Obstructive sleep apnea syndrome (OSAS) is a prevalent sleep-related breathing disorder characterized by recurrent episodes of upper airway obstruction during sleep, resulting in intermittent reductions or complete cessation of airflow. These interruptions reduce oxygen saturation and disrupt normal sleep architecture, frequently resulting in daytime fatigue and adverse health outcomes. Recent research has provided increasing evidence that OSAS may be associated with neuroinflammation, defined as inflammation within the brain and nervous system. Such neuroinflammation may contribute to the development of conditions including depression, anxiety, Alzheimer’s disease, and Parkinson’s disease. This narrative review examines the association between OSAS and neuroinflammation and outlines the potential biological mechanisms involved. Intermittent hypoxemia and recurrent sleep fragmentation are thought to promote oxidative stress, neuroinflammation, and neuronal injury, ultimately contributing to impaired memory, executive function, emotional regulation, and overall neurological function. Over time, these processes can impair memory, executive function, emotional regulation, and overall neurological function. The review also highlights key risk factors and clinical manifestations and emphasizes the importance of early diagnosis and intervention for OSAS. Evidence from both experimental animal studies and human clinical studies is discussed to highlight current understanding while distinguishing established findings from emerging hypotheses. In summary, this review indicates that neuroinflammation may represent an important mechanistic pathway linking OSAS with depression, anxiety, cognitive impairment, and neurodegenerative disorders. However, much of the available evidence remains associative, and further longitudinal and biomarker-driven studies are required to clarify causal relationships and determine the long-term impact of interventions such as continuous positive airway pressure (CPAP) therapy. Improved understanding of these mechanisms may facilitate earlier diagnosis, risk stratification, and the development of targeted therapeutic strategies for individuals with OSAS.
Mehdi et al. (Sun,) studied this question.