ArticleSleep & breathing = Schlaf & Atmung2024
Chronic intermittent hypoxia induces cognitive impairment in Alzheimer's disease mouse model via postsynaptic mechanisms.
Article in Sleep & breathing = Schlaf & Atmung, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Short-lived Niemann-Pick type C mice with accelerated brain aging as a novel model for Alzheimer's disease research.Neural regeneration research · 2026Article
- Association of bedtime with co-morbid hypertension in OSA: a community-based study.Sleep & breathing = Schlaf & Atmung · 2026Article
- Dysfunctional respiration as a risk factor for Alzheimer disease: a hypothesis.Metabolic brain disease · 2026Review
- Chronic Intermittent Hypoxia Exposure Induces a Unique Microglial Transcriptome in 5XFAD Mice.Molecular neurobiology · 2025Article
- Sleep Abnormalities and Risk of Alzheimer's Disease.Current neurology and neuroscience reports · 2025Review
- Chronic Intermittent Hypoxia-Induced Neural Injury: Pathophysiology, Neurodegenerative Implications, and Therapeutic Insights.CNS neuroscience & therapeutics · 2025Review
- Intermittent Hypoxia as a Model of Obstructive Sleep Apnea: Present and Future.Sleep medicine clinics · 2025Review
- The relationship between hypoxia and Alzheimer's disease: an updated review.Frontiers in aging neuroscience · 2024Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
purposeObstructive sleep apnea (OSA) is highly comorbid with Alzheimer's disease (AD) and may represent a risk factor for inducing or accelerating cognitive impairment in AD. Chronic intermittent hypoxia (CIH) has been considered to be a predictor of developing cognitive decline and AD. However, the precise underlying mechanisms by which CIH contributes to cognitive impairment remain unknown. In the present study, we examined the effects of CIH on cognition and hippocampal function in APP/PS1 mice, an animal model of AD.
methodsWild-type (WT) and APP/PS1 mice were subjected to one of the following conditions for 2 weeks: (1) sham condition (continuous room air) or (2) CIH condition. The oxygen concentration of the CIH condition transitioned from 5 to 21%. Behavioral tests, electrophysiological recording, real-time polymerase chain reaction, and Western blot were used to assess the effect of CIH on cognitive performance and synaptic plasticity.
resultsCIH exposure did not affect motor coordination, general locomotor activity, anxiety, or willingness to explore. However, behavioral test results indicated that APP/PS1-CIH mice showed more spatial learning and memory deficits. CIH induced long-term potentiation (LTP) dysfunction of the hippocampus in WT mice. These effects were aggravated in APP/PS1 mice. The N-methyl-D-aspartic acid receptor (NMDAR) NR1 subunit and postsynaptic density 95 (PSD95) in the hippocampus of WT and APP/PS1 mice were downregulated.
conclusionsThese findings showed that a postsynaptic mechanism was involved in the effect of CIH on cognitive impairment.
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Registered trials
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