The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Proteomic and oxidative stress analysis in human brain samples of Huntington disease
Open accessAbstract
Huntington disease (HD) is a neurodegenerative disorder caused by expansion of CAG repeats in exon 1 of the huntingtin gene, affecting initially the striatum and progressively the cortex. This work reports a proteomic analysis of human brain postmortem samples obtained from striatum and cortex of patients with HD compared to samples of age- and sex-matched controls. Antioxidant defense proteins that were strongly induced in striatum, but also detectable in cortex, were identified as peroxiredoxins 1, 2, and 6, as well as glutathione peroxidases 1 and 6. The activities of other antioxidant enzymes such as mitochondrial superoxide dismutase and catalase were also increased in HD. Aconitase, a protein involved in energy metabolism, showed decreased activities in striatum of HD patients. Protein carbonyls, used as markers of oxidative stress, were increased in HD, and glial fibrillary acidic protein, aconitase, gamma-enolase, and creatine kinase B were identified as the main targets. Taken together, these results indicate that oxidative stress and damage to specific macromolecules would participate in the disease progression. Also, these data support the rationale for therapeutic strategies that either potentiate antioxidant defenses or avoid oxidative stress generation to delay disease progression.
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Grx5 Is a Mitochondrial Glutaredoxin Required for the Activity of Iron/Sulfur Enzymes
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Self-citationMicroglial activation correlates with severity in Huntington disease: A clinical and PET study
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Oxidative Stress in Neurodegenerative Diseases: From Molecular Mechanisms to Clinical Applications
Liu, Z., Zhou, T., Ziegler, A. C., Dimitrion, P., & Zuo, L. (2017) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2017/2525967 · Cited by 810
Huntington’s Disease: Mechanisms of Pathogenesis and Therapeutic Strategies
Jimenez-Sanchez, M., Licitra, F., Underwood, B. R., & Rubinsztein, D. C. (2017) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a024240 · Cited by 507
Rose, S., Melnyk, S., Pavliv, O., Bai, S., Nick, T. G., Frye, R. E., & James, S. J. (2012) · Translational Psychiatry · doi:10.1038/tp.2012.61 · Cited by 480
Lipid peroxidation and neurodegenerative disease
Reed, T. T. (2011) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2011.06.027 · Cited by 379
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Brandes, M. S., & Gray, N. E. (2020) · ASN Neuro · doi:10.1177/1759091419899782 · Cited by 297
Metadata
- Authors
- Sorolla, M. A., Reverter-Branchat, G., Tamarit, J., Ferrer, I., Ros, J., & Cabiscol, E.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 45
- Issue
- 5
- Pages
- 667-678
- ISSN
- 0891-5849
- OpenAlex
- W1971851525
- Cited by
- 301
- References
- 9
- FWCI
- 7.12
- Type
- journal article
- Language
- en
- Open access
- green
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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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