The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Oxidative stress in Alzheimer’s disease
Open accessAbstract
Oxidative balance is emerging as an important issue in understanding the pathogenesis of Alzheimer's disease. Examination of Alzheimer's disease brain has demonstrated a great deal of oxidative damage, associated with both hallmark pathologies (senile plaques and neurofibrillary tangles) as well as in normal appearing pyramidal neurons. While this suggests that oxidative stress is a proximal event in Alzheimer's disease pathogenesis, the mechanisms by which redox balance is altered in the disease remains elusive. Determining which of the proposed sources of free radicals, which include mitochondrial dysfunction, amyloid-beta-mediated processes, transition metal accumulation and genetic factors like apolipoprotein E and presenilins, is responsible for redox imbalance will lead to a better understanding of Alzheimer's disease pathogenesis and novel therapeutic approaches.
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“All of these markers of OS have been described as an early alteration in the AD brain, and this concept has been used in the past to support the ‘oxidative stress hypothesis’ in the pathogenesis of AD [20,28,29,30].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [30]
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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 [108]
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1 retracted
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RetractedCloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
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Iron accumulation in Alzheimer disease is a source of redox-generated free radicals
Smith, M. A., Harris, P. L. R., Sayre, L. M., & Perry, G. L. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.18.9866 · Cited by 1,365
Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.
Smith, C. D., Carney, J. M., Starke-Reed, P. E., Oliver, C. N., Stadtman, E. R., Floyd, R. A., & Markesbery, W. R. (1991) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.88.23.10540 · Cited by 1,296
Widespread Peroxynitrite-Mediated Damage in Alzheimer’s Disease
Smith, M. A., Richey Harris, P. L., Sayre, L. M., Beckman, J. S., & Perry, G. (1997) · The Journal of Neuroscience · doi:10.1523/jneurosci.17-08-02653.1997 · Cited by 1,239
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Cited by
Sorted by citations
Oxidative DNA damage: mechanisms, mutation, and disease
Cooke, M. S., Evans, M. D., Dizdaroglu, M., & Lunec, J. (2003) · The FASEB Journal · doi:10.1096/fj.02-0752rev · Cited by 3,245
Copper toxicity, oxidative stress, and antioxidant nutrients
Gaetke, L. M. (2003) · Toxicology · doi:10.1016/s0300-483x(03)00159-8 · Cited by 2,223
Long-Term Potentiation and Memory
Lynch, M. A. (2004) · Physiological Reviews · doi:10.1152/physrev.00014.2003 · Cited by 2,074
Oxidative Damage Is the Earliest Event in Alzheimer Disease
Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., Jones, P. K., Ghanbari, H., Wataya, T., Shimohama, S., et al. (2001) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/60.8.759 · Cited by 1,885
Self-citationReview on in vivo and in vitro methods evaluation of antioxidant activity
Alam, M. N., Bristi, N. J., & Rafiquzzaman, M. (2012) · Saudi Pharmaceutical Journal · doi:10.1016/j.jsps.2012.05.002 · Cited by 1,868
Metadata
- Authors
- Smith, M. A., Rottkamp, C. A., Nunomura, A., Raina, A. K., & Perry, G.
- Affiliations
- Case Western Reserve University (US)
- Asahikawa Medical College Hospital (JP)
- Corresponding author
- Smith, Mark A.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2000-07
- Volume
- 1502
- Issue
- 1
- Pages
- 139-144
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W1983789627
- Cited by
- 895
- References
- 52
- Citations by year
- 2026: 13 · 2025: 22 · 2024: 30 · 2023: 33 · 2022: 31 · 2021: 38 · 2020: 36 · 2019: 40 · 2018: 37 · 2017: 26 · 2016: 33 · 2015: 34 · 2014: 32 · 2013: 39 · 2012: 39
- FWCI
- 5.89
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- Biochimica et Biophysica Acta
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- oxidative stress, Alzheimer's disease, redox imbalance, free radicals, mitochondrial dysfunction, amyloid-beta, apolipoprotein E, presenilin, amyloid plaques, neurofibrillary tangles, pyramidal neurons, pathogenesis
- MeSH terms
- Alzheimer Disease, Antioxidants, Free Radicals, Humans, Neurons, Oxidation-Reduction, Peptide Fragments, Amyloid beta-Peptides, Neurofibrillary Tangles, Oxidative Stress, Plaque, Amyloid
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