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首页> 外文期刊>The American journal of geriatric psychiatry: official journal of the American Association for Geriatric Psychiatry >Obstructive Sleep Apnea is Linked to Depression and Cognitive Impairment: Evidence and Potential Mechanisms
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Obstructive Sleep Apnea is Linked to Depression and Cognitive Impairment: Evidence and Potential Mechanisms

机译：阻塞性睡眠呼吸暂停与抑郁和认知障碍有关：证据和潜在机制

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Obstructive sleep apnea (OSA) is highly prevalent but very frequently undiagnosed. OSA is an independent risk factor for depression and cognitive impairment/dementia. Herein the authors review studies in the literature pertinent to the effects of OSA on the cerebral microvascular and neurovascular systems and present a model to describe the key pathophysiologic mechanisms that may underlie the associations, including hypoperfusion, endothelial dysfunction, and neuroinflammation. Intermittent hypoxia plays a critical role in initiating and amplifying these pathologic processes. Hypoperfusion and impaired cerebral vasomotor reactivity lead to the development or progression of cerebral small vessel disease (C-SVD). Hypoxemia exacerbates these processes, resulting in white matter lesions, white matter integrity abnormalities, and gray matter loss. Blood-brain barrier (BBB) hyperpermeability and neuroinflammation lead to altered synaptic plasticity, neuronal damage, and worsening C-SVD. Thus, OSA may initiate or amplify the pathologic processes of C-SVD and BBB dysfunction, resulting in the development or exacerbation of depressive symptoms and cognitive deficits. Given the evidence that adequate treatment of OSA with continuous positive airway pressure improves depression and neurocognitive functions, it is important to identify OSA when assessing patients with depression or cognitive impairment. Whether treatment of OSA changes the deteriorating trajectory of elderly patients with already-diagnosed vascular depression and cognitive impairment/dementia remains to be determined in randomized controlled trials.
机译：阻塞性睡眠呼吸暂停（OSA）高度流行，但经常无法诊断。 OSA是抑郁症和认知障碍/痴呆症的独立危险因素。本文作者回顾了与OSA对脑微血管和神经血管系统的影响有关的文献研究，并提出了一个模型来描述可能是这种关联基础的关键病理生理机制，包括灌注不足，内皮功能障碍和神经炎症。间歇性缺氧在启动和放大这些病理过程中起关键作用。灌注不足和脑血管舒缩反应性受损会导致脑小血管疾病（C-SVD）的发生或发展。低氧血症加剧了这些过程，导致白质损害，白质完整性异常和灰质流失。血脑屏障（BBB）的高通透性和神经炎症导致突触可塑性改变，神经元损伤和C-SVD恶化。因此，OSA可能会引发或放大C-SVD和BBB功能障碍的病理过程，从而导致抑郁症状和认知缺陷的发展或加剧。鉴于有证据表明，持续持续的气道正压对OSA进行充分的治疗可以改善抑郁症和神经认知功能，因此在评估患有抑郁症或认知障碍的患者时，确定OSA非常重要。 OSA的治疗是否会改变已被诊断为血管性抑郁症和认知障碍/痴呆症的老年患者的恶化轨迹，尚需进行随机对照试验来确定。

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