Amyloid β-peptide (1-42)-induced Oxidative Stress and Neurotoxicity: Implications for Neurodegeneration in Alzheimer's Disease Brain. A Review
By D. Allan Butterfield. 2002
799 citations recorded by the source corpus.
Subfields: Pathology and Forensic Medicine, Physiology
View Paper: https://www.semanticscholar.org/paper/e57c7f4364e037d4663e8f59ae915f6a1eb39a9e
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Pathology and Forensic Medicine
- Richard O'Brien
- I. Dalle-Donne
- Sarah S Kellerby
- Barry Halliwell
- Xia Zhang
- Wei-Wei Chen
- A. Milzani
- Wenjuan Huang
In Physiology
- Barry Halliwell
- I. Dalle-Donne
- A. Milzani
- R. Rossi
- R. Colombo
- D. Giustarini
- Richard O'Brien
- Sarah S Kellerby
Citations in the corpus
- Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives (2022, neutral): “[66], respiratory diseases [67,68], rheumatoid arthritis [69], neurological disorders [70], liver and kidney diseases, reproductive diseases and diabetes [71,72].”
- Antioxidant Activity of Proteins and Peptides (2008, positive): “…has been suggested that the symptoms of Alzheimer’s disease is attributable to the accumulation of aggregated amyloid β-protein as neurofibrillary tangles in the brain resulting from oxidation reactions (Butterfield, 2002; Nunomura et al., 2001; Shringarpure et al., 2000; Varadarajan et al., 2000).”
- Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean? (2004, background): “…interest is the use of isoprostane measurements to study Alzheimer’s disease (AD), a condition in which lipid peroxidation and other oxidative damage seem to play significant pathological roles (Montine et al., 1998; 1999; Pratico et al., 2000; 2001; 2002; Halliwell, 2001; Butterfield, 2002).”
- Role of oxidative stress in Alzheimer's disease (2016, positive): “This seems to be associated with the length of Aβ fragments, with Aβ (1-42) being more toxic than Aβ (1-40) and the most likely candidate to generate hydrogen peroxide and other ROS (54).”
- Biomarkers of oxidative damage in human disease. (2006, positive): “Concentrations of F2- and F4-isoprostanes [which arise from oxidation of docosahexaenoic acid, an abundant unsaturated fatty acid in the central nervous system (CNS) and are often called neuroprostanes], are increased in the cerebrospinal fluid from AD patients (2, 43, 50– 52, 83, 84) and may even b”
- Oxidative Stress: Harms and Benefits for Human Health (2017, background): “β-amyloid, a toxic peptide often found present in AD patients’ brain, is produced by free radical action and it is known to be at least in part responsible for neurodegeneration observed during AD onset and progression [35].”
- Amyloid Precursor Protein Processing and Alzheimer’s Disease (2011, background): “N IH -PA Author M anuscript N IH -PA Author M anuscript N IH -PA Author M anuscript created the interest of Elan’s initial AN1792 trial, which was an active immunization protocol against the full-length Aβ42 peptide (Schenk et al. 2005).”