Altered brain glucose metabolism and connectivity in young adults with obstructive sleep apnea

Abstract INTRODUCTION Obstructive sleep apnea syndrome (OSAS) is a recognized risk factor for neurodegenerative disorders. However, a causal link between OSAS and brain damage has yet to be established. METHODS Thirty cognitively normal patients with moderate‐to‐severe OSAS, free from systemic or neurological comorbidities, were enrolled and underwent 18 F‐fluorodeoxyglucose positron emission tomography imaging. Their scans were compared to those of cognitively normal, OSAS‐free controls from the Alzheimer's Disease Neuroimaging Initiative database. Additional analyses included commonality mapping, correlations with polysomnographic parameters, and seed‐based metabolic connectivity of major resting‐state networks. RESULTS Group‐level analyses showed fronto‐parietal glucose hypometabolism and cerebellar glucose hypermetabolism in patients with OSAS compared to controls. Cerebellar glucose hypermetabolism was associated with reduced rapid eye movement sleep latency and duration. Seed‐based connectivity analysis revealed alterations in attentional and limbic networks. DISCUSSION Moderate‐to‐severe OSAS may represent a cause of brain dysfunction, highlighting the importance of its early diagnosis and appropriate treatment to prevent worsening brain damage and possible future neurodegenerative processes. Highlights Moderate‐to‐severe obstructive sleep apnea syndrome (OSAS) is associated with altered brain glucose metabolism. Cerebellar glucose hypermetabolism is associated with rapid eye movement sleep impairment. Attentional and limbic networks connectivity is disrupted in moderate‐to‐severe OSAS. Early recognition of patients with moderate‐to‐severe OSAS has the potential to overcome the risk of worsening brain damage that may lead to neurodegeneration.