Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death.
By D. Allan Butterfield, Alessandra Castegna, C. Lauderback, J. Drake. Neurobiology of Aging, 2002
730 citations recorded by the source corpus.
View Paper: https://www.semanticscholar.org/paper/9ea28bcfdf6a33c954e109a73f19218461aa20a8
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Citations in the corpus
- Oxidative Stress and Neurodegenerative Diseases: A Review of Upstream and Downstream Antioxidant Therapeutic Options (2009, background): “Double bonds of unsaturated fatty acids are hot spots for attack by free radicals those initiate cascade or chain reaction to damage neighboring unsaturated fatty acids [13].”
- Docosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model. (2004, unknown): “…and in the brain of the Tg2576 mouse model, is the probable cause of the transgene-dependent loss of one of the most peroxidizable CNS lipids (DHA) and has been increasingly implicated as a significant factor in AD pathogenesis (Aksenov et al., 2001; Butterfield et al., 2002; Montine et al., 2004).”
- Free radicals and antioxidants in normal physiological functions and human disease. (2007, background): “In addition to Cu2+, A also binds Zn2+ and e3+ in vitro and the amounts of these metals are lso markedly elevated in the neocortex and especially nriched in amyloid plaque deposits in individuals with lzheimer’s disease (Butterfield et al., 2002).”
- Biomarkers of oxidative damage in human disease. (2006, background): “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”
- Nrf2 and Oxidative Stress: A General Overview of Mechanisms and Implications in Human Disease (2022, background): “The brain consumes 20% of the body’s oxygen relative to its small mass (~2% of total body mass) and is particularly susceptible to oxidative damage due to its high rate of metabolic activity, high rate of oxygen metabolite production, relatively low levels of antioxidants, low capacity for repair, a”
- Protein aggregation kinetics, mechanism, and curve-fitting: a review of the literature. (2009, background): “Several research groups have also looked at the toxicity of soluble oligomers of amyloid-β and proposed that toxicity could occur by way of (i) reacting with O2 in the neuronal cell membrane to start a chain of radical reactions leading to the formation of lipid peroxidation products [66]; (ii) gene”