The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
The Identification and Characterization of Oxidized RNAs in Alzheimer's Disease
Open accessAbstract
It has been shown that cytoplasmic RNA oxidation occurs to a great extent in the brains of Alzheimer's disease (AD) patients. The goal of this study was to isolate and identify oxidized RNA species in AD. We show that significant amounts of poly(A)+mRNAs are oxidized in AD brains. RNA oxidation is not random but highly selective. Importantly, many identified oxidized mRNA species have been implicated in the pathogenesis of AD. Quantitative analysis revealed that some mRNA species are more susceptible to oxidative damage. We also investigated the biological consequence of oxidatively damaged mRNAs by expressing them in cell lines. Our data indicated that abnormal processing of proteins occurred to the oxidized mRNAs. This may implicate the potential contribution of RNA oxidation in the pathogenesis of AD.
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Cites
Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.
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Oxidative damage to mitochondrial DNA is increased in Alzheimer’s disease
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Oxidative damage to mitochondrial DNA shows marked age-dependent increases in human brain
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“…functional and structural damages in neurons including lipid peroxidation (Subbarao et al., 1990; Sayre et al., 1997), protein oxidation (Smith et al., 1991; Castegna et al., 2002a,b), mitochondrial abnormality (Hirai et al., 2001), as well as nucleic acid oxidation (Mecocci et al., 1993, 1994).”
BackgroundA mutation in succinate dehydrogenase cytochrome b causes oxidative stress and ageing in nematodes.
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“A mutation in cytochrome b causes oxidative stress and aging in nematodes (Ishii et al., 1998).”
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Transferrin and Iron in Normal, Alzheimer's Disease, and Parkinson's Disease Brain Regions
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Mitochondrial membrane fluidity and oxidative damage to mitochondrial DNA in aged and AD human brain
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Cited by
Oxidative stress and mitochondrial dysfunction in Alzheimer’s disease
Wang, X., Wang, W., Li, L., Perry, G., Lee, H.-G., & Zhu, X. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.10.015 · Cited by 1,357
A “mitochondrial cascade hypothesis” for sporadic Alzheimer’s disease
Swerdlow, R. H., & Khan, S. M. (2004) · Medical Hypotheses · doi:10.1016/j.mehy.2003.12.045 · Cited by 758
The epitranscriptome beyond m6A
Wiener, D., & Schwartz, S. (2021) · Nature Reviews Genetics · doi:10.1038/s41576-020-00295-8 · Cited by 709
Butterfield, D. A., Reed, T., Newman, S. F., & Sultana, R. (2007) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2007.05.037 · Cited by 564
Butterfield, D. A., Swomley, A. M., & Sultana, R. (2013) · Antioxidants & Redox Signaling · doi:10.1089/ars.2012.5027 · Cited by 526
Metadata
- Authors
- Shan, X., Tashiro, H., & Lin, C.-L. G.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2003-06-15
- Volume
- 23
- Issue
- 12
- Pages
- 4913-4921
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W1752358945
- Cited by
- 185
- References
- 9
- FWCI
- 4.16
- Type
- journal article
- Language
- en
- Open access
- bronze
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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