Obstructive Sleep Apnea May Lead to Early Cognitive Decline in Men

Distinct cognitive changes in male patients with obstructive sleep apnoea without co-morbidities

Valentina Gnoni1, Michel Mesquita2, David O'Regan1,3,4, Alessio Delogu5, Ivan Chakalov6,7, Andrea Antal7, Allan H. Young8,9, Romola S. Bucks10,11, Melinda L. Jackson12 and Ivana Rosenzweig1,3,4*

• 1Sleep and Brain Plasticity Centre, Department of Neuroimaging, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom
• 2L&M Data Science Ltd., London, United Kingdom
• 3Sleep Disorder Centre, Nuffield House, Guy's Hospital, London, United Kingdom
• 4Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom
• 5Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom
• 6Department of Anesthesiology, University Medical Center Göttingen, Göttingen, Germany
• 7Department of Neurology, University Medical Center Göttingen, Göttingen, Germany
• 8Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom
• 9South London and Maudsley National Health Service (NHS) Foundation Trust, Bethlem Royal Hospital, Beckenham, United Kingdom
• 10School of Psychological Science, University of Western Australia, Perth, WA, Australia
• 11The Raine Study, School of Population and Global Health, University of Western Australia, Perth, WA, Australia
• 12Turner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, Melbourne, VIC, Australia

Introduction: Obstructive sleep apnoea (OSA) is a multisystem, debilitating, chronic disorder of breathing during sleep, resulting in a relatively consistent pattern of cognitive deficits. More recently, it has been argued that those cognitive deficits, especially in middle-aged patients, may be driven by cardiovascular and metabolic comorbidities, rather than by distinct OSA-processes, such as are for example ensuing nocturnal intermittent hypoxaemia, oxidative stress, neuroinflammation, and sleep fragmentation.

Methods: Thus, we undertook to define cognitive performance in a group of 27 middle-aged male patients with untreated OSA, who had no concomitant comorbidities, compared with seven matched controls (AHI mean ± S.D.: 1.9 ± 1.4 events/h; mean age 34.0 ± 9.3 years; mean BMI 23.8 ± 2.3 kg/m2). Of the 27 patients, 16 had mild OSA (AHI mean ± S.D.:11.7 ± 4.0 events/h; mean age 42.6 ± 8.2 years; mean BMI 26.7 ± 4.1 kg/m2), and 11 severe OSA (AHI 41.8 ± 20.7 events/h; age: 46.9 ± 10.9 years, BMI: 28.0 ± 3.2 kg/m2).

Results: In our patient cohort, we demonstrate poorer executive-functioning, visuospatial memory, and deficits in vigilance sustained attention, psychomotor and impulse control. Remarkably, we also report, for the first time, effects on social cognition in this group of male, middle-aged OSA patients.

Conclusion: Our findings suggest that distinct, OSA-driven processes may be sufficient for cognitive changes to occur as early as in middle age, in otherwise healthy individuals.

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