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Oxidative Stress and Huntington’s Disease: The Good, The Bad, and The Ugly
Open accessAbstract
Redox homeostasis is crucial for proper cellular functions, including receptor tyrosine kinase signaling, protein folding, and xenobiotic detoxification. Under basal conditions, there is a balance between oxidants and antioxidants. This balance facilitates the ability of oxidants, such as reactive oxygen species, to play critical regulatory functions through a direct modification of a small number of amino acids (e.g. cysteine) on signaling proteins. These signaling functions leverage tight spatial, amplitude, and temporal control of oxidant concentrations. However, when oxidants overwhelm the antioxidant capacity, they lead to a harmful condition of oxidative stress. Oxidative stress has long been held to be one of the key players in disease progression for Huntington's disease (HD). In this review, we will critically review this evidence, drawing some intermediate conclusions, and ultimately provide a framework for thinking about the role of oxidative stress in the pathophysiology of HD.
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“Oxidative damage has been implicated in all major neurodegenerative diseases including Alzheimer’s disease (AD) [108,109], Parkinson’s disease (PD) [110,111], Huntington’s disease (HD) [112,113], amyotrophic lateral sclerosis (ALS) [114], and multiple sclerosis (MS) [115].”
From Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022) · cites this paper as [113]
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Metadata
- Authors
- Kumar, A., & Ratan, R. R.
- Affiliations
- Cornell University (US)
- Corresponding author
- Ratan, Rajiv R.
- Venue
- Journal of Huntington s Disease
- Publisher
- SAGE Publications
- Published
- 2016-09-20
- Volume
- 5
- Issue
- 3
- Pages
- 217-237
- ISSN
- 1879-6397 (ISSN-L)
- 1879-6400
- PMC
- PMC5310831
- OpenAlex
- W2522941116
- Cited by
- 236
- References
- 183
- Citations by year
- 2026: 19 · 2025: 32 · 2024: 31 · 2023: 26 · 2022: 34 · 2021: 31 · 2020: 21 · 2019: 20 · 2018: 18 · 2017: 4
- FWCI
- 1.53
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Huntington s Disease (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion, cc-by-nc)
- Funders
- Dr. Miriam and Sheldon G. Adelson Medical Research Foundation
- National Institutes of Health (P01 AG14930-15A1)
- National Institute on Aging (P01AG014930, AG14930)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- oxidative stress, Huntington's disease, redox homeostasis, reactive oxygen species, antioxidants, cysteine oxidation, protein oxidation, receptor tyrosine kinase signaling, protein folding, xenobiotic detoxification, disease pathophysiology
- MeSH terms
- Humans, Huntington Disease, Oxidative Stress
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