Affiliations: [a] Department of Psychiatry, Healthy Brain Aging Sleep Center, NYU Grossman School of Medicine, New York, NY, USA
| [b] Department of Population Health, Institute of Excellence in Health Equity, Center for Healthful Behavior Change, NYU Grossman School of Medicine, New York, NY, USA
| [c] Department of Neurology, NYU Alzheimer’s Disease Research Center, Center for Cognitive Neurology, NYU Grossman School of Medicine, New York, NY, USA
| [d] Department of Neuroscience and Physiology, NYU Neuroscience Institute, NYU Grossman School of Medicine, New York, NY, USA
Correspondence:
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Correspondence to: Omonigho M. Bubu, MD, MPH, PhD, 145 East 32nd St., 8th Floor, New York, NY 10016, USA. Tel.: +1 646 501 3440; E-mail: omonigho.bubu@nyulangone.org.
Abstract: Impairments of the sleep architecture due to disrupted sleep in individuals with obstructive sleep apnea (OSA) may result in reduced slow wave sleep (SWS), intermittent hypoxemia, and excessive day time sleepiness— all factors that have been shown to impact Alzheimer’s disease (AD) risk. In this commentary, we comment on the work by Cavuoto and colleagues in which they examine the associations between nocturnal hypoxemia or sleep disruptions (during SWS) and amyloid-β burden in individuals with OSA. We review the findings in the context of other similar studies and highlight the strengths and weaknesses of these published studies. We note the importance of examining these relationships longitudinally with a large sample size, including considering sleep health disparities, vascular components, and multiple cognitive domain tests.
