Purpose of Review <p>Alzheimer’s disease (AD) is multifactorial, and it is believed that several factors, including genetic, metabolic, bioenergetics, and environmental factors, have a role in the onset and development of this disease. Obstructive sleep apnea (OSA) has a high prevalence in patients with AD and is considered a risk factor for the development of AD. Besides, several features, including shared comorbidities, the induction of cognitive impairment and neurodegeneration make both pathologies highly interconnected. We reviewed the existing knowledge about the possible OSA-induced brain alterations that can potentially participate in the development and progression of AD.</p> Recent Findings <p>Intermittent hypoxia and sleep fragmentation have been considered as the most important OSA-induced alterations that can trigger dysregulation of multiple pathways at the cerebral tissue. Although both events can act synergistically, here we discussed the possible role of each event in development and progression of AD individually. Intermittent hypoxia has been linked to increased oxidative stress, systemic and neuroinflammation, and consequently cerebrovascular dysfunctionality. On the other hand, sleep fragmentation and deprivation can challenge memory consolidation and the brain clearance.</p> Summary <p>OSA-induced pathophysiological alterations in AD patients can lead to synaptic damage, neurodegeneration and increased AD-related brain pathology that will manifest by progressive cognitive impairment in this disease.</p>

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The Physiological Association between Obstructive Sleep Apnea and Alzheimer’s Disease

  • Farida Dakterzada,
  • Nathalia Montero-Castilla,
  • Anna Carnes-Vendrell,
  • Gerard Piñol Ripoll

摘要

Purpose of Review

Alzheimer’s disease (AD) is multifactorial, and it is believed that several factors, including genetic, metabolic, bioenergetics, and environmental factors, have a role in the onset and development of this disease. Obstructive sleep apnea (OSA) has a high prevalence in patients with AD and is considered a risk factor for the development of AD. Besides, several features, including shared comorbidities, the induction of cognitive impairment and neurodegeneration make both pathologies highly interconnected. We reviewed the existing knowledge about the possible OSA-induced brain alterations that can potentially participate in the development and progression of AD.

Recent Findings

Intermittent hypoxia and sleep fragmentation have been considered as the most important OSA-induced alterations that can trigger dysregulation of multiple pathways at the cerebral tissue. Although both events can act synergistically, here we discussed the possible role of each event in development and progression of AD individually. Intermittent hypoxia has been linked to increased oxidative stress, systemic and neuroinflammation, and consequently cerebrovascular dysfunctionality. On the other hand, sleep fragmentation and deprivation can challenge memory consolidation and the brain clearance.

Summary

OSA-induced pathophysiological alterations in AD patients can lead to synaptic damage, neurodegeneration and increased AD-related brain pathology that will manifest by progressive cognitive impairment in this disease.