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Genomes and Genes | D A ButterfieldSummaryAffiliation: University of Kentucky Country: USA Publications
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Publications
Rodent Abeta(1-42) exhibits oxidative stress properties similar to those of human Abeta(1-42): Implications for proposed mechanisms of toxicityDebra Boyd-Kimball
Department of Chemistry, Center for Membrane Sciences, University of Kentucky Lexington, KY 40506-0055, USA
J Alzheimers Dis 6:515-25. 2004....
Redox proteomics in selected neurodegenerative disorders: from its infancy to future applicationsD 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....
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 brainD 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...
Effects of UVB-induced oxidative stress on protein expression and specific protein oxidation in normal human epithelial keratinocytes: a proteomic approachMarzia Perluigi
Laboratory of Virology, IFO Regina Elena National Cancer Institute V, Messi d Oro, 156 00156 Rome, Italy
Proteome Sci 8:13. 2010....
Amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity: implications for neurodegeneration in Alzheimer's disease brain. A reviewD Allan Butterfield
Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506, USA
Free Radic Res 36:1307-13. 2002....
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 progressionFabio 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...
Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal deathD 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....
Amyloid beta-peptide and amyloid pathology are central to the oxidative stress and inflammatory cascades under which Alzheimer's disease brain existsD 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...
Vitamin E and neurodegenerative disorders associated with oxidative stressD 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...
The critical role of methionine 35 in Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicityD 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...
Lipid peroxidation and protein oxidation in Alzheimer's disease brain: potential causes and consequences involving amyloid beta-peptide-associated free radical oxidative stressD 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....
Alzheimer's amyloid beta-peptide (1-42): involvement of methionine residue 35 in the oxidative stress and neurotoxicity properties of this peptideD 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...
The glutamatergic system and Alzheimer's disease: therapeutic implicationsD 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...
Oxidatively modified glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and Alzheimer's disease: many pathways to neurodegenerationD 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...
Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brainD 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...
Proteomics for the identification of specifically oxidized proteins in brain: technology and application to the study of neurodegenerative disordersD 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....
Amyloid beta-peptide [1-42]-associated free radical-induced oxidative stress and neurodegeneration in Alzheimer's disease brain: mechanisms and consequencesD 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...
Proteomic analysis of oxidatively modified proteins in Alzheimer's disease brain: insights into neurodegenerationD 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...
Involvements of the lipid peroxidation product, HNE, in the pathogenesis and progression of Alzheimer's diseaseD 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...
Proteomics in Alzheimer's disease: insights into potential mechanisms of neurodegenerationD 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...
Multifunctional roles of enolase in Alzheimer's disease brain: beyond altered glucose metabolismD 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...
Lectin-affinity chromatography brain glycoproteomics and Alzheimer disease: insights into protein alterations consistent with the pathology and progression of this dementing disorderD 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...
Redox proteomics identification of oxidatively modified brain proteins in inherited Alzheimer's disease: an initial assessmentD 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...
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 diseaseD 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...
Oxidative stress in Alzheimer's disease brain: new insights from redox proteomicsD 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...
Redox proteomics in some age-related neurodegenerative disorders or models thereofD 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...
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 stresH 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...
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 diseaseD 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...
Elevated protein-bound levels of the lipid peroxidation product, 4-hydroxy-2-nonenal, in brain from persons with mild cognitive impairmentD Allan Butterfield
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
Neurosci Lett 397:170-3. 2006....
Redox proteomics identification of oxidatively modified hippocampal proteins in mild cognitive impairment: insights into the development of Alzheimer's diseaseD 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...
Roles of amyloid beta-peptide-associated oxidative stress and brain protein modifications in the pathogenesis of Alzheimer's disease and mild cognitive impairmentD 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...
Redox proteomics identification of oxidatively modified brain proteins in Alzheimer's disease and mild cognitive impairment: insights into the progression of this dementing disorderD Allan Butterfield
Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
J Alzheimers Dis 12:61-72. 2007....
Cholesterol-independent neuroprotective and neurotoxic activities of statins: perspectives for statin use in Alzheimer disease and other age-related neurodegenerative disordersD 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...
Roles of 3-nitrotyrosine- and 4-hydroxynonenal-modified brain proteins in the progression and pathogenesis of Alzheimer's diseaseD Allan Butterfield
Department of Chemistry, University of Kentucky, Lexington, KY 40506 0055, USA
Free Radic Res 45:59-72. 2011....
In vivo oxidative stress in brain of Alzheimer disease transgenic mice: Requirement for methionine 35 in amyloid beta-peptide of APPD 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...
In vivo protection by the xanthate tricyclodecan-9-yl-xanthogenate against amyloid beta-peptide (1-42)-induced oxidative stressM 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...
Antioxidant activity of the organotellurium compound 3-[4-(N,N-dimethylamino)benzenetellurenyl]propanesulfonic acid against oxidative stress in synaptosomal membrane systems and neuronal culturesJ 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...
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....
Vulnerability of synaptosomes from apoE knock-out mice to structural and oxidative modifications induced by A beta(1-40): implications for Alzheimer's diseaseC 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...
Redox proteomics in aging rat brain: involvement of mitochondrial reduced glutathione status and mitochondrial protein oxidation in the aging processM 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...
Redox modulation of heat shock protein expression by acetylcarnitine in aging brain: relationship to antioxidant status and mitochondrial functionV 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...
5-Aminosalicylic acid protection against oxidative damage to synaptosomal membranes by alkoxyl radicals in vitroJ 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...
The glial glutamate transporter, GLT-1, is oxidatively modified by 4-hydroxy-2-nonenal in the Alzheimer's disease brain: the role of Abeta1-42C 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...
Increased expression of heat shock proteins in rat brain during aging: relationship with mitochondrial function and glutathione redox stateV 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...
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 ED 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...
Redox regulation of heat shock protein expression in aging and neurodegenerative disorders associated with oxidative stress: a nutritional approachV 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...
Evidence of increased oxidative damage in subjects with mild cognitive impairmentJ 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)...
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 chemobrainG 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...
Glutathione elevation and its protective role in acrolein-induced protein damage in synaptosomal membranes: relevance to brain lipid peroxidation in neurodegenerative diseaseC B Pocernich
Department of Chemistry, 125 Chemistry-Physics Building, University of Kentucky, Lexington, KY 40506, USA
Neurochem Int 39:141-9. 2001....
Disruption of thiol homeostasis and nitrosative stress in the cerebrospinal fluid of patients with active multiple sclerosis: evidence for a protective role of acetylcarnitineV Calabrese
Department of Chemistry, Section of Biochemistry and Molecular Biology Faculty of Medicine, University of Catania, Catania, Italy
Neurochem Res 28:1321-8. 2003....
Protein oxidation in the brain in Alzheimer's diseaseM Y Aksenov
Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
Neuroscience 103:373-83. 2001....
Antisense directed at the Abeta region of APP decreases brain oxidative markers in aged senescence accelerated miceH 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...
Long-term ethanol administration enhances age-dependent modulation of redox state in different brain regions in the rat: protection by acetyl carnitineV 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...
Free radical oxidation of brain proteins in accelerated senescence and its modulation by N-tert-butyl-alpha-phenylnitroneD 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...
Nitrosative stress, cellular stress response, and thiol homeostasis in patients with Alzheimer's diseaseVittorio 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...
A neuronal model of Alzheimer's disease: an insight into the mechanisms of oxidative stress-mediated mitochondrial injuryP 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...
Proteomic identification of proteins specifically oxidized by intracerebral injection of amyloid beta-peptide (1-42) into rat brain: implications for Alzheimer's diseaseD Boyd-Kimball
Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, KY 40506 0055, USA
Neuroscience 132:313-24. 2005....
Identification of nitrated proteins in Alzheimer's disease brain using a redox proteomics approachRukhsana 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...
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 diseaseHafiz 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...
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 synthesisH 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...
Quantitative proteomics analysis of differential protein expression and oxidative modification of specific proteins in the brains of old miceH 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...
Role of spermine in amyloid beta-peptide-associated free radical-induced neurotoxicityS M Yatin
Department of Chemistry and Center of Membrane Sciences, University of Kentucky, Lexington, 40506-0055, USA
J Neurosci Res 63:395-401. 2001....
Amyloid beta-peptide effects on synaptosomes from apolipoprotein E-deficient miceJ 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...
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 diseaseM 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...
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 AbeRukhsana 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...
Proteomic identification of oxidized mitochondrial proteins following experimental traumatic brain injuryWycliffe 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...
Proteomic identification of oxidatively modified proteins in Alzheimer's disease brain. Part I: creatine kinase BB, glutamine synthase, and ubiquitin carboxy-terminal hydrolase L-1Alessandra 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...
Apolipoprotein E modulates Alzheimer's Abeta(1-42)-induced oxidative damage to synaptosomes in an allele-specific mannerChristopher 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...
Proteomic analysis of 4-hydroxy-2-nonenal-modified proteins in G93A-SOD1 transgenic mice--a model of familial amyotrophic lateral sclerosisMarzia 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...
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 diseaseHafiz 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...
Oxidative modification of glutamine synthetase by amyloid beta peptideM 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...
Evidence of oxidative damage in Alzheimer's disease brain: central role for amyloid beta-peptideD 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...
D609 inhibits ionizing radiation-induced oxidative damage by acting as a potent antioxidantD 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...
Oxidative modification and down-regulation of Pin1 in Alzheimer's disease hippocampus: A redox proteomics analysisRukhsana 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...
Proteomics analysis of the Alzheimer's disease hippocampal proteomeRukhsana 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...
Free radical mediated oxidative stress and toxic side effects in brain induced by the anti cancer drug adriamycin: insight into chemobrainGururaj 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...
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...
Oxidatively modified, mitochondria-relevant brain proteins in subjects with Alzheimer disease and mild cognitive impairmentRukhsana 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...
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 diseaseGiovanna 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...
Methamphetamine toxicity is attenuated in mice that overexpress human manganese superoxide dismutaseW 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...
The expression of key oxidative stress-handling genes in different brain regions in Alzheimer's diseaseM Y Aksenov
Sanders Brown Center on Aging, University of Kentucky, Lexington 40536, USA
J Mol Neurosci 11:151-64. 1998....
Brain protein oxidation in age-related neurodegenerative disorders that are associated with aggregated proteinsD 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...
Oxidative damage in rat brain during aging: interplay between energy and metabolic key target proteinsF 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...
Oxidative damage in brain from human mutant APP/PS-1 double knock-in mice as a function of ageHafiz 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...
Protective effect of quercetin in primary neurons against Abeta(1-42): relevance to Alzheimer's diseaseMubeen 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...
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 diseaseMiranda 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...
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 oxidativMubeen 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...
Redox proteomics analysis of oxidatively modified proteins in G93A-SOD1 transgenic mice--a model of familial amyotrophic lateral sclerosisH Fai Poon
Department of Chemistry, University of Kentucky, Lexington KY 40506, USA
Free Radic Biol Med 39:453-62. 2005....
Neurotoxicity and oxidative stress in D1M-substituted Alzheimer's A beta(1-42): relevance to N-terminal methionine chemistry in small model peptidesDebra 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...
Role of glycine-33 and methionine-35 in Alzheimer's amyloid beta-peptide 1-42-associated oxidative stress and neurotoxicityJaroslaw 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...
Oxidatively modified GST and MRP1 in Alzheimer's disease brain: implications for accumulation of reactive lipid peroxidation productsRukhsana 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...
Protective effect of the xanthate, D609, on Alzheimer's amyloid beta-peptide (1-42)-induced oxidative stress in primary neuronal cellsRukhsana 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...
Proteomic identification of nitrated proteins in Alzheimer's disease brainAlessandra Castegna
Department of Chemistry, Center of Membrane Sciences, University of Kentucky, Lexington, Kentucky 40506 0055, USA
J Neurochem 85:1394-401. 2003....
Protective effect of ferulic acid ethyl ester against oxidative stress mediated by UVB irradiation in human epidermal melanocytesF 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...
Brain oxidative stress in animal models of accelerated aging and the age-related neurodegenerative disorders, Alzheimer's disease and Huntington's diseaseD 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....
APP and PS-1 mutations induce brain oxidative stress independent of dietary cholesterol: implications for Alzheimer's diseaseHafiz 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...
Oxidatively modified proteins in Alzheimer's disease (AD), mild cognitive impairment and animal models of AD: role of Abeta in pathogenesisRukhsana 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...
Proteomic identification of HNE-bound proteins in early Alzheimer disease: Insights into the role of lipid peroxidation in the progression of ADTanea 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....
Detection of 4-hydroxy-2-nonenal- and 3-nitrotyrosine-modified proteins using a proteomics approachRukhsana 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...
Proteomic identification of oxidatively modified proteins in Alzheimer's disease brain. Part II: dihydropyrimidinase-related protein 2, alpha-enolase and heat shock cognate 71Alessandra 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...
Oxidative stress precedes fibrillar deposition of Alzheimer's disease amyloid beta-peptide (1-42) in a transgenic Caenorhabditis elegans modelJennifer 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...
