Pocernich, C. ., & Butterfield, D. . Acrolein inhibits NADH-linked mitochondrial enzyme activity: implications for Alzheimer’s disease. Neurotoxicity Research, 5(7), 515-20. https://doi.org/10.1007/BF03033161 (Original work published 2003)
DA Butterfield
First name:
DA
Last name:
Butterfield
Castegna, A. ., , Klein, J. ., Lynn, B. ., Wang, Y. ., Osaka, H. ., … Butterfield, D. . (2004). Proteomic analysis of brain proteins in the gracile axonal dystrophy (gad) mouse, a syndrome that emanates from dysfunctional ubiquitin carboxyl-terminal hydrolase L-1, reveals oxidation of key proteins. Journal of Neurochemistry, 88(6), 1540-6. https://doi.org/10.1046/j.1471-4159.2003.02288.x
Castegna, A. ., Lauderback, C. ., Mohmmad-Abdul, H. ., & Butterfield, D. . (2004). Modulation of phospholipid asymmetry in synaptosomal membranes by the lipid peroxidation products, 4-hydroxynonenal and acrolein: implications for Alzheimer’s disease. Brain Research, 1004(1-2), 193-7. https://doi.org/10.1016/j.brainres.2004.01.036 (Original work published 2004)
Drake, J. ., Petroze, R. ., Castegna, A. ., Ding, Q. ., Keller, J. ., Markesbery, W. ., … Butterfield, D. . (2004). 4-Hydroxynonenal oxidatively modifies histones: implications for Alzheimer’s disease. Neuroscience Letters, 356(3), 155-8. https://doi.org/10.1016/j.neulet.2003.11.047 (Original work published 2004)
Butterfield, D. . (2004). Proteomics: a new approach to investigate oxidative stress in Alzheimer’s disease brain. Brain Research, 1000(1-2), 1-7. https://doi.org/10.1016/j.brainres.2003.12.012 (Original work published 2004)
Maragos, W. ., Young, K. ., Altman, C. ., Pocernich, C. ., Drake, J. ., Butterfield, D. ., … Shih, J. . (2004). Striatal damage and oxidative stress induced by the mitochondrial toxin malonate are reduced in clorgyline-treated rats and MAO-A deficient mice. Neurochemical Research, 29(4), 741-6. https://doi.org/10.1023/b:nere.0000018845.82808.45
Poon, H. ., , Scapagnini, G. ., & Butterfield, D. . (2004). Free radicals: key to brain aging and heme oxygenase as a cellular response to oxidative stress. The Journals of Gerontology. Series A, Biological Sciences and Medical Sciences, 59(5), 478-93. https://doi.org/10.1093/gerona/59.5.m478
Butterfield, D. ., & Bush, A. . (1969). Alzheimer’s amyloid beta-peptide (1-42): involvement of methionine residue 35 in the oxidative stress and neurotoxicity properties of this peptide. Neurobiology of Aging, 25(5), 563-8. https://doi.org/10.1016/j.neurobiolaging.2003.12.027 (Original work published 1969)
Poon, H. ., , Scapagnini, G. ., & Butterfield, D. . (2004). Free radicals and brain aging. Clinics in Geriatric Medicine, 20(2), 329-59. https://doi.org/10.1016/j.cger.2004.02.005
Boyd-Kimball, D. ., Abdul, M. ., Reed, T. ., Sultana, R. ., & Butterfield, D. . (2004). Role of phenylalanine 20 in Alzheimer’s amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity. Chemical Research in Toxicology, 17(12), 1743-9. https://doi.org/10.1021/tx049796w