AUTHOR=Turner Arlener D. , Locklear Clarence E. , Oruru Daisha , Briggs Anthony Q. , Bubu Omonigho M. , Seixas Azizi 

TITLE=Exploring the combined effects of sleep apnea and APOE-e4 on biomarkers of Alzheimer’s disease

JOURNAL=Frontiers in Aging Neuroscience

VOLUME=14

YEAR=2023

URL=https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2022.1017521

DOI=10.3389/fnagi.2022.1017521

ISSN=1663-4365

ABSTRACT=<sec><title>Objective</title><p>We determined the interactive associations of apolipoprotein e4 (APOE-e4), and obstructive sleep apnea (OSA) on biomarkers of Alzheimer’s disease and examined for racial/ethnic differences of this association.</p></sec><sec><title>Methods</title><p>We used data from the National Alzheimer’s Coordinating Center Uniform Dataset (NACC UDS). All participants undergo annual observations, including demographic survey, battery of neuropsychological tests, blood draw (with genotyping), and a clinical evaluation with medical and cognitive/dementia status assessment, while a subset of participants have cerebrospinal fluid (CSF) biomarkers and neuroimaging data. Biomarkers of AD were characterized as the presence of abnormally low amyloid in CSF, <italic>via</italic> validated Aβ<sub>42</sub> cut off protocols, and total segmented hippocampal volume, and volume of white matter hyper intensities (WMH). While clinical markers (to preview cognitive relationships) were characterized <italic>via</italic> the Montreal Cognitive Assessment (MOCA).</p></sec><sec><title>Results</title><p>Biomarker and clinical marker data were derived from 1,387 participants at baseline (mean age = 69.73 ± 8.32; 58.6% female; 13.7% Black/African American), 18.4% of the sample had sleep apnea, and 37.9% were APOE-e4 carriers. Our results confirmed previous reports that OSA and APOE-e4 were independently associated with AD through abnormal levels of amyloid (<italic>F</italic><sub>(1,306)</sub> = 4.27; <italic>p</italic> = 0.040; <italic>F</italic><sub>(1,285)</sub> = 60.88; <italic>p</italic> &lt; 0.000, respectively), WMH volume (<italic>F</italic><sub>(1,306)</sub> = 4.27; <italic>p</italic> = 0.040; <italic>F</italic><sub>(1,285)</sub> = 60.88; <italic>p</italic> &lt; 0.000, respectively), and MOCA scores (<italic>F</italic><sub>(1,306)</sub> = 4.27; <italic>p</italic> = 0.040; <italic>F</italic><sub>(1,285)</sub> = 60.88; <italic>p</italic> &lt; 0.000, respectively). No significant interaction between OSA and APOE-e4 relative to amyloid emerged, however, race stratified analyses indicated the interaction of OSA and APOE-e4 and was significantly associated with WMH and hippocampal volume in Black/African American, but not white participants.</p></sec><sec><title>Conclusion</title><p>OSA and APOE-e4 are interactively associated with WHM in Black/African Americans. This interaction may partially explicate increased levels of risk in this population.</p></sec>