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Oxidative Damage Is the Earliest Event in Alzheimer Disease
Open accessAbstract
Recently, we demonstrated a significant increase of an oxidized nucleoside derived from RNA, 8-hydroxyguanosine (8OHG), and an oxidized amino acid, nitrotyrosine in vulnerable neurons of patients with Alzheimer disease (AD). To determine whether oxidative damage is an early- or end-stage event in the process of neurodegeneration in AD, we investigated the relationship between neuronal 8OHG and nitrotyrosine and histological and clinical variables, i.e. amyloid-beta (A beta) plaques and neurofibrillary tangles (NFT), as well as duration of dementia and apolipoprotein E (ApoE) genotype. Our findings show that oxidative damage is quantitatively greatest early in the disease and reduces with disease progression. Surprisingly, we found that increases in A beta deposition are associated with decreased oxidative damage. These relationships are more significant in ApoE epsilon4 carriers. Moreover, neurons with NFT show a 40%-56% decrease in relative 8OHG levels compared with neurons free of NFT. Our observations indicate that increased oxidative damage is an early event in AD that decreases with disease progression and lesion formation. These findings suggest that AD is associated with compensatory changes that reduce damage from reactive oxygen.
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“Past and recent studies have demonstrated that oxidative damage is not only an early event in the pathogenesis of AD, occurring before the onset of clinical symptoms but also a factor contributing to the disease progression [17,18,19,20,21].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [19]
Experimental — accuracy not yet measuredIn the citing paper
“In the brains of individuals with AD and preclinical AD (i.e., evidence of Aβ and tau deposition in the brain without any clinical manifestation of the disease), as well as patients with MCI (a mild clinical impairment with no proof of underlying pathology with biomarkers), many oxidative damage products are measured, and numerous investigations have pointed to OS as a key and early player in the”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [19]
In the citing paper
“In the AD brain, mitochondria can be sources of ROS and also the target of OS, especially mitochondrial DNA (mtDNA) is susceptible to oxidative damage [19,53,63].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [19]
In the citing paper
“Oxidative damage to RNA in EC, hippocampus, subiculum, and temporal neocortex of subjects with AD has been described. The levels of 8-OHdG increase early before pathological changes occur, and this can explain that the selective vulnerability of neurons in the EC during AD may be related to the vulnerability of these particular neurons to oxidative damage [19].”
From Role of Oxidative Damage in Alzheimer’s Disease and Neurodegeneration: From Pathogenic Mechanisms to Biomarker Discovery (2021) · cites this paper as [19]
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Self-citation
Metadata
- Authors
- Nunomura, A., Perry, G., Aliev, G., Hirai, K., Takeda, A., Balraj, E. K., Jones, P. K., Ghanbari, H., Wataya, T., Shimohama, S., Chiba, S., Atwood, C. S., Petersen, R. B., & Smith, M. A.
- Affiliations
- Asahikawa Medical University (JP)
- Case Western Reserve University (US)
- Takeda (Japan) (JP)
- Sensei Biotherapeutics (United States) (US)
- Kyoto University (JP)
- Corresponding author
- Nunomura, Akihiko
- ORCID
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2001-08
- Volume
- 60
- Issue
- 8
- Pages
- 759-767
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W1542215809
- Cited by
- 1,885
- References
- 59
- Citations by year
- 2026: 46 · 2025: 31 · 2024: 52 · 2023: 61 · 2022: 80 · 2021: 98 · 2020: 86 · 2019: 82 · 2018: 69 · 2017: 73 · 2016: 70 · 2015: 83 · 2014: 86 · 2013: 86 · 2012: 104
- FWCI
- 33.08
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Asahikawa Medical University Collection and Research (Asahikawa Medical University) (submittedVersion)
- Institutional Repositories DataBase (IRDB) (submittedVersion)
- Funders
- Alzheimer's Association
- National Institutes of Health (5r01ag009287-08, AG09287)
- Japan Society for the Promotion of Science (12670918)
- National Institute on Aging (AG-14249, R01AG014249, AG 09287)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, oxidative damage, 8-hydroxyguanosine, nitrotyrosine, amyloid plaques, neurofibrillary tangles, APOE ε4, disease progression, neurodegeneration, reactive oxygen species, RNA oxidation
- MeSH terms
- Aged, Alzheimer Disease, Apolipoproteins E, Brain, Female, Genotype, Guanosine, Heterozygote, Humans, Male, Middle Aged, Neurons, Tyrosine, Amyloid beta-Peptides, Neurofibrillary Tangles, Oxidative Stress, Disease Progression, Plaque, Amyloid
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