D A Butterfield

Summary

Affiliation: University of Kentucky
Country: USA

Publications

  1. ncbi request reprint Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid beta-peptide
    D A Butterfield
    Dept of Chemistry, Center of Membrane Sciences and Sanders Brown Center on Aging, University of Kentucky, Lexington 40506 0055, USA
    Trends Mol Med 7:548-54. 2001
  2. pmc Free radical oxidation of brain proteins in accelerated senescence and its modulation by N-tert-butyl-alpha-phenylnitrone
    D A Butterfield
    Department of Chemistry, University of Kentucky, Lexington 40506, USA
    Proc Natl Acad Sci U S A 94:674-8. 1997
  3. ncbi request reprint Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteins
    D A Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, 121 Chemistry Physics Building, University of Kentucky, Lexington, KY 40506 0055, USA
    Mech Ageing Dev 122:945-62. 2001
  4. ncbi request reprint Structural and functional changes in proteins induced by free radical-mediated oxidative stress and protective action of the antioxidants N-tert-butyl-alpha-phenylnitrone and vitamin E
    D A Butterfield
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington 40506 0055, USA
    Ann N Y Acad Sci 854:448-62. 1998
  5. ncbi request reprint Brain oxidative stress in animal models of accelerated aging and the age-related neurodegenerative disorders, Alzheimer's disease and Huntington's disease
    D A Butterfield
    Department of Chemistry, Center of Membrane Sciences and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Curr Med Chem 8:815-28. 2001
  6. ncbi request reprint Methionine residue 35 is critical for the oxidative stress and neurotoxic properties of Alzheimer's amyloid beta-peptide 1-42
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Peptides 23:1299-309. 2002
  7. ncbi request reprint Different mechanisms of oxidative stress and neurotoxicity for Alzheimer's A beta(1--42) and A beta(25--35)
    S Varadarajan
    Departments of Chemistry, University of Kentucky, Lexington, Kentucky 40506-0055, USA
    J Am Chem Soc 123:5625-31. 2001
  8. ncbi request reprint Vulnerability of synaptosomes from apoE knock-out mice to structural and oxidative modifications induced by A beta(1-40): implications for Alzheimer's disease
    C M Lauderback
    Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40506, USA
    Biochemistry 40:2548-54. 2001
  9. ncbi request reprint Antioxidant activity of the organotellurium compound 3-[4-(N,N-dimethylamino)benzenetellurenyl]propanesulfonic acid against oxidative stress in synaptosomal membrane systems and neuronal cultures
    J Kanski
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Brain Res 911:12-21. 2001
  10. ncbi request reprint 5-Aminosalicylic acid protection against oxidative damage to synaptosomal membranes by alkoxyl radicals in vitro
    J Kanski
    Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington 04506, USA
    Neurochem Res 26:23-9. 2001

Collaborators

Detail Information

Publications110 found, 100 shown here

  1. ncbi request reprint Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid beta-peptide
    D A Butterfield
    Dept of Chemistry, Center of Membrane Sciences and Sanders Brown Center on Aging, University of Kentucky, Lexington 40506 0055, USA
    Trends Mol Med 7:548-54. 2001
    ..Here, we summarize current research on phospholipid peroxidation, as well as protein and DNA oxidation, in AD brain, and discuss the potential role of Abeta in this oxidative stress...
  2. pmc Free radical oxidation of brain proteins in accelerated senescence and its modulation by N-tert-butyl-alpha-phenylnitrone
    D A Butterfield
    Department of Chemistry, University of Kentucky, Lexington 40506, USA
    Proc Natl Acad Sci U S A 94:674-8. 1997
    ..The results are discussed with reference to the use of free radical scavengers as potential anti-aging agents...
  3. ncbi request reprint Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteins
    D A Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, 121 Chemistry Physics Building, University of Kentucky, Lexington, KY 40506 0055, USA
    Mech Ageing Dev 122:945-62. 2001
    ..The current rapid progress in elucidation of mechanisms of protein oxidation in neuronal loss should provide further insight into the importance of free radical oxidative stress in these neurodegenerative disorders...
  4. ncbi request reprint Structural and functional changes in proteins induced by free radical-mediated oxidative stress and protective action of the antioxidants N-tert-butyl-alpha-phenylnitrone and vitamin E
    D A Butterfield
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington 40506 0055, USA
    Ann N Y Acad Sci 854:448-62. 1998
    ..These components may be critical targets for the beneficial effects of gerontotherapeutics both in normal aging and in disease of aging...
  5. ncbi request reprint Brain oxidative stress in animal models of accelerated aging and the age-related neurodegenerative disorders, Alzheimer's disease and Huntington's disease
    D A Butterfield
    Department of Chemistry, Center of Membrane Sciences and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Curr Med Chem 8:815-28. 2001
    ....
  6. ncbi request reprint Methionine residue 35 is critical for the oxidative stress and neurotoxic properties of Alzheimer's amyloid beta-peptide 1-42
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Peptides 23:1299-309. 2002
    ..This work is of obvious relevance to AD and provides a coupling between the centrality of Abeta(1-42) in the pathogenesis of AD and the oxidative stress under which the AD brain exists...
  7. ncbi request reprint Different mechanisms of oxidative stress and neurotoxicity for Alzheimer's A beta(1--42) and A beta(25--35)
    S Varadarajan
    Departments of Chemistry, University of Kentucky, Lexington, Kentucky 40506-0055, USA
    J Am Chem Soc 123:5625-31. 2001
    ....
  8. ncbi request reprint Vulnerability of synaptosomes from apoE knock-out mice to structural and oxidative modifications induced by A beta(1-40): implications for Alzheimer's disease
    C M Lauderback
    Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40506, USA
    Biochemistry 40:2548-54. 2001
    ..Together, these data support a role for apoE in the modulation of oxidative injury and in the maintenance of synaptic integrity and are discussed with reference to alterations in AD brain...
  9. ncbi request reprint Antioxidant activity of the organotellurium compound 3-[4-(N,N-dimethylamino)benzenetellurenyl]propanesulfonic acid against oxidative stress in synaptosomal membrane systems and neuronal cultures
    J Kanski
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Brain Res 911:12-21. 2001
    ..These findings demonstrate the great potential of the antioxidant and are consistent with the notion that NDBT may have a role to play in modulating oxidative stress in neurodegenerative disorders, including Alzheimer's disease...
  10. ncbi request reprint 5-Aminosalicylic acid protection against oxidative damage to synaptosomal membranes by alkoxyl radicals in vitro
    J Kanski
    Department of Chemistry, Center of Membrane Sciences, and Sanders-Brown Center on Aging, University of Kentucky, Lexington 04506, USA
    Neurochem Res 26:23-9. 2001
    ..These results are consistent with the notion of antioxidant protection against free radical induced oxidative stress in synaptosomal membrane system by this agent...
  11. ncbi request reprint Antisense directed at the Abeta region of APP decreases brain oxidative markers in aged senescence accelerated mice
    H Fai Poon
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington 40506 0055, USA
    Brain Res 1018:86-96. 2004
    ..Therefore, we conclude that Abeta may contribute to the oxidative stress found in aged SAMP8 mice that have learning and memory impairments. These results are discussed in reference to AD...
  12. pmc Alterations in brain antioxidant enzymes and redox proteomic identification of oxidized brain proteins induced by the anti-cancer drug adriamycin: implications for oxidative stress-mediated chemobrain
    G Joshi
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
    Neuroscience 166:796-807. 2010
    ..These results further support the notion ADR induces oxidative stress in brain despite not crossing the BBB, and that antioxidant intervention may prevent ADR-induced cognitive dysfunction...
  13. ncbi request reprint Protein oxidation in the brain in Alzheimer's disease
    M Y Aksenov
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Neuroscience 103:373-83. 2001
    ....
  14. ncbi request reprint Glutathione elevation and its protective role in acrolein-induced protein damage in synaptosomal membranes: relevance to brain lipid peroxidation in neurodegenerative disease
    C B Pocernich
    Department of Chemistry, 125 Chemistry-Physics Building, University of Kentucky, Lexington, KY 40506, USA
    Neurochem Int 39:141-9. 2001
    ....
  15. ncbi request reprint Rodent Abeta(1-42) exhibits oxidative stress properties similar to those of human Abeta(1-42): Implications for proposed mechanisms of toxicity
    Debra Boyd-Kimball
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky Lexington, KY 40506 0055, USA
    J Alzheimers Dis 6:515-25. 2004
    ....
  16. ncbi request reprint Quantitative proteomics analysis of differential protein expression and oxidative modification of specific proteins in the brains of old mice
    H Fai Poon
    Department of Chemistry, Center of Mambrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Aging 27:1010-9. 2006
    ..Our results establish an initial basis for understanding protein alterations that may lead to age-related cellular dysfunction in the brain...
  17. ncbi request reprint Proteomics analysis provides insight into caloric restriction mediated oxidation and expression of brain proteins associated with age-related impaired cellular processes: Mitochondrial dysfunction, glutamate dysregulation and impaired protein synthesis
    H Fai Poon
    Department of Chemistry, University of Kentucky, Center of Membrane Sciences, Sanders Brown Center on Aging, 255 Bowman Hall, Lexington, KY 40506 0055, USA
    Neurobiol Aging 27:1020-34. 2006
    ..This study provides valuable insights into the mechanisms of the beneficial factors on brain aging by CR...
  18. pmc Involvement of PI3K/PKG/ERK1/2 signaling pathways in cortical neurons to trigger protection by cotreatment of acetyl-L-carnitine and alpha-lipoic acid against HNE-mediated oxidative stress and neurotoxicity: implications for Alzheimer's disease
    Hafiz Mohmmad Abdul
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    Free Radic Biol Med 42:371-84. 2007
    ..This evidence supports the pharmacological potential of cotreatment of ALCAR and LA in the management of neurodegenerative disorders associated with HNE-induced oxidative stress and neurotoxicity, including AD...
  19. ncbi request reprint Identification of nitrated proteins in Alzheimer's disease brain using a redox proteomics approach
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Dis 22:76-87. 2006
    ..Our results are discussed in context of the role of oxidative stress as one of the important mechanisms of neurodegeneration in AD...
  20. ncbi request reprint Amyloid beta-peptide effects on synaptosomes from apolipoprotein E-deficient mice
    J N Keller
    Sanders Brown Center on Aging, University of Kentucky, Lexington 40536 0230, USA
    J Neurochem 74:1579-86. 2000
    ..Together, these data are consistent with a role for apoE in maintaining homeostasis by attenuating oxidative stress, caspase activation, and mitochondrial homeostasis in synapses...
  21. ncbi request reprint The glial glutamate transporter, GLT-1, is oxidatively modified by 4-hydroxy-2-nonenal in the Alzheimer's disease brain: the role of Abeta1-42
    C M Lauderback
    Department of Chemistry, and Center of Membrane Sciences, University of Kentucky, Lexington, Kentucky, USA
    J Neurochem 78:413-6. 2001
    ..Furthermore, our data suggests that Abeta may be a possible causative agent in this cascade...
  22. ncbi request reprint Role of spermine in amyloid beta-peptide-associated free radical-induced neurotoxicity
    S M Yatin
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington, 40506-0055, USA
    J Neurosci Res 63:395-401. 2001
    ....
  23. pmc Decreased levels of PSD95 and two associated proteins and increased levels of BCl2 and caspase 3 in hippocampus from subjects with amnestic mild cognitive impairment: Insights into their potential roles for loss of synapses and memory, accumulation of Abe
    Rukhsana Sultana
    University of Kentucky, Lexington, Kentucky, USA
    J Neurosci Res 88:469-77. 2010
    ..The data obtained from the current study suggest a possible involvement of these proteins in synaptic alterations, apoptosis and consequent decrements in learning and memory associated with the progression of MCI to AD...
  24. ncbi request reprint Proteomic identification of oxidatively modified proteins in Alzheimer's disease brain. Part I: creatine kinase BB, glutamine synthase, and ubiquitin carboxy-terminal hydrolase L-1
    Alessandra Castegna
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington 40506 0055, USA
    Free Radic Biol Med 33:562-71. 2002
    ..Proteomics offers a rapid means of identifying oxidatively modified proteins in aging and age-related neurodegenerative disorders without the limitations of the immunochemical detection method...
  25. ncbi request reprint Proteomic identification of oxidized mitochondrial proteins following experimental traumatic brain injury
    Wycliffe O Opii
    Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506, USA
    J Neurotrauma 24:772-89. 2007
    ..The identification of these proteins provides new insights into the mechanisms that take place following TBI and may provide avenues for possible therapeutic interventions after TBI...
  26. ncbi request reprint Apolipoprotein E modulates Alzheimer's Abeta(1-42)-induced oxidative damage to synaptosomes in an allele-specific manner
    Christopher M Lauderback
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Brain Res 924:90-7. 2002
    ..These results are discussed with reference to mechanistic implications for neurodegeneration in the AD brain...
  27. ncbi request reprint Acetyl-L-carnitine-induced up-regulation of heat shock proteins protects cortical neurons against amyloid-beta peptide 1-42-mediated oxidative stress and neurotoxicity: implications for Alzheimer's disease
    Hafiz Mohmmad Abdul
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, 40506, USA
    J Neurosci Res 84:398-408. 2006
    ..This evidence supports the pharmacological potential of acetyl carnitine in the management of Abeta(1-42)-induced oxidative stress and neurotoxicity. Therefore, ALCAR may be useful as a possible therapeutic strategy for patients with AD...
  28. ncbi request reprint The expression of several mitochondrial and nuclear genes encoding the subunits of electron transport chain enzyme complexes, cytochrome c oxidase, and NADH dehydrogenase, in different brain regions in Alzheimer's disease
    M Y Aksenov
    Sanders Brown Center on Aging, University of Kentucky, Lexington 40536, USA
    Neurochem Res 24:767-74. 1999
    ..This study suggests that changes of the expression of mitochondrial and nuclear genes, encoding parts of ND and CO enzyme complexes, may contribute to alterations of oxidative metabolism in AD...
  29. ncbi request reprint Oxidative modification of glutamine synthetase by amyloid beta peptide
    M Y Aksenov
    Department of Pharmacology, University of Kentucky, Lexington 40536, USA
    Free Radic Res 27:267-81. 1997
    ..Here we report also that A beta(25-35) induces carbonyl formation in BSA. Our results demonstrate that beta-peptide, as well as other free radical generators, induces carbonyl formation when brought into contact with different proteins...
  30. ncbi request reprint Proteomic identification of proteins specifically oxidized by intracerebral injection of amyloid beta-peptide (1-42) into rat brain: implications for Alzheimer's disease
    D Boyd-Kimball
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    Neuroscience 132:313-24. 2005
    ....
  31. doi request reprint Elevated levels of pro-apoptotic p53 and its oxidative modification by the lipid peroxidation product, HNE, in brain from subjects with amnestic mild cognitive impairment and Alzheimer's disease
    Giovanna Cenini
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    J Cell Mol Med 12:987-94. 2008
    ..In addition, HNE may be a novel non-protein mediator of oxidative stress-induced neuronal apoptosis...
  32. ncbi request reprint Proteomics analysis of the Alzheimer's disease hippocampal proteome
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    J Alzheimers Dis 11:153-64. 2007
    ..26-fold increase in protein level compared to control (p<0.04). Thus, proteomics has provided knowledge of the levels of key proteins in AD brain. We discuss the functions regulated by these proteins with respect to AD pathology...
  33. pmc Oxidatively modified, mitochondria-relevant brain proteins in subjects with Alzheimer disease and mild cognitive impairment
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
    J Bioenerg Biomembr 41:441-6. 2009
    ..In this review, we discuss the role of the oxidation of mitochondria-relevant brain proteins to the pathogenesis and progression of AD...
  34. ncbi request reprint Oxidative modification and down-regulation of Pin1 in Alzheimer's disease hippocampus: A redox proteomics analysis
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Aging 27:918-25. 2006
    ..Taken together, these results provide evidence supporting a direct link between oxidative damage to neuronal Pin1 and the pathobiology of AD...
  35. ncbi request reprint Mutations in amyloid precursor protein and presenilin-1 genes increase the basal oxidative stress in murine neuronal cells and lead to increased sensitivity to oxidative stress mediated by amyloid beta-peptide (1-42), HO and kainic acid: implications for
    Hafiz Mohmmad Abdul
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506, USA
    J Neurochem 96:1322-35. 2006
    ..The results are consonant with the hypothesis that Abeta(1-42)-associated oxidative stress and increased vulnerability to oxidative stress may contribute significantly to neuronal apoptosis and death in familial early onset AD...
  36. ncbi request reprint Free radical mediated oxidative stress and toxic side effects in brain induced by the anti cancer drug adriamycin: insight into chemobrain
    Gururaj Joshi
    Department of Chemistry, University of Kentucky, Lexington, 40506, USA
    Free Radic Res 39:1147-54. 2005
    ..p injection of ADR. These results are discussed with reference to potential use of this redox cycling chemotheraputic agent in the treatement of cancer and its chemobrain side effect in brain...
  37. pmc A neuronal model of Alzheimer's disease: an insight into the mechanisms of oxidative stress-mediated mitochondrial injury
    P Sompol
    Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40536, USA
    Neuroscience 153:120-30. 2008
    ..However, continuing development of neurons under oxidative damage conditions may suppress the expression of MnSOD and enhance cell death in mature neurons...
  38. ncbi request reprint Methamphetamine toxicity is attenuated in mice that overexpress human manganese superoxide dismutase
    W F Maragos
    Department of Neurology, Kentucky Clinic, Room L 445, University of Kentucky, Lexington, KY 40536 0284, USA
    Brain Res 878:218-22. 2000
    ..non-transgenic littermates. These findings support the notion that ROS contribute to MA-induced brain damage and suggest that mitochondria may play an important role in this form of neurodegeneration...
  39. ncbi request reprint Proteomics for the identification of specifically oxidized proteins in brain: technology and application to the study of neurodegenerative disorders
    D A Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington 40506 0055, USA
    Amino Acids 25:419-25. 2003
    ....
  40. ncbi request reprint Methionine residue 35 is important in amyloid beta-peptide-associated free radical oxidative stress
    S Varadarajan
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington 40506 0055, USA
    Brain Res Bull 50:133-41. 1999
    ....
  41. ncbi request reprint Redox proteomics analysis of oxidatively modified proteins in G93A-SOD1 transgenic mice--a model of familial amyotrophic lateral sclerosis
    H Fai Poon
    Department of Chemistry, University of Kentucky, Lexington KY 40506, USA
    Free Radic Biol Med 39:453-62. 2005
    ....
  42. ncbi request reprint Oxidatively modified GST and MRP1 in Alzheimer's disease brain: implications for accumulation of reactive lipid peroxidation products
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Neurochem Res 29:2215-20. 2004
    ..The results from this study also imply that augmenting endogenous oxidative defense capacity through dietary or pharmacological intake of antioxidants may slow down the progression of neurodegenerative processes in AD...
  43. ncbi request reprint Neurotoxicity and oxidative stress in D1M-substituted Alzheimer's A beta(1-42): relevance to N-terminal methionine chemistry in small model peptides
    Debra Boyd-Kimball
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    Peptides 26:665-73. 2005
    ..The results of this study validate the chemistry reported for short peptides with N-terminal methionines in a disease-relevant peptide...
  44. ncbi request reprint Protective effect of the xanthate, D609, on Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress in primary neuronal cells
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Free Radic Res 38:449-58. 2004
    ..Our results suggest that D609 exerts protective effects against Abeta(1-42) toxicity by modulating oxidative stress. These results may be of importance for the treatment of AD and other oxidative stress-related diseases...
  45. pmc Protective effect of quercetin in primary neurons against Abeta(1-42): relevance to Alzheimer's disease
    Mubeen Ahmad Ansari
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    J Nutr Biochem 20:269-75. 2009
    ..These findings provide motivation to test the hypothesis that quercetin may provide a promising approach for the treatment of AD and other oxidative-stress-related neurodegenerative diseases...
  46. ncbi request reprint Role of glycine-33 and methionine-35 in Alzheimer's amyloid beta-peptide 1-42-associated oxidative stress and neurotoxicity
    Jaroslaw Kanski
    Department of Chemistry, University of Kentucky, Lexington 40506 0055, USA
    Biochim Biophys Acta 1586:190-8. 2002
    ..The results suggest that Gly33 may be a possible site of free radical propagation processes that are initiated on Met35 of Abeta(1-42) and that contribute to the peptide's toxicity in Alzheimer's disease brain...
  47. ncbi request reprint Proteomic identification of nitrated proteins in Alzheimer's disease brain
    Alessandra Castegna
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    J Neurochem 85:1394-401. 2003
    ....
  48. pmc Age-related loss of phospholipid asymmetry in APP(NLh)/APP(NLh) x PS-1(P264L)/PS-1(P264L) human double mutant knock-in mice: relevance to Alzheimer disease
    Miranda L Bader Lange
    Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Dis 38:104-15. 2010
    ..These results are discussed with relevance to loss of lipid asymmetry and consequent neurotoxicity in brain of subjects with Alzheimer disease...
  49. pmc In vivo administration of D609 leads to protection of subsequently isolated gerbil brain mitochondria subjected to in vitro oxidative stress induced by amyloid beta-peptide and other oxidative stressors: relevance to Alzheimer's disease and other oxidativ
    Mubeen Ahmad Ansari
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Free Radic Biol Med 41:1694-703. 2006
    ..These antiapoptotic findings are discussed with reference to the potential use of this brain-accessible glutathione mimetic in the treatment of oxidative stress-related neurodegenerative disorders, including AD...
  50. pmc Oxidative damage in brain from human mutant APP/PS-1 double knock-in mice as a function of age
    Hafiz Mohmmad Abdul
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    Free Radic Biol Med 45:1420-5. 2008
    ..These results are discussed with reference to the importance of Abeta42-associated oxidative stress in the pathogenesis of AD...
  51. ncbi request reprint D609 inhibits ionizing radiation-induced oxidative damage by acting as a potent antioxidant
    D Zhou
    Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, University of Kentucky, Lexington, Kentucky, USA
    J Pharmacol Exp Ther 298:103-9. 2001
    ..5 and 8.5 Gy), it protected the mice from IR-induced lethality. Thus, these results indicate that D609 is a potent antioxidant and has the ability to inhibit IR-induced cellular oxidative stress...
  52. ncbi request reprint Evidence of increased oxidative damage in subjects with mild cognitive impairment
    J N Keller
    Department of Anatomy, University of Kentucky, Lexington 40536 0230, USA
    Neurology 64:1152-6. 2005
    ..To determine if increased levels of oxidative damage are present in the brains of persons with mild cognitive impairment (MCI), a condition that often precedes Alzheimer disease (AD)...
  53. ncbi request reprint Proteomic identification of oxidatively modified proteins in Alzheimer's disease brain. Part II: dihydropyrimidinase-related protein 2, alpha-enolase and heat shock cognate 71
    Alessandra Castegna
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506, USA
    J Neurochem 82:1524-32. 2002
    ..These results are discussed with reference to potential involvement of these oxidatively modified proteins in neurodegeneration in AD brain...
  54. doi request reprint Proteomic identification of HNE-bound proteins in early Alzheimer disease: Insights into the role of lipid peroxidation in the progression of AD
    Tanea T Reed
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Brain Res 1274:66-76. 2009
    ....
  55. pmc Effects of oxidative and nitrosative stress in brain on p53 proapoptotic protein in amnestic mild cognitive impairment and Alzheimer disease
    Giovanna Cenini
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    Free Radic Biol Med 45:81-5. 2008
    ....
  56. pmc Preclinical Alzheimer disease: brain oxidative stress, Abeta peptide and proteomics
    Christopher D Aluise
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Dis 39:221-8. 2010
    ..Our analyses may reveal processes involved in a period of protection from neurodegeneration that mimic the clinical phenotype of PCAD...
  57. ncbi request reprint Protective effect of D609 against amyloid-beta1-42-induced oxidative modification of neuronal proteins: redox proteomics study
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, 40506, USA
    J Neurosci Res 84:409-17. 2006
    ..We discuss the implications of these Abeta(1-42)-mediated oxidatively modified proteins for AD pathology and for potential therapeutic intervention in this dementing disorder...
  58. ncbi request reprint Mitochondrial associated metabolic proteins are selectively oxidized in A30P alpha-synuclein transgenic mice--a model of familial Parkinson's disease
    H Fai Poon
    Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Dis 18:492-8. 2005
    ..Our findings suggest that proteins associated with impaired energy metabolism and mitochondria are particularly prone to oxidative stress associated with A30P-mutant alpha-synuclein...
  59. ncbi request reprint Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans model
    Jennifer Drake
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Aging 24:415-20. 2003
    ..These results are discussed with reference to Alzheimer's disease...
  60. pmc Oxidative stress and toxicity induced by the nucleoside reverse transcriptase inhibitor (NRTI)--2',3'-dideoxycytidine (ddC): relevance to HIV-dementia
    Wycliffe O Opii
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Exp Neurol 204:29-38. 2007
    ..These findings are consistent with the notion of a possible role of the NRTIs, and in particular, ddC, in the mechanisms involved in HIVD...
  61. ncbi request reprint APP and PS-1 mutations induce brain oxidative stress independent of dietary cholesterol: implications for Alzheimer's disease
    Hafiz Mohmmad Abdul
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Neurosci Lett 368:148-50. 2004
    ..The APP and PS-1 mice displayed increased oxidative stress as measured by protein oxidation and lipid peroxidation, independent of dietary cholesterol. These results are discussed with reference to proposed therapeutic strategies of AD...
  62. ncbi request reprint Gamma-glutamylcysteine ethyl ester-induced up-regulation of glutathione protects neurons against Abeta(1-42)-mediated oxidative stress and neurotoxicity: implications for Alzheimer's disease
    Debra Boyd-Kimball
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    J Neurosci Res 79:700-6. 2005
    ..These results are consistent with the notion that up-regulation of GSH by GCEE may play a viable protective role in the oxidative and neurotoxicity induced by Abeta(1-42) in AD brain...
  63. doi request reprint Redox proteomic identification of 4-hydroxy-2-nonenal-modified brain proteins in amnestic mild cognitive impairment: insight into the role of lipid peroxidation in the progression and pathogenesis of Alzheimer's disease
    Tanea Reed
    Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Dis 30:107-20. 2008
    ..We suggest that impairment of target proteins through the production of HNE adducts leads to protein dysfunction and eventually neuronal death, thus contributing to the biological events that may lead MCI patients to progress to AD...
  64. doi request reprint Detection of 4-hydroxy-2-nonenal- and 3-nitrotyrosine-modified proteins using a proteomics approach
    Rukhsana Sultana
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Methods Mol Biol 519:351-61. 2009
    ..Since the protein levels and the protein oxidation can be obtained from 2DE and 2D blots, specific nitration or HNE modification of each protein spot can be easily calculated...
  65. ncbi request reprint Role of phenylalanine 20 in Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity
    Debra Boyd-Kimball
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    Chem Res Toxicol 17:1743-9. 2004
    ..Taken together, these results suggest that long distance electron transfer from methionine 35 through phenylalanine 20 may not play a pivotal role in Abeta(1-42)-mediated oxidative stress and neurotoxicity...
  66. ncbi request reprint An increase in S-glutathionylated proteins in the Alzheimer's disease inferior parietal lobule, a proteomics approach
    Shelley F Newman
    Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506, USA
    J Neurosci Res 85:1506-14. 2007
    ..This study demonstrates that specific proteins are sensitive to S-glutathionylation, which most likely is due to their sensitivity to cysteine oxidation initiated by the increase in oxidative stress in the AD brain...
  67. ncbi request reprint Gamma-glutamylcysteine ethyl ester protection of proteins from Abeta(1-42)-mediated oxidative stress in neuronal cell culture: a proteomics approach
    Debra Boyd-Kimball
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    J Neurosci Res 79:707-13. 2005
    ....
  68. pmc Proteomics-determined differences in the concanavalin-A-fractionated proteome of hippocampus and inferior parietal lobule in subjects with Alzheimer's disease and mild cognitive impairment: implications for progression of AD
    Joshua B Owen
    Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    J Proteome Res 8:471-82. 2009
    ..These results are discussed with reference to biochemical and pathological alterations in and progression of AD...
  69. pmc Oxidatively modified proteins in Alzheimer's disease (AD), mild cognitive impairment and animal models of AD: role of Abeta in pathogenesis
    Rukhsana Sultana
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    Acta Neuropathol 118:131-50. 2009
    ..In this review, we summarized our findings of redox proteomics identified oxidatively modified proteins in AD, MCI and AD models...
  70. ncbi request reprint Nutritional approaches to modulate oxidative stress in Alzheimer's disease
    C B Pocernich
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Curr Alzheimer Res 8:452-69. 2011
    ..Brain-accessible antioxidants with both radical scavenging properties and ability to induce protective genes are hypothesized to be helpful in treatment for AD...
  71. pmc Differential expression and redox proteomics analyses of an Alzheimer disease transgenic mouse model: effects of the amyloid-β peptide of amyloid precursor protein
    R A S Robinson
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
    Neuroscience 177:207-22. 2011
    ..Overall, these studies provide information about changes in the brain proteome as a result of Aβ deposition and clues with which to further direct studies on elucidating AD pathogenesis...
  72. ncbi request reprint Oxidative stress in HIV demented patients and protection ex vivo with novel antioxidants
    J Turchan
    Department of Neurology, Pharmaceutical Sciences, University of Kentucky, Lexington, USA
    Neurology 60:307-14. 2003
    ..To determine the role of oxidative stress in mediating HIV dementia and to identify novel therapeutic compounds that may block this oxidative stress...
  73. ncbi request reprint Quantitative proteomics analysis of specific protein expression and oxidative modification in aged senescence-accelerated-prone 8 mice brain
    H F Poon
    Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
    Neuroscience 126:915-26. 2004
    ....
  74. ncbi request reprint Proteomic analysis of oxidatively modified proteins in Alzheimer's disease brain: insights into neurodegeneration
    D A Butterfield
    Department of Chemistry, Center of Membrane Sciences, Sanders Brown Center on Aging, 121 Chemistry Physics Building, University of Kentucky, Lexington, KY 40506 0055, USA
    Cell Mol Biol (Noisy-le-grand) 49:747-51. 2003
    ..There are limitations to proteomics, and these, too, are discussed...
  75. ncbi request reprint Proteomic identification of nitrated brain proteins in amnestic mild cognitive impairment: a regional study
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    J Cell Mol Med 11:839-51. 2007
    ..The identified nitrated proteins in MCI brain were compared to those previously reported to be nitrated and oxidatively modified in AD brain, a comparison that might provide an invaluable insight into the progression of the disease...
  76. ncbi request reprint Proteomics analysis in Alzheimer's disease: new insights into mechanisms of neurodegeneration
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences University of Kentucky, Lexington, KY 40506, USA
    Int Rev Neurobiol 61:159-88. 2004
  77. pmc Proteomic identification of brain proteins in the canine model of human aging following a long-term treatment with antioxidants and a program of behavioral enrichment: relevance to Alzheimer's disease
    Wycliffe O Opii
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, United States
    Neurobiol Aging 29:51-70. 2008
    ..These results support the combination treatments as a possible therapeutic approach that could be translated to the aging human population who are at risk for age-related neurodegenerative disorders, including Alzheimer's disease...
  78. ncbi request reprint Protein oxidation and lipid peroxidation in brain of subjects with Alzheimer's disease: insights into mechanism of neurodegeneration from redox proteomics
    Rukhsana Sultana
    Department of Chemistry, and Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    Antioxid Redox Signal 8:2021-37. 2006
    ..Particular attention is given to the current knowledge about the redox proteomics identification of oxidatively modified proteins in AD brain...
  79. ncbi request reprint Free radicals: key to brain aging and heme oxygenase as a cellular response to oxidative stress
    H Fai Poon
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington 40506 0055, USA
    J Gerontol A Biol Sci Med Sci 59:478-93. 2004
    ..Therefore, this review supports the proposition that free radicals are, indeed, a key to brain aging...
  80. ncbi request reprint Protection against amyloid beta-peptide (1-42)-induced loss of phospholipid asymmetry in synaptosomal membranes by tricyclodecan-9-xanthogenate (D609) and ferulic acid ethyl ester: implications for Alzheimer's disease
    Hafiz Mohmmad Abdul
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
    Biochim Biophys Acta 1741:140-8. 2005
    ..Rather, other mechanisms that could modulate the function of flippase might be important in the modulation of phospholipid asymmetry. The results of this study are discussed with relevance to neuronal loss in the AD brain...
  81. ncbi request reprint Proteomic identification of proteins specifically oxidized in Caenorhabditis elegans expressing human Abeta(1-42): implications for Alzheimer's disease
    Debra Boyd-Kimball
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, 121 Chemistry Physics Building, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Aging 27:1239-49. 2006
    ..We identified 16 oxidized proteins involved in energy metabolism, proteasome function, and scavenging of oxidants that are more oxidized compared to control lines. These results are discussed with reference to Alzheimer's disease...
  82. ncbi request reprint Redox proteomics identification of oxidized proteins in Alzheimer's disease hippocampus and cerebellum: an approach to understand pathological and biochemical alterations in AD
    Rukhsana Sultana
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Aging 27:1564-76. 2006
    ..The identification of common oxidized proteins in different brain regions of AD brain suggests a potential role for these oxidized proteins and thereby oxidative stress in the pathogenesis of Alzheimer's disease...
  83. ncbi request reprint Antioxidant activity of X-34 in synaptosomal and neuronal systems
    Jaroslaw Kanski
    Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Rose Street 125, Chemistry Physics Building, Lexington, KY 40506 0055, USA
    Brain Res 988:173-9. 2003
    ..Protein oxidation was not prevented by X-34. These results are discussed in terms of potential therapeutic use of X-34 and related compounds in AD...
  84. pmc Spin-labeling studies of the conformation of the Ca(2+)-regulatory protein calmodulin in solution and bound to the membrane skeleton in erythrocyte ghosts: implications to transmembrane signaling
    M A Yacko
    Department of Chemistry, University of Kentucky, Lexington 40506 0055
    Biophys J 63:317-22. 1992
    ..P < 0.00001). These results suggest that electron paramagnetic resonance spectra of spin-labeled CaM can provide useful information about protein structure and function when in solution and when bound to membranes...
  85. doi request reprint Multifunctional roles of enolase in Alzheimer's disease brain: beyond altered glucose metabolism
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    J Neurochem 111:915-33. 2009
    ..This review examines potential altered function(s) of brain enolase in MCI, early-onset AD, and AD, alterations that may contribute to the biochemical, pathological, clinical characteristics, and progression of this dementing disorder...
  86. ncbi request reprint Striatal damage and oxidative stress induced by the mitochondrial toxin malonate are reduced in clorgyline-treated rats and MAO-A deficient mice
    William F Maragos
    University of Kentucky, Department of Neurology, USA
    Neurochem Res 29:741-6. 2004
    ..These findings indicate that normal levels of MAO-A participate in expression of malonate toxicity by a mechanism involving oxidative stress...
  87. ncbi request reprint Amyloid beta-peptide [1-42]-associated free radical-induced oxidative stress and neurodegeneration in Alzheimer's disease brain: mechanisms and consequences
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Curr Med Chem 10:2651-9. 2003
    ..This review presents evidence in support of this model and provides insight into the molecular basis of this devastating dementing disorder...
  88. ncbi request reprint Stimulation of Epstein-Barr virus-infected human B cell growth by physiological concentrations of 4-hydroxynonenal
    Dinesh Ranjan
    Department of Surgery, University of Kentucky, College of Medicine, Lexington, 40536, USA
    Cell Biochem Funct 24:147-52. 2006
    ..This observation provides evidence for further understanding the mechanism of CsA-induced oxidative stress on EBV-related post-transplant lymphoproliferative disorder (PTLD)...
  89. ncbi request reprint Vitamin E and neurodegenerative disorders associated with oxidative stress
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington 40506, USA
    Nutr Neurosci 5:229-39. 2002
    ..This review presents some of the chemistry of vitamin E as an antioxidant and summarizes studies in which vitamin E has been employed in these disorders and models thereof...
  90. doi request reprint The wheat germ agglutinin-fractionated proteome of subjects with Alzheimer's disease and mild cognitive impairment hippocampus and inferior parietal lobule: Implications for disease pathogenesis and progression
    Fabio Di Domenico
    Department of Biochemical Sciences, Sapienza University of Rome, Rome, Italy
    J Neurosci Res 88:3566-77. 2010
    ..This study, the first to use proteomics to identify WGA-fractionated proteins isolated from brains from subjects with MCI and AD, provides additional information about the active proteome of the brain throughout AD progression...
  91. doi request reprint Lectin-affinity chromatography brain glycoproteomics and Alzheimer disease: insights into protein alterations consistent with the pathology and progression of this dementing disorder
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Proteomics Clin Appl 5:50-6. 2011
    ..This is a relatively nascent field of proteomics research in brain, so future studies of lectin-based brain protein separations may lead to additional insights into AD pathogenesis and progression...
  92. ncbi request reprint The glutamatergic system and Alzheimer's disease: therapeutic implications
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    CNS Drugs 17:641-52. 2003
    ..Recently, memantine, an NMDA receptor antagonist that addresses the hyperactivity of these receptors, has been approved in some countries for use in Alzheimer's disease...
  93. pmc Redox proteomic identification of HNE-bound mitochondrial proteins in cardiac tissues reveals a systemic effect on energy metabolism after doxorubicin treatment
    Y Zhao
    Graduate Center for Toxicology, University of Kentucky, Lexington, KY 40506, USA
    Free Radic Biol Med 72:55-65. 2014
    ....
  94. pmc Acrolein induces selective protein carbonylation in synaptosomes
    C F Mello
    Department of Chemistry, Center of Membrane Sciences and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Neuroscience 147:674-9. 2007
    ..Our results suggest that acrolein may significantly contribute to oxidative damage in AD brain...
  95. ncbi request reprint The expression of key oxidative stress-handling genes in different brain regions in Alzheimer's disease
    M Y Aksenov
    Sanders Brown Center on Aging, University of Kentucky, Lexington 40536, USA
    J Mol Neurosci 11:151-64. 1998
    ....
  96. ncbi request reprint Amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity: implications for neurodegeneration in Alzheimer's disease brain. A review
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
    Free Radic Res 36:1307-13. 2002
    ....
  97. ncbi request reprint Lipid peroxidation and protein oxidation in Alzheimer's disease brain: potential causes and consequences involving amyloid beta-peptide-associated free radical oxidative stress
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Free Radic Biol Med 32:1050-60. 2002
    ....
  98. ncbi request reprint Amyloid beta-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain exists
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    J Alzheimers Dis 4:193-201. 2002
    ..This review briefly examines each of these sources of oxidative stress and inflammation in AD brain and discusses their potential roles in the clinical progression of AD dementia...
  99. ncbi request reprint Proteomics in Alzheimer's disease: insights into potential mechanisms of neurodegeneration
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    J Neurochem 86:1313-27. 2003
    ..This review surveys the proteomics studies relevant to AD, from which new understandings of the pathology, biochemistry, and physiology of AD are beginning to emerge...
  100. ncbi request reprint Alzheimer's amyloid beta-peptide (1-42): involvement of methionine residue 35 in the oxidative stress and neurotoxicity properties of this peptide
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Neurobiol Aging 25:563-8. 2004
    ..This brief review summarizes some of our findings relevant to the role of the single methionine residue of Abeta(1-42) in the oxidative stress and neurotoxic properties of this peptide...
  101. ncbi request reprint Acetylcarnitine and cellular stress response: roles in nutritional redox homeostasis and regulation of longevity genes
    Vittorio Calabrese
    Department of Chemistry, Biochemistry and Molecular Biology Section, Faculty of Medicine, University of Catania, 95100 Catania, Italy
    J Nutr Biochem 17:73-88. 2006
    ....