiable targets for preserving cognition in CAA and may reflect glymphatic clearance dysfunction contributing to vascular amyloid accumulation.