Self‐reported OSA risk, but not daytime sleepiness, is related to memory decline in autosomal dominant Alzheimer’s disease: Preliminary findings from the COLBOS biomarker study

Abstract

AbstractBackgroundSleep disturbances may increase the risk of developing Alzheimer’s Disease (AD). Research suggests that excessive daytime sleepiness and obstructive sleep apnea (OSA) may be linked to increased AD pathology and cognitive dysfunction. This study aimed to investigate the relation between subjective sleepiness and OSA risk, memory, and amyloid and tau, as measured by PET in preclinical AD.MethodOur ongoing sleep study includes members of a Colombian kindred with a Presenilin1 (PSEN1) E280A mutation for autosomal dominant AD. PSEN1 mutation carriers develop dementia in their late forties. 19 carriers (mean age 38+‐6,12 females) and 15 non‐carrier family members (mean age 36+‐5,10 females) completed the Epworth Sleepiness Scale and the STOP‐BANG for OSA risk, and underwent cognitive testing and PET examinations. A subset (n=15, 8 carriers, 7 non‐carriers) also completed these tests after 18mo. Mann‐Whitney tests were used to test between‐group differences in sleepiness and OSA risk. Spearman correlations were used to examine associations among outcome measures and cortical amyloid, entorhinal tau, and verbal memory (delayed word list recall). Change scores between baseline and follow‐up were calculated (timepoint2‐timepoint1) to assess longitudinal relations.ResultCross‐sectional results showed no differences between carriers and non‐carriers in daytime sleepiness or OSA risk (p’s<0.34). Sleep metrics were not related to cortical amyloid, entorhinal tau, or verbal memory (r’s>0.14, p’s<0.62). Longitudinal results revealed an increase in OSA risk score from baseline to 1.5‐year follow‐up was correlated to lower verbal memory performance for all subjects who had two time points (r=‐0.73,p=0.002). A change in sleepiness score was not associated with any of the variables of interest (r’s>0.44,p’s<0.10).ConclusionPreliminary baseline results showed that carriers and non‐carriers from a kindred with autosomal dominant AD did not differ in sleep‐related risk factors, such as self‐reported daytime sleepiness and OSA risk. These results suggest that baseline daytime sleepiness and OSA risk may not be related to pathology burden in early AD. In contrast, preliminary longitudinal results suggest that an increase in self‐reported OSA risk within a 1.5‐year timeframe may be related to memory decline. Future research with a larger sample is required to further assess sleep metrics in this population.