ReviewOxidative medicine and cellular longevity2020
RNA and Oxidative Stress in Alzheimer's Disease: Focus on microRNAs.
Review in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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.
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Who cites it
61 citing papers in PubMed, 105 citations in OpenAlex.
- Combined metabolic activators improve cognitive functions in Alzheimer's disease patients: a randomised, double-blinded, placebo-controlled phase-II trial.Translational neurodegeneration · 2023Trial
- Oxidative Stress in Alzheimer's Disease: Can Dietary Interventions Provide Neuroprotection?Nutrients · 2026Review
- From Inflammatory RNAs to Therapeutic Silencing: Deciphering the RNA-Inflammation Axis in Cancer and Neurodegeneration.Biology · 2026Review
- miR-125b Mediates Tau-induced Mitochondrial Dysfunction in a Cellular Model of Alzheimer's Disease.Molecular neurobiology · 2026Article
- A Bioinformatic Analysis of BAG Protein Interactors and Pathways in Alzheimer's and Parkinson's Disease.Journal of molecular neuroscience : MN · 2026Review
- Oxidative Stress and Lysosomal Dysfunction in Neurodegenerative Diseases: Underlying Mechanisms and Nanotherapeutic Targeting Strategies.Antioxidants (Basel, Switzerland) · 2026Review
- The process of angiogenesis in neurodegeneration-pathomechanisms and new therapeutic interventions.Psychopharmacology · 2026Review
- Epigenetics in Alzheimer's disease: from molecular mechanisms to emerging novel biomarkers.Frontiers in aging neuroscience · 2026Review
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Insulin resistance: fueling oxidative stress and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- MiR-21-5p promotes RPE cell necroptosis by targeting Peli1 in a rat model of AMD.In vitro cellular & developmental biology. Animal · 2025Article
- Role of mGluR7 in Alzheimer's disease: pathophysiological insights and therapeutic approaches.Inflammopharmacology · 2025Review
- Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2025Article
- Intracranial self-stimulation mitigates spatial task deficits, modifies miR-146a and miR-495 serum levels and restores hippocampal NRF2 levels in a rat model of sporadic Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Mapping the future of oxidative RNA damage in neurodegeneration: Rethinking the status quo with new tools.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Circulating metabolome in relation to cognitive impairment: a community-based cohort of older adults.Translational psychiatry · 2024Article
- Observational
- Role of miRNAs in neurovascular injury and repair.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024Review
- NRF2 Deficiency Promotes Ferroptosis of Astrocytes Mediated by Oxidative Stress in Alzheimer's Disease.Molecular neurobiology · 2024Article
- Treatment of Acute and Long-COVID, Diabetes, Myocardial Infarction, and Alzheimer's Disease: The Potential Role of a Novel Nano-Compound-The Transdermal Glutathione-Cyclodextrin Complex.Antioxidants (Basel, Switzerland) · 2024Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress (OS) is one of the major pathomechanisms of Alzheimer's disease (AD), which is closely associated with other key events in neurodegeneration such as mitochondrial dysfunction, inflammation, metal dysregulation, and protein misfolding. Oxidized RNAs are identified in brains of AD patients at the prodromal stage. Indeed, oxidized mRNA, rRNA, and tRNA lead to retarded or aberrant protein synthesis. OS interferes with not only these translational machineries but also regulatory mechanisms of noncoding RNAs, especially microRNAs (miRNAs). MiRNAs can be oxidized, which causes misrecognizing target mRNAs. Moreover, OS affects the expression of multiple miRNAs, and conversely, miRNAs regulate many genes involved in the OS response. Intriguingly, several miRNAs embedded in upstream regulators or downstream targets of OS are involved also in neurodegenerative pathways in AD. Specifically, seven upregulated miRNAs (miR-125b, miR-146a, miR-200c, miR-26b, miR-30e, miR-34a, miR-34c) and three downregulated miRNAs (miR-107, miR-210, miR-485), all of which are associated with OS, are found in vulnerable brain regions of AD at the prodromal stage. Growing evidence suggests that altered miRNAs may serve as targets for developing diagnostic or therapeutic tools for early-stage AD. Focusing on a neuroprotective transcriptional repressor, REST, and the concept of hormesis that are relevant to the OS response may provide clues to help us understand the role of the miRNA system in cellular and organismal adaptive mechanisms to OS.
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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 OpenQuestion graph.