Affiliations: [a]
Department of Neurology, Alzheimer’s Disease Center, NYU Langone Medical Center, New York, NY, USA
| [b]
Department of Psychiatry, Center for Brain Health, NYU Langone Medical Center, New York, NY, USA
| [c]
Department of Epidemiology and Biostatistics, College of Public Health, University of South Florida, Tampa, FL, USA
| [d] Division of Pulmonary, Critical Care and Sleep Medicine at the Icahn School of Medicine at Mount Sinai, New York, NY, USA
| [e]
Nathan S. Kline Institute for Psychiatric Research, Orangeburg, New York, NY, USA
Correspondence:
[*]
Correspondence to: Andreia Andrade and Ricardo Osorio, NYU Langone Medical Center, 145 East 32nd Street, New
York NY 10016, USA. Tel.: +1 212 263 3255; E-mails: Andreia.GodinhoDeAndrade@nyumc.org and Ricardo.Osorio@nyumc.org.
Abstract: Obstructive sleep apnea (OSA) and Alzheimer’s disease (AD) are highly prevalent conditions with growing impact on our aging society. While the causes of OSA are now better characterized, the mechanisms underlying AD are still largely unknown, challenging the development of effective treatments. Cognitive impairment, especially affecting attention and executive functions, is a recognized clinical consequence of OSA. A deeper contribution of OSA to AD pathogenesis is now gaining support from several lines of research. OSA is intrinsically associated with disruptions of sleep architecture, intermittent hypoxia and oxidative stress, intrathoracic and hemodynamic changes as well as cardiovascular comorbidities. All of these could increase the risk for AD, rendering OSA as a potential modifiable target for AD prevention. Evidence supporting the relevance of each of these mechanisms for AD risk, as well as a possible effect of AD in OSA expression, will be explored in this review.
Keywords: AD risk, Alzheimer’s disease, amyloid, obstructive sleep apnea, OSA phenotypes
