ArticleInternational journal of molecular sciences2008
Sublethal RNA oxidation as a mechanism for neurodegenerative disease.
Article in International journal of molecular sciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04287543 (Effect of Melatonin Administration on the PER1 and BMAL1 Clock Genes in Patients With Parkinson's Disease), which is not on this map. Cited by 21 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.
Effect of Melatonin Administration on the PER1 and BMAL1 Clock Genes in Patients With Parkinson's Disease
Who cites it
21 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Biology of aging: Oxidative stress and RNA oxidation.Molecular biology reports · 2022Review
- Essential Roles and Risks of G-Quadruplex Regulation: Recognition Targets of ALS-Linked TDP-43 and FUS.Frontiers in molecular biosciences · 2022Review
- Current perspectives on the clinical implications of oxidative RNA damage in aging research: challenges and opportunities.GeroScience · 2021Review
- Tau Oligomers Neurotoxicity.Life (Basel, Switzerland) · 2021Review
- Role of RNA Oxidation in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Recent Advances: Molecular Mechanism of RNA Oxidation and Its Role in Various Diseases.Frontiers in molecular biosciences · 2020Review
- Article
- Biophysical properties, thermal stability and functional impact of 8-oxo-7,8-dihydroguanine on oligonucleotides of RNA-a study of duplex, hairpins and the aptamer for preQ1 as models.Nucleic acids research · 2017Article
- Alzheimer's disease and CADASIL are heritable, adult-onset dementias that both involve damaged small blood vessels.Cellular and molecular life sciences : CMLS · 2014Article
- Diabetes and the brain: oxidative stress, inflammation, and autophagy.Oxidative medicine and cellular longevity · 2014 · on this mapReview
- Oxidative stress and neurodegenerative disorders.International journal of molecular sciences · 2013Review
- Autophagy in the brains of young patients with poorly controlled T1DM and fatal diabetic ketoacidosis.Experimental and molecular pathology · 2012Review
- A novel origin for granulovacuolar degeneration in aging and Alzheimer's disease: parallels to stress granules.Laboratory investigation; a journal of technical methods and pathology · 2011Article
- tRNA structural and functional changes induced by oxidative stress.Cellular and molecular life sciences : CMLS · 2011Review
- Oxidative damage is present in the fatal brain edema of diabetic ketoacidosis.Brain research · 2011Article
- No increased chromosomal damage in L-DOPA-treated patients with Parkinson's disease: a pilot study.Journal of neural transmission (Vienna, Austria : 1996) · 2010Article
- Basic mechanisms of neurodegeneration: a critical update.Journal of cellular and molecular medicine · 2010Review
- Getting the iron out: phlebotomy for Alzheimer's disease?Medical hypotheses · 2009Article
- Molecular pathogenesis of Alzheimer's disease: reductionist versus expansionist approaches.International journal of molecular sciences · 2009Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although cellular RNA is subjected to the same oxidative insults as DNA and other cellular macromolecules, oxidative damage to RNA has not been a major focus in investigations of the biological consequences of free radical damage. In fact, because it is largely single-stranded and its bases lack the protection of hydrogen bonding and binding by specific proteins, RNA may be more susceptible to oxidative insults than is DNA. Oxidative damage to protein-coding RNA or non-coding RNA will, in turn, potentially cause errors in proteins and/or dysregulation of gene expression. While less lethal than mutations in the genome, such sublethal insults to cells might be associated with underlying mechanisms of several chronic diseases, including neurodegenerative disease. Recently, oxidative RNA damage has been described in several neurodegenerative diseases including Alzheimer disease, Parkinson disease, dementia with Lewy bodies, and prion diseases. Of particular interest, oxidative RNA damage can be demonstrated in vulnerable neurons early in disease, suggesting that RNA oxidation may actively contribute to the onset of the disease. An increasing body of evidence suggests that, mechanistically speaking, the detrimental effects of oxidative RNA damage to protein synthesis are attenuated, at least in part, by the existence of protective mechanisms that prevent the incorporation of the damaged ribonucleotides into the translational machinery. Further investigations aimed at understanding the processing mechanisms related to oxidative RNA damage and its consequences may provide significant insights into the pathogenesis of neurodegenerative and other degenerative diseases and lead to better therapeutic strategies.
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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.