短暂的睡眠呼吸暂停会导致β-淀粉样蛋白生成和tau过度磷酸化的长期增加。

IF 2.4 4区医学 Q3 NEUROSCIENCES

Neuroscience Research Pub Date : 2024-08-01 DOI:10.1016/j.neures.2024.03.003

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引用次数: 0

摘要

睡眠呼吸暂停被认为是阿尔茨海默病（AD）发病机制中的一个重要风险因素。在实验动物昼夜节律周期的睡眠期给予慢性间歇性缺氧治疗（IHT）是一种行之有效的睡眠呼吸暂停模型。在此，我们报告了对AD模型小鼠进行为期4天的短暂间歇性缺氧治疗会导致Aβ在间歇性缺氧治疗2个月后过度生成，这可能是通过突触BACE1的上调以及tau的过度磷酸化实现的。这些结果表明，即使是短暂的 IHT 也足以导致大脑中作为 AD 生物标志物的分子发生长期变化。

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Transient sleep apnea results in long-lasting increase in β-amyloid generation and tau hyperphosphorylation

Sleep apnea is regarded as an important risk factor in the pathogenesis of Alzheimer disease (AD). Chronic intermittent hypoxia treatment (IHT) given during the sleep period of the circadian cycle in experimental animals is a well-established sleep apnea model. Here we report that transient IHT for 4 days on AD model mice causes Aβ overproduction 2 months after IHT presumably via upregulation of synaptic BACE1, side-by-side with tau hyperphosphorylation. These results suggest that even transient IHT may be sufficient to cause long-lasting changes in the molecules measured as AD biomarkers in the brain.

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来源期刊

Neuroscience Research 医学-神经科学

CiteScore

5.60

自引率

3.40%

发文量

136

审稿时长

28 days

期刊介绍： The international journal publishing original full-length research articles, short communications, technical notes, and reviews on all aspects of neuroscience Neuroscience Research is an international journal for high quality articles in all branches of neuroscience, from the molecular to the behavioral levels. The journal is published in collaboration with the Japan Neuroscience Society and is open to all contributors in the world.