D A Butterfield

Summary

Affiliation: University of Kentucky
Country: USA

Publications

  1. 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
  2. pmc Amyloid β-peptide (1-42)-induced oxidative stress in Alzheimer disease: importance in disease pathogenesis and progression
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    Antioxid Redox Signal 19:823-35. 2013
  3. pmc Redox proteomics in selected neurodegenerative disorders: from its infancy to future applications
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Antioxid Redox Signal 17:1610-55. 2012
  4. doi request reprint Atorvastatin treatment in a dog preclinical model of Alzheimer's disease leads to up-regulation of haem oxygenase-1 and is associated with reduced oxidative stress in brain
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Int J Neuropsychopharmacol 15:981-7. 2012
  5. pmc Effects of UVB-induced oxidative stress on protein expression and specific protein oxidation in normal human epithelial keratinocytes: a proteomic approach
    Marzia Perluigi
    Laboratory of Virology, IFO Regina Elena National Cancer Institute V, Messi d Oro, 156 00156 Rome, Italy
    Proteome Sci 8:13. 2010
  6. ncbi request reprint Redox proteomics identification of oxidatively modified brain proteins in inherited Alzheimer's disease: an initial assessment
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    J Alzheimers Dis 10:391-7. 2006
  7. 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
  8. 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
  9. pmc Elevated levels of 3-nitrotyrosine in brain from subjects with amnestic mild cognitive impairment: implications for the role of nitration in the progression of Alzheimer's disease
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Brain Res 1148:243-8. 2007
  10. pmc Roles of amyloid beta-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairment
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Free Radic Biol Med 43:658-77. 2007

Collaborators

Detail Information

Publications129 found, 100 shown here

  1. 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
    ....
  2. pmc Amyloid β-peptide (1-42)-induced oxidative stress in Alzheimer disease: importance in disease pathogenesis and progression
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    Antioxid Redox Signal 19:823-35. 2013
    ..The main component of SPs is amyloid beta-peptide (Aβ) that is derived from the proteolytic cleavage of amyloid precursor protein...
  3. pmc Redox proteomics in selected neurodegenerative disorders: from its infancy to future applications
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Antioxid Redox Signal 17:1610-55. 2012
    ....
  4. doi request reprint Atorvastatin treatment in a dog preclinical model of Alzheimer's disease leads to up-regulation of haem oxygenase-1 and is associated with reduced oxidative stress in brain
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Int J Neuropsychopharmacol 15:981-7. 2012
    ..HO-1 up-regulation significantly correlated with lower discrimination learning error scores in aged beagles. Reference to therapeutic applications of atorvastatin in AD is discussed...
  5. pmc Effects of UVB-induced oxidative stress on protein expression and specific protein oxidation in normal human epithelial keratinocytes: a proteomic approach
    Marzia Perluigi
    Laboratory of Virology, IFO Regina Elena National Cancer Institute V, Messi d Oro, 156 00156 Rome, Italy
    Proteome Sci 8:13. 2010
    ....
  6. ncbi request reprint Redox proteomics identification of oxidatively modified brain proteins in inherited Alzheimer's disease: an initial assessment
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    J Alzheimers Dis 10:391-7. 2006
    ..To identify oxidatively modified proteins in brains of persons with inherited Alzheimer's disease...
  7. 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...
  8. 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...
  9. pmc Elevated levels of 3-nitrotyrosine in brain from subjects with amnestic mild cognitive impairment: implications for the role of nitration in the progression of Alzheimer's disease
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Brain Res 1148:243-8. 2007
    ..Immunohistochemistry analysis of hippocampus confirmed this result. These findings suggest that nitrosative damage occurs early in the course of MCI, and that protein nitration may be important for conversion of MCI to AD...
  10. pmc Roles of amyloid beta-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairment
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Free Radic Biol Med 43:658-77. 2007
    ..In addition, redox proteomics studies in in vivo models of AD centered around human Abeta(1-42) are discussed...
  11. ncbi request reprint Redox proteomics identification of oxidatively modified brain proteins in Alzheimer's disease and mild cognitive impairment: insights into the progression of this dementing disorder
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    J Alzheimers Dis 12:61-72. 2007
    ....
  12. ncbi request reprint Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Aging 23:655-64. 2002
    ....
  13. 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...
  14. 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...
  15. 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...
  16. 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
    ....
  17. ncbi request reprint The senescence-accelerated prone mouse (SAMP8): a model of age-related cognitive decline with relevance to alterations of the gene expression and protein abnormalities in Alzheimer's disease
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506 0055, USA
    Exp Gerontol 40:774-83. 2005
    ..The SAMP8 is a good animal model to investigate the fundamental mechanisms of age-related learning and memory deficits at the gene and protein levels...
  18. ncbi request reprint The critical role of methionine 35 in Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity
    D Allan Butterfield
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
    Biochim Biophys Acta 1703:149-56. 2005
    ..In this review, we discuss the role of methionine 35 in the oxidative stress and neurotoxicity induced by Abeta(1-42) and the implications of these findings in the pathogenesis of AD...
  19. ncbi request reprint Redox proteomics identification of oxidatively modified hippocampal proteins in mild cognitive impairment: insights into the development of Alzheimer's disease
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
    Neurobiol Dis 22:223-32. 2006
    ..The current study provides a framework for future studies on the development of AD from MCI relevant to oxidative stress...
  20. ncbi request reprint Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain
    D Allan Butterfield
    Department of Chemistry, Center for Membrane Sciences, University of Kentucky, Lexington, 40506 0055, USA
    Brain Pathol 14:426-32. 2004
    ..Additionally, we discuss the critical role of methionine 35 in the oxidative stress and neurotoxic properties exhibited by Abeta1-42...
  21. ncbi request reprint Proteomics analyses of specific protein oxidation and protein expression in aged rat brain and its modulation by L-acetylcarnitine: insights into the mechanisms of action of this proposed therapeutic agent for CNS disorders associated with oxidative stres
    H Fai Poon
    Department of Chemistry, University of Kentucky, Lexington, Kentucky 40506 0055, USA
    Antioxid Redox Signal 8:381-94. 2006
    ..Moreover, those proteins that are reduced in oxidation status were identified in aged brains from rats treated in vivo with LAC. The findings are discussed in reference to brain aging and age-related cognitive impairment...
  22. pmc Redox proteomics in some age-related neurodegenerative disorders or models thereof
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, 40506, USA
    NeuroRx 3:344-57. 2006
    ..Here we review redox proteomic studies of some neurodegenerative diseases...
  23. ncbi request reprint Elevated protein-bound levels of the lipid peroxidation product, 4-hydroxy-2-nonenal, in brain from persons with mild cognitive impairment
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Neurosci Lett 397:170-3. 2006
    ....
  24. ncbi request reprint Oxidative stress in Alzheimer's disease brain: new insights from redox proteomics
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Eur J Pharmacol 545:39-50. 2006
    ..Further, redox proteomics may provide potential targets for drug therapy in Alzheimer's disease...
  25. 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...
  26. 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...
  27. 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
    ....
  28. 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...
  29. pmc Involvements of the lipid peroxidation product, HNE, in the pathogenesis and progression of Alzheimer's disease
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, Sanders Brown Center on Aging, University of Kentucky, Lexington KY 40506 0055, USA
    Biochim Biophys Acta 1801:924-9. 2010
    ..Based on the research conducted so far in the area of lipid peroxidation, it is suggested that lipid accessible antioxidant molecules could be a promising therapeutic approach to treat or slow progression of MCI and AD...
  30. doi request reprint Roles of 3-nitrotyrosine- and 4-hydroxynonenal-modified brain proteins in the progression and pathogenesis of Alzheimer's disease
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
    Free Radic Res 45:59-72. 2011
    ....
  31. 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...
  32. pmc Oxidatively modified glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and Alzheimer's disease: many pathways to neurodegeneration
    D Allan Butterfield
    Department of Chemistry, University of Kentucky, Center of Membrane Sciences, Lexington, KY40506 0055, USA
    J Alzheimers Dis 20:369-93. 2010
    ..In this review, we examine the many functions of GAPDH with respect to AD brain; in particular, the apparent role(s) of GAPDH in AD-related apoptotic cell death is emphasized...
  33. 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...
  34. pmc Cholesterol-independent neuroprotective and neurotoxic activities of statins: perspectives for statin use in Alzheimer disease and other age-related neurodegenerative disorders
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Pharmacol Res 64:180-6. 2011
    ..This perspective paper outlines pros and cons of the use of statins in neurodegenerative disorders, with particular emphasis on Alzheimer disease...
  35. pmc In vivo oxidative stress in brain of Alzheimer disease transgenic mice: Requirement for methionine 35 in amyloid beta-peptide of APP
    D Allan Butterfield
    Department of Chemistry, Center of Membrane Sciences, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40506, USA
    Free Radic Biol Med 48:136-44. 2010
    ..However, in this specific transgenic mouse model of AD, oxidative stress is neither required nor sufficient for memory abnormalities...
  36. 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
    ....
  37. ncbi request reprint In vivo protection by the xanthate tricyclodecan-9-yl-xanthogenate against amyloid beta-peptide (1-42)-induced oxidative stress
    M Perluigi
    Department of Biochemical Sciences, University of Rome La Sapienza, Rome 00185, Italy
    Neuroscience 138:1161-70. 2006
    ..Based on the above data, we suggest that tricyclodecan-9-yl-xanthogenate is a potent antioxidant and could be of importance for the treatment of Alzheimer's disease and other oxidative stress-related disorders...
  38. 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
    ....
  39. 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...
  40. 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...
  41. doi request reprint Redox proteomics in aging rat brain: involvement of mitochondrial reduced glutathione status and mitochondrial protein oxidation in the aging process
    M Perluigi
    Department of Biochemical Sciences, Sapienza University of Rome, Rome, Italy
    J Neurosci Res 88:3498-507. 2010
    ..In additon, our results further contribute to identifying common pathological pathways involved both in aging and in neurodegenerative disease development...
  42. ncbi request reprint Redox modulation of heat shock protein expression by acetylcarnitine in aging brain: relationship to antioxidant status and mitochondrial function
    V Calabrese
    Section of Biochemistry and Molecular Biology, Department of Chemistry, Faculty of Medicine, University of Catania, Catania, Italy
    Antioxid Redox Signal 8:404-16. 2006
    ..Particularly, modulation of endogenous cellular defense mechanisms via acetyl-L-carnitine may represent an innovative approach to therapeutic intervention in diseases causing tissue damage, such as neurodegeneration...
  43. 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...
  44. doi request reprint Decreased expression and increased oxidation of plasma haptoglobin in Alzheimer disease: Insights from redox proteomics
    A Cocciolo
    Department of Biochemical Sciences, Sapienza University of Rome, Rome, Italy
    Free Radic Biol Med 53:1868-76. 2012
    ..Our findings suggest that alterations in proteins acting as extracellular chaperones may contribute to exacerbating amyloid-β toxicity in the peripheral system and may be considered a putative marker of disease progression...
  45. ncbi request reprint Redox regulation of heat shock protein expression in aging and neurodegenerative disorders associated with oxidative stress: a nutritional approach
    V Calabrese
    Department of Chemistry, Section of Biochemistry and Molecular Biology, Faculty of Medicine, University of Catania, Catania, Italy
    Amino Acids 25:437-44. 2003
    ..Consistent with this notion, maintenance or recovery of the activity of vitagenes, such as the HO gene, conceivably may delay the aging process and decrease the occurrence of age-related neurodegenerative diseases...
  46. 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...
  47. 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...
  48. ncbi request reprint Increased expression of heat shock proteins in rat brain during aging: relationship with mitochondrial function and glutathione redox state
    V Calabrese
    Section of Biochemistry and Molecular Biology, Department of Chemistry, Faculty of Medicine, University of Catania, Viale Andrea Doria No 6, 95100 Catania, Italy
    Mech Ageing Dev 125:325-35. 2004
    ..Conceivably, heat shock signal pathway by increasing cellular stress resistance may represent a crucial mechanism of defence against free radical-induced damage occurring in aging brain and in neurodegenerative disorders...
  49. ncbi request reprint Nitrosative stress, cellular stress response, and thiol homeostasis in patients with Alzheimer's disease
    Vittorio Calabrese
    Department of Chemistry, Biochemistry, and Molecular Biology Section, Faculty of Medicine, University of Catania, Catania, Italy
    Antioxid Redox Signal 8:1975-86. 2006
    ..Our data support a role for nitrative stress in the pathogenesis of AD and indicate that the stress-responsive genes, such as HO-1 and TRXr, may represent important targets for novel cytoprotective strategies...
  50. 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
    ....
  51. 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
    ....
  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. 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...
  54. ncbi request reprint Disruption of thiol homeostasis and nitrosative stress in the cerebrospinal fluid of patients with active multiple sclerosis: evidence for a protective role of acetylcarnitine
    V Calabrese
    Department of Chemistry, Section of Biochemistry and Molecular Biology Faculty of Medicine, University of Catania, Catania, Italy
    Neurochem Res 28:1321-8. 2003
    ....
  55. 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...
  56. ncbi request reprint Long-term ethanol administration enhances age-dependent modulation of redox state in different brain regions in the rat: protection by acetyl carnitine
    V Calabrese
    Biochemistry and Molecular Biology Section, Department of Chemistry, Faculty of Medicine, University of Catania, Catania, Italy
    Int J Tissue React 24:97-104. 2002
    ..Administration of acetyl carnitine greatly reduces these metabolic abnormalities. This evidence supports the pharmacological potential of acetyl carnitine in the management of alcoholic disturbances...
  57. 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...
  58. 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
    ....
  59. 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...
  60. 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...
  61. 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...
  62. 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...
  63. 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...
  64. 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...
  65. 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...
  66. 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...
  67. 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
    ....
  68. 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...
  69. 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...
  70. 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...
  71. 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...
  72. 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...
  73. ncbi request reprint Proteomic analysis of 4-hydroxy-2-nonenal-modified proteins in G93A-SOD1 transgenic mice--a model of familial amyotrophic lateral sclerosis
    Marzia Perluigi
    Department of Biochemical Sciences, University of Rome La Sapienza, Rome 00185, Italy
    Free Radic Biol Med 38:960-8. 2005
    ..These results support the role of oxidative stress as a major mechanism in the pathogenesis of ALS. Structural alteration and activity decline of functional proteins may consistently contribute to the neurodegeneration process in ALS...
  74. 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...
  75. 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...
  76. 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...
  77. 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...
  78. 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...
  79. 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...
  80. 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...
  81. 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...
  82. doi request reprint Oxidative damage in rat brain during aging: interplay between energy and metabolic key target proteins
    F Di Domenico
    Department of Biochemical Sciences, Sapienza University of Rome, P le A Moro 5, 00185 Rome, Italy
    Neurochem Res 35:2184-92. 2010
    ..These results further confirm that increased protein oxidation coupled with decreased reducing systems are characteristic hallmarks of aging and aging-related degenerative processes...
  83. 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...
  84. 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...
  85. 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
    ....
  86. 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...
  87. 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...
  88. 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...
  89. 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...
  90. 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...
  91. 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...
  92. 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...
  93. 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
    ....
  94. 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...
  95. 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
    ....
  96. doi request reprint Protective effect of ferulic acid ethyl ester against oxidative stress mediated by UVB irradiation in human epidermal melanocytes
    F Di Domenico
    Department of Biochemical Sciences, University of Rome La Sapienza, P le Aldo Moro, 5 00185 Rome, Italy
    Free Radic Res 43:365-75. 2009
    ..Moreover FAEE prevented iNOS induction, thus suppressing the secondary generation of NO-derived oxidizing agents. FAEE may represent a potentially effective pharmacological approach to reduce UV radiation-induced skin damage...
  97. 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
    ....
  98. 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...
  99. 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...
  100. 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...
  101. 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...