The DOI matches its Crossref record; 95 of the 95 references it cites were found in a registry or an index.
Methionine-35 of A β (1–42): Importance for Oxidative Stress in Alzheimer Disease
Open accessAbstract
Alzheimer disease (AD) is an age-related progressive neurodegenerative disorder. This devastating disease is characterized by the presence of senile plaques (SP), neurofibrillary tangles (NFTs), and loss of synapses. Amyloid beta-peptide 1–42 (A β (1–42)) is the main component of SP and is pivotal to AD pathogenesis. Brain of subjects with AD and arguably its earliest manifestation, mild cognitive impairment (MCI), demonstrate increased levels of oxidative stress markers. Our laboratory combined these two aspects of AD and MCI and proposed the A β (1–42)-associated free radical oxidative stress hypothesis to explain oxidative stress under which the MCI and AD brain exist and the loss of synapses in both disorders. A large number of in vitro and in vivo studies showed that A β causes protein oxidation, lipid peroxidation, reactive oxygen species formation, and cell death in neuronal and synaptosomal systems. Methionine located at residue 35 of A β (1–42) is an important contributor to the oxidative stress associated with this neurotoxic peptide. In this paper, we summarize studies involving Met-35 of A β (1–42). Understanding the role of the single methionine residue of A β (1–42) may help in understanding underlying disease mechanisms in AD and MCI.
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“Given the complexity and low abundance of many PTMs, AI-based analytical methods are increasingly used for enrichment, site identification, and functional network modeling139,169,178,179.”
From Artificial intelligence-driven multi-omics approaches in Alzheimer's disease: Progress, challenges, and future directions (2025) · cites this paper as [139]
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Oxidative stress and the amyloid beta peptide in Alzheimer’s disease
Cheignon, C., Tomas, M., Bonnefont-Rousselot, D., Faller, P., Hureau, C., & Collin, F. (2018) · Redox Biology · doi:10.1016/j.redox.2017.10.014 · Cited by 2,185
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Self-citationImplications of peptide assemblies in amyloid diseases
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Oxidative stress, protein modification and Alzheimer disease
Tramutola, A., Lanzillotta, C., Perluigi, M., & Butterfield, D. A. (2017) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2016.06.005 · Cited by 303
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Metadata
- Authors
- Butterfield, D. A., & Sultana, R.
- Affiliations
- University of Kentucky (US)
- Department of Chemistry, University of Kentucky, Lexington, KY 40506-0055, USA
- Corresponding author
- Butterfield, D. Allan
- Venue
- Journal of Amino Acids
- Publisher
- Wiley
- Published
- 2011-06-04
- Volume
- 2011
- Pages
- 1-10
- ISSN
- 2090-0104 (ISSN-L)
- 2090-0112
- PMC
- PMC3268025
- OpenAlex
- W2015089109
- Cited by
- 124
- References
- 95
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 11 · 2023: 26 · 2022: 5 · 2021: 6 · 2020: 7 · 2019: 6 · 2018: 8 · 2017: 8 · 2016: 6 · 2015: 6 · 2014: 8 · 2013: 9 · 2012: 9
- FWCI
- 6.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Journal of Amino Acids (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- UKnowledge (University of Kentucky) (submittedVersion, cc-by)
- Funders
- National Institutes of Health (AG-05119)
- 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
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, amyloid beta peptide 1-42, 35S-methionine, oxidative stress, mild cognitive impairment, amyloid plaques, neurofibrillary tangles, synaptic loss, protein oxidation, lipid peroxidation, reactive oxygen species, neurotoxicity
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