ArticleExperimental and therapeutic medicine2020
The role of reactive oxygen species in cognitive impairment associated with sleep apnea.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.
- Cerebral oxidative stress, inflammation and apoptosis induced by intermittent hypoxia: a systematic review and meta-analysis of rodent data.European respiratory review : an official journal of the European Respiratory Society · 2024Pooled it
- Relationship between acute glucose variability and cognitive decline in type 2 diabetes: A systematic review and meta-analysis.PloS one · 2023Pooled it
- iNOS/NOX-mediated stress, telomerase activity, and hTERT expression as potential biomarkers in sleep apnea.Irish journal of medical science · 2026Article
- Dietary Protocols to Promote and Improve Restful Sleep: A Narrative Review.Nutrition reviews · 2026Review
- Research status and progress on the relationship between obstructive sleep apnea and pulmonary nodules.Frontiers in medicine · 2026Review
- The mitochondrial theory of sleep: an integrative framework for understanding sleep-wake regulation.Frontiers in psychiatry · 2026Review
- The Role of Mitochondria in Obstructive Sleep Apnea: Implications for the Upper Airway Muscles.International journal of molecular sciences · 2025Review
- Intermittent Hypoxia Induces Cognitive Dysfunction and Hippocampal Gene Expression Changes in a Mouse Model of Obstructive Sleep Apnea.International journal of molecular sciences · 2025Article
- NLRP3 Inflammasome Triggers Inflammation of Obstructive Sleep Apnea.Current molecular medicine · 2025Review
- Unraveling the interplay between sleep, redox metabolism, and aging: implications for brain health and longevity.Frontiers in aging · 2025Review
- Role of Oxidative Stress in the Occurrence and Development of Cognitive Dysfunction in Patients with Obstructive Sleep Apnea Syndrome.Molecular neurobiology · 2024Review
- Can we obtain a reliable marker that shows the hypoxic burden in patients with sleep disordered breathing?Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- Overnight changes in uric acid, xanthine oxidoreductase and oxidative stress levels and their relationships with sleep-disordered breathing in patients with coronary artery disease.Hypertension research : official journal of the Japanese Society of Hypertension · 2023Article
- The oDGal Mouse: A Novel, Physiologically Relevant Rodent Model of Sporadic Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Summary of drug therapy to treat cognitive impairment-induced obstructive sleep apnea.Frontiers in cellular neuroscience · 2023Review
- The effect of sleep disorders on dementia risk in patients with traumatic brain injury: A large-scale cohort study.Alzheimer's & dementia (Amsterdam, Netherlands)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obstructive sleep apnea (OSA), a common breathing and sleeping disorder, is associated with a broad range of neurocognitive difficulties. Intermittent hypoxia (IH), one major characteristic of OSA, has been shown to impair learning and memory due to increased levels of reactive oxygen species (ROS). Under normal conditions, ROS are produced in low concentrations and act as signaling molecules in different processes. However, IH treatment leads to elevated ROS production via multiple pathways, including mitochondrial electron transport chain dysfunction and in particular complex I dysfunction, and induces oxidative tissue damage. Moreover, elevated ROS results in the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER) and increased activity of peroxisomes, such as NADPH oxidase, xanthine oxidase and phospholipase A2. Furthermore, oxidative tissue damage has been found in regions of the brains of patients with OSA, including the cortex and hippocampus, which are associated with memory and executive function. Furthermore, increased ROS levels in these regions of the brain induce damage via inflammation, apoptosis, ER stress and neuronal activity disturbance. The present review focuses on the mechanism of excessive ROS production in an OSA model and the relationship between ROS and cognitive impairment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.