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

被引：1

作者：

Nagayama, Takeru ^{[1
]}

Yagishita, Sosuke ^{[1
]}

Shibata, Megumi ^{[1
]}

Furuno, Akiko ^{[1
]}

Saito, Takashi ^{[2
,3
]}

Saido, Takaomi C. ^{[3
]}

Wakatsuki, Shuji ^{[1
]}

Araki, Toshiyuki ^{[1
]}

机构：

[1] Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Peripheral Nervous Syst Res, Tokyo 1878502, Japan

[2] Nagoya City Univ, Inst Brain Sci, Grad Sch Med Sci, Dept Neurocognit Sci, Nagoya, Aichi 4678601, Japan

[3] RIKEN, Ctr Brain Sci, Lab Proteolyt Neurosci, Wako, Saitama 3510198, Japan

来源：

NEUROSCIENCE RESEARCH | 2024年 / 205卷

关键词：

Sleep-disordered breathing; Sleep apnea; Chronic intermittent hypoxia; Alzheimer; Disease (AD); beta-Secretase 1 (BACE1); Tau; Hyperphosphorylation; INTERMITTENT HYPOXIA; OXIDATIVE STRESS; PRECURSOR PROTEIN; GAMMA-SECRETASE; MOUSE MODEL; BACE1; PHOSPHORYLATION; CLEAVAGE; RELEASE; BRAIN;

D O I：

10.1016/j.neures.2024.03.003

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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 A beta 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.

引用

页码：40 / 46

页数：7

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