Study objectives
We evaluated if self-reported sleepiness was associated with neuroimaging markers of brain aging and ischemic damage in a large community-based sample.
Methods
Participants from the Framingham Heart Study Offspring cohort (n=468, 62.5±8.7, 49.6%M) free of dementia, stroke, and neurological diseases, completed sleep questionnaires and polysomnography followed by MRI, three years later on average. We used linear and logistic regression models to evaluate the associations between Epworth Sleepiness Scale scores and total brain, cortical and subcortical gray matter, and white matter hyperintensities volumes, and the presence of covert brain infarcts.
Results
Higher sleepiness scores were associated with larger total brain, greater cortical gray matter volume, and a lower prevalence of covert brain infarcts, even when adjusting for a large array of potential confounders, including demographics, sleep profiles and disorders, organic health diseases, and proxies for daytime cognitive and physical activities. Interactions indicated that more sleepiness associated with larger cortical gray matter volume in men only and in APOE ε4 non-carriers, whereas a trend for smaller cortical gray matter volume was observed in carriers. In longitudinal analyses, those with stable excessive daytime sleepiness over time had greater cortical total brain and cortical gray matter volumes, whereas baseline sleepiness scores were not associated with subsequent atrophy or cognitive decline.
Conclusion
Our findings suggest that sleepiness is not necessarily a marker of poor brain health when not explained by diseases or sleep debt and disorders. Rather, sleepiness could be a marker of preserved sleep-regulatory processes and brain health in some cases.