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<p>Obstructive sleep apnea (OSA), a disorder characterized by recurrent episodes of apnea or hypopnea due to upper airway collapse, has been linked to various respiratory, cardiovascular, and metabolic sequelae. It has been associated with sleep fragmentation, nocturnal hypoxia, and sympathetic surges, thereby contributing to cognitive and neurological decline. Literature remains divided on whether OSA acts as a direct risk factor for neurodegenerative diseases or as a bidirectional exacerbator intensifying pre-existing cognitive impairments. Accumulating evidence suggests that OSA may act as a multifactorial risk modifier of neurodegenerative processes, potentially contributing through cycles of intermittent hypoxia and consequent oxidative stress, in addition to neuroinflammatory mechanisms and glymphatic dysfunction. In conjunction with autonomic dysregulation, blood-brain barrier disruption, sleep fragmentation, and dysfunction of synaptic homeostasis, these processes represent proposed mechanisms underlying cognitive decline in patients with OSA. For management, continuous positive airway pressure (CPAP) has been accepted as the gold-standard therapy, with hypoglossal nerve stimulation (HNS) serving as an alternative for selected CPAP-intolerant patients, and mandibular advancement devices (MADs) and pharmacological approaches representing additional emerging options. This manuscript presents a narrative review of the current evidence. While causal relationships have not been definitively established, OSA may function as a significant risk modifier for neurodegenerative diseases, underscoring the value of timely screening and management in patients with or at risk of neurodegenerative disorders. Further longitudinal and interventional studies are needed to clarify causality and determine whether early treatment of OSA can influence cognitive decline or disease progression.</p>

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Obstructive Sleep Apnea as a Potentially Modifiable Risk Factor in Neurodegeneration: Mechanisms, Evidence, and Clinical Implications

  • 期刊论文

  • 发表日期：

    2026年7月23日

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  • Kasana Smith,
  • Naomi Châtelain,
  • Vansh Patel,
  • Himanshi Banker,
  • Gunn Goel,
  • Arihant Senthil,
  • Rohit Jain

摘要

Obstructive sleep apnea (OSA), a disorder characterized by recurrent episodes of apnea or hypopnea due to upper airway collapse, has been linked to various respiratory, cardiovascular, and metabolic sequelae. It has been associated with sleep fragmentation, nocturnal hypoxia, and sympathetic surges, thereby contributing to cognitive and neurological decline. Literature remains divided on whether OSA acts as a direct risk factor for neurodegenerative diseases or as a bidirectional exacerbator intensifying pre-existing cognitive impairments. Accumulating evidence suggests that OSA may act as a multifactorial risk modifier of neurodegenerative processes, potentially contributing through cycles of intermittent hypoxia and consequent oxidative stress, in addition to neuroinflammatory mechanisms and glymphatic dysfunction. In conjunction with autonomic dysregulation, blood-brain barrier disruption, sleep fragmentation, and dysfunction of synaptic homeostasis, these processes represent proposed mechanisms underlying cognitive decline in patients with OSA. For management, continuous positive airway pressure (CPAP) has been accepted as the gold-standard therapy, with hypoglossal nerve stimulation (HNS) serving as an alternative for selected CPAP-intolerant patients, and mandibular advancement devices (MADs) and pharmacological approaches representing additional emerging options. This manuscript presents a narrative review of the current evidence. While causal relationships have not been definitively established, OSA may function as a significant risk modifier for neurodegenerative diseases, underscoring the value of timely screening and management in patients with or at risk of neurodegenerative disorders. Further longitudinal and interventional studies are needed to clarify causality and determine whether early treatment of OSA can influence cognitive decline or disease progression.