Clinical Research Studies

African-Americans (blacks) have two times the risk of developing Alzheimer’s disease (AD) compared to non-Hispanic whites.1-6 Neuropathological studies show blacks with more mixed pathology1-6. Recent evidence demonstrate differences in AD biomarkers with blacks having decreased cortical thickness, and lower cerebrospinal fluid (CSF) P-tau, and T-tau.7-10. Notably, area-based socio-economic status (SES) partly explain racial differences in cortical thickness.11 This suggests the possible existence of additional physiologic differences on AD-risk by race, mediated by SES and resulting to greater neuronal loss, similar or less CSF-tau for similar levels of amyloid. Recent studies suggest that obstructive sleep apnea (OSA) increases AD-risk,12-14 is associated with higher brain amyloid and tau in cognitive normal (CN) participants.15-22. Notably, blacks have a higher burden of symptomatic OSA, particularly with excessive daytime sleepiness (EDS),23 which is associated with longitudinal amyloid-PET uptake.24. Potential intermediate mechanisms linking OSA and AD, such as decreased non rapid eye movement (NREM) slow wave activity (SWA) and increased inflammation affect amyloid and tau pathology,25,26 are associated with changes in cognition in late-life,27 and are more burdensome in blacks.28 OSA effects changes in circulating levels of CRP, TNFa, IL-6, and IL-17A.29,30 . More importantly, inflammation arising from cumulative stress exposure placed blacks at a greater risk for developing vascular risk factors,31-33 that increase AD-risk. In addition, SES and psychosocial factors11,34-36 may contribute to increase OSA and AD-risk in blacks. This highlights the need to utilize OSA as a unique disease model to explore racial differences in AD biomarkers.