J N Keller

Summary

Affiliation: University of Kentucky
Country: USA

Publications

  1. ncbi The many nuances of oxidative stress and proteolysis
    Jeffrey N Keller
    Antioxid Redox Signal 8:119-20. 2006
  2. ncbi Oxidized lipoproteins increase reactive oxygen species formation in microglia and astrocyte cell lines
    J N Keller
    Sanders Brown Center on Aging, University of Kentucky, 101 Sanders Brown Building, Lexington, KY, 40536 0230, USA
    Brain Res 830:10-5. 1999
  3. ncbi 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
  4. ncbi Age-related neuropathology, cognitive decline, and Alzheimer's disease
    Jeffrey N Keller
    Department of Anatomy and Neurobiology and Sanders Brown Center on Aging, University of Kentucky, 800 South Limestone, Lexington, KY 40536 0230, USA
    Ageing Res Rev 5:1-13. 2006
  5. ncbi Autophagy, proteasomes, lipofuscin, and oxidative stress in the aging brain
    Jeffrey N Keller
    203 Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    Int J Biochem Cell Biol 36:2376-91. 2004
  6. ncbi The proteasome in brain aging
    Jeffrey N Keller
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536 0230, USA
    Ageing Res Rev 1:279-93. 2002
  7. ncbi Dopamine induces proteasome inhibition in neural PC12 cell line
    J N Keller
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    Free Radic Biol Med 29:1037-42. 2000
  8. ncbi Anti-death properties of TNF against metabolic poisoning: mitochondrial stabilization by MnSOD
    A J Bruce-Keller
    Sanders Brown Research Center on Aging, Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neuroimmunol 93:53-71. 1999
  9. ncbi 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
  10. ncbi Proteasome inhibition in oxidative stress neurotoxicity: implications for heat shock proteins
    Q Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky, USA
    J Neurochem 77:1010-7. 2001

Collaborators

Detail Information

Publications58

  1. ncbi The many nuances of oxidative stress and proteolysis
    Jeffrey N Keller
    Antioxid Redox Signal 8:119-20. 2006
  2. ncbi Oxidized lipoproteins increase reactive oxygen species formation in microglia and astrocyte cell lines
    J N Keller
    Sanders Brown Center on Aging, University of Kentucky, 101 Sanders Brown Building, Lexington, KY, 40536 0230, USA
    Brain Res 830:10-5. 1999
    ....
  3. ncbi 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)...
  4. ncbi Age-related neuropathology, cognitive decline, and Alzheimer's disease
    Jeffrey N Keller
    Department of Anatomy and Neurobiology and Sanders Brown Center on Aging, University of Kentucky, 800 South Limestone, Lexington, KY 40536 0230, USA
    Ageing Res Rev 5:1-13. 2006
    ....
  5. ncbi Autophagy, proteasomes, lipofuscin, and oxidative stress in the aging brain
    Jeffrey N Keller
    203 Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    Int J Biochem Cell Biol 36:2376-91. 2004
    ....
  6. ncbi The proteasome in brain aging
    Jeffrey N Keller
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536 0230, USA
    Ageing Res Rev 1:279-93. 2002
    ....
  7. ncbi Dopamine induces proteasome inhibition in neural PC12 cell line
    J N Keller
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    Free Radic Biol Med 29:1037-42. 2000
    ..Together, these data indicate that dopamine induces proteasome inhibition that is dependent, in part, on ROS and dopamine uptake, and suggest a possible role for proteasome inhibition in dopamine toxicity...
  8. ncbi Anti-death properties of TNF against metabolic poisoning: mitochondrial stabilization by MnSOD
    A J Bruce-Keller
    Sanders Brown Research Center on Aging, Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536 0230, USA
    J Neuroimmunol 93:53-71. 1999
    ..Additional studies showed that levels of oxidative stress and striatal lesion size following 3-NP administration in vivo are increased in mice lacking TNF receptors...
  9. ncbi 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...
  10. ncbi Proteasome inhibition in oxidative stress neurotoxicity: implications for heat shock proteins
    Q Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky, USA
    J Neurochem 77:1010-7. 2001
    ....
  11. ncbi 4-hydroxynonenal increases neuronal susceptibility to oxidative stress
    J N Keller
    Sanders Brown Center on Aging, University of Kentucky, Lexington 40536 0230, USA
    J Neurosci Res 58:823-30. 1999
    ..In addition, the present study indicates a possible mechanism for reactive oxygen species and lipid peroxidation toxicity in neurodegenerative conditions...
  12. ncbi Antiinflammatory effects of estrogen on microglial activation
    A J Bruce-Keller
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington 40536, USA
    Endocrinology 141:3646-56. 2000
    ..These results describe a novel mechanism by which estrogen may attenuate the progression of neurodegenerative disease and suggest new pathways for therapeutic intervention in clinical settings...
  13. ncbi 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...
  14. ncbi Oxidative stress-associated impairment of proteasome activity during ischemia-reperfusion injury
    J N Keller
    Sanders Bronwn Research Center on Aging, Department of Biochemistry, University of Kentucky, Lexington 40536 0230, USA
    J Cereb Blood Flow Metab 20:1467-73. 2000
    ..Together, these data indicate that proteasome inhibition occurs during cerebral ischemia-reperfusion injury and is mediated, at least in part, by oxidative stress...
  15. ncbi Proteasomes and proteasome inhibition in the central nervous system
    Q Ding
    Department of Anatomy, University of Kentucky, Lexington, KY, USA
    Free Radic Biol Med 31:574-84. 2001
    ..The focus of this review is to describe what is currently known about proteasome biology in the central nervous system and to discuss the possible role of proteasome inhibition in the neurodegenerative process...
  16. ncbi Lysophosphatidic acid induction of neuronal apoptosis and necrosis
    M R Steiner
    Department of Microbiology and Immunology, University of Kentucky, Lexington 40536, USA
    Ann N Y Acad Sci 905:132-41. 2000
    ..Thus, LPA-induced neuronal apoptosis is associated with mitochondrial alterations, the generation of reactive oxygen species and nitric oxide, and protection by pretreatment with a serum constituent, insulin-like growth factor 1...
  17. ncbi 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...
  18. ncbi Pro-inflammatory and pro-oxidant properties of the HIV protein Tat in a microglial cell line: attenuation by 17 beta-estradiol
    A J Bruce-Keller
    Department of Anatomy, University of Kentucky, Lexington, Kentucky, USA
    J Neurochem 78:1315-24. 2001
    ..Together, these data elucidate specific components of the microglial response to Tat and suggest that Tat could contribute to the neuropathology associated with HIV infection through microglial promulgation of oxidative stress...
  19. ncbi Ribosome dysfunction is an early event in Alzheimer's disease
    Qunxing Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536-0230, USA
    J Neurosci 25:9171-5. 2005
    ....
  20. ncbi Ump1 extends yeast lifespan and enhances viability during oxidative stress: central role for the proteasome?
    Qinghua Chen
    Sanders Brown Center on Aging, Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536 0230, USA
    Free Radic Biol Med 40:120-6. 2006
    ..Taken together these data strongly support a role for the proteasome serving as a central regulator of cellular viability during oxidative stress and during aging...
  21. ncbi 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...
  22. ncbi LMP2 knock-out mice have reduced proteasome activities and increased levels of oxidatively damaged proteins
    Qunxing Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536, USA
    Antioxid Redox Signal 8:130-5. 2006
    ..Results from this study demonstrate for the first time that individual proteasome subunits are important for the regulation of age-related changes in both proteasome activity and protein oxidation...
  23. ncbi Proteasome regulation of oxidative stress in aging and age-related diseases of the CNS
    Qunxing Ding
    Sanders-Brown Center on Aging, Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536-0230, USA
    Antioxid Redox Signal 8:163-72. 2006
    ..Additionally we discuss the likelihood that the 20S proteasome and 26S proteasome may play different roles in regulating oxidative stress and neurotoxicity in the aging CNS, and in age-related disorders of the CNS...
  24. ncbi Decreased RNA, and increased RNA oxidation, in ribosomes from early Alzheimer's disease
    Qunxing Ding
    Anatomy and Neurobiology, University of Kentucky, 205 Sanders-Brown Center on Aging, Lexington, KY 40536-0230, USA
    Neurochem Res 31:705-10. 2006
    ..Together, these data strongly suggest a role for RNA alterations within the ribosome as a mediator of decreased protein synthesis in both MCI and AD...
  25. ncbi Age-related alterations of Apolipoprotein E and interleukin-1beta in the aging brain
    Jillian R Gee
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536 0230, USA
    Biogerontology 7:69-79. 2006
    ..Taken together, these studies demonstrate that ApoE expression is not altered during normal brain aging, but suggest that there may be a relationship between ApoE and IL-1beta transcription in the cerebral cortex...
  26. ncbi Aging and dietary restriction effects on ubiquitination, sumoylation, and the proteasome in the heart
    Feng Li
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
    Mech Ageing Dev 129:515-21. 2008
    ....
  27. ncbi Amyloid peptides in different assembly states and related effects on isolated and cellular proteasomes
    Valentina Cecarini
    Department of Molecular, Cellular and Animal Biology, University of Camerino, 62032 Camerino MC, Italy
    Brain Res 1209:8-18. 2008
    ..Furthermore, the altered proteasome functionality is not associated with a decrease in cell viability, but is linked with increased levels of protein oxidation...
  28. ncbi Oxidative stress alters neuronal RNA- and protein-synthesis: Implications for neural viability
    Qunxing Ding
    Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536 0230, USA
    Free Radic Res 41:903-10. 2007
    ..These data also suggest that there is a complex relationship between the ability of oxidative stressors to modulate RNA- and protein-synthesis, and the ability of oxidative stressors to ultimately induce neuron death...
  29. ncbi Abeta solubility and deposition during AD progression and in APPxPS-1 knock-in mice
    M Paul Murphy
    Department of Molecular and Cellular Biochemistry, Sanders Brown Center on Aging, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    Neurobiol Dis 27:301-11. 2007
    ..These data suggest that distinct changes in Abeta occur throughout the progression of AD, and that elevations in Abeta42 occur at an early, clinically defined stage...
  30. ncbi RNA in brain disease: no longer just "the messenger in the middle"
    Peter T Nelson
    Department of Pathology and Division of Neuropathology, University of Kentucky, Sanders Brown Center on Aging, Lexington, Kentucky 40536 0230, USA
    J Neuropathol Exp Neurol 66:461-8. 2007
    ....
  31. ncbi Oxidative inactivation of the proteasome in Alzheimer's disease
    Valentina Cecarini
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    Free Radic Res 41:673-80. 2007
    ..Together, these data confirm that impairments in the function of purified proteasomes occurs in the earliest stages of AD, and directly support a role for oxidative inactivation contributing to declines in proteasome function in AD...
  32. ncbi 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...
  33. ncbi Oxidative damage, protein synthesis, and protein degradation in Alzheimer's disease
    Qunxing Ding
    Anatomy and Neurobiology, Sanders Brown Center on Aging, University of Kentucky, Lexington KY 40536, USA
    Curr Alzheimer Res 4:73-9. 2007
    ....
  34. ncbi Protein oxidation and cellular homeostasis: Emphasis on metabolism
    Valentina Cecarini
    Post Graduate School of Clinical Biochemistry, Departments of Molecular and Cellular and Animal Biology, University of Camerino, Camerino, Italy
    Biochim Biophys Acta 1773:93-104. 2007
    ..Together, this review describes a potential role for elevated levels of protein oxidation contributing to cellular dysfunction and oxidative stress via impacts on cellular metabolism...
  35. ncbi Alpha-synuclein alters proteasome function, protein synthesis, and stationary phase viability
    Qinghua Chen
    Sanders Brown Center on Aging, The Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536, USA
    J Biol Chem 280:30009-17. 2005
    ....
  36. ncbi Polyglutamine expansion, protein aggregation, proteasome activity, and neural survival
    Qunxing Ding
    Department of Anatomy, University of Kentucky, Lexington, Kentucky 40536, USA
    J Biol Chem 277:13935-42. 2002
    ....
  37. ncbi The neuregulin GGF2 attenuates free radical release from activated microglial cells
    Filomena O Dimayuga
    Department of Anatomy and Neurobiology, MN 222 Chandler Medical Center, University of Kentucky, Lexington 40536-0298, USA
    J Neuroimmunol 136:67-74. 2003
    ..Overall, these results indicate that the neuregulin rhGGF2 may have anti-inflammatory and antioxidant properties in the brain, and may also provide trophic support for brain-resident microglial cells...
  38. ncbi Role of the proteasome in protein oxidation and neural viability following low-level oxidative stress
    Qunxing Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA
    FEBS Lett 546:228-32. 2003
    ..Taken together, these data indicate that maintaining neural proteasome function may be critical to preventing neurotoxicity, but not the increase in protein oxidation, following low-level oxidative stress...
  39. ncbi Characterization of chronic low-level proteasome inhibition on neural homeostasis
    Qunxing Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky 40536 0230, USA
    J Neurochem 86:489-97. 2003
    ....
  40. ncbi Does proteasome inhibition play a role in mediating neuropathology and neuron death in Alzheimer's disease?
    Qunxing Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington KY 40536, USA
    J Alzheimers Dis 5:241-5. 2003
    ..Experimental evidence supporting this hypothesis, as well as the scientific implications of this hypothesis are discussed...
  41. ncbi Synaptic transport of human immunodeficiency virus-Tat protein causes neurotoxicity and gliosis in rat brain
    Annadora J Bruce-Keller
    Department of Anatomy and Neurobiology, MN 222 Chandler Medical Center, University of Kentucky, Lexington, Kentucky 40536 0298, USA
    J Neurosci 23:8417-22. 2003
    ..Tat may thus be an important participant in brain dysfunction in HIV dementia...
  42. ncbi Proteasome inhibition alters neural mitochondrial homeostasis and mitochondria turnover
    Patrick G Sullivan
    Department of Anatomy and Neurobiology, 205 Sanders-Brown Building, University of Kentucky, Lexington, KY 40536, USA
    J Biol Chem 279:20699-707. 2004
    ....
  43. ncbi Analysis of gene expression in neural cells subject to chronic proteasome inhibition
    Qunxing Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA
    Free Radic Biol Med 36:445-55. 2004
    ....
  44. ncbi Loss of an individual proteasome subunit alters motor function but not cognitive function or ambulation in mice
    Sarah Martin
    Sanders Brown Center on Aging, University of Kentucky, 205 Sanders Brown Center on Aging, 800 S Limestone, Lexington, KY 40536, USA
    Neurosci Lett 357:76-8. 2004
    ..These data demonstrate for the first time that specific proteasome subunits may play a role in regulating both brain function and body weight...
  45. ncbi Proteasome synthesis and assembly are required for survival during stationary phase
    Qinghua Chen
    Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Free Radic Biol Med 37:859-68. 2004
    ..These data also suggest a role for impaired proteasome-mediated protein degradation in increased protein oxidation and cell death observed during the aging of eukaryotic cells...
  46. ncbi Estrogen increases proteasome activity in murine microglial cells
    Janelle L Reed
    Department of Anatomy and Neurobiology, MN 222 Chandler Medical Center, University of Kentucky, 800 S. Rose Street, Lexington, KY 40536-0298, USA
    Neurosci Lett 367:60-5. 2004
    ..Hence, these data demonstrate that through the MAPK pathway, estrogen can upregulate proteasome activity, suggesting a possible mechanism for estrogen's cytoprotective effects...
  47. ncbi Proteasome inhibition increases DNA and RNA oxidation in astrocyte and neuron cultures
    Qunxing Ding
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, Kentucky, USA
    J Neurochem 91:1211-8. 2004
    ....
  48. ncbi RNA interference toward UMP1 induces proteasome inhibition in Saccharomyces cerevisiae: evidence for protein oxidation and autophagic cell death
    Qinghua Chen
    Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA
    Free Radic Biol Med 38:226-34. 2005
    ..cerevisiae and demonstrate the ability of proteasome inhibition to induce cytotoxic alterations in S. cerevisiae...
  49. ncbi The stationary phase model of aging in yeast for the study of oxidative stress and age-related neurodegeneration
    Quinghua Chen
    Sanders-Brown Center on Aging, University of Kentucky, Lexington, 40536-0230, USA
    Biogerontology 6:1-13. 2005
    ..cerevisiae as a model system with which to explore the molecular basis for neuronal alterations observed in normal brain aging as well as multiple age-related diseases of the CNS...
  50. ncbi Proteasome inhibition induces reversible impairments in protein synthesis
    Qunxing Ding
    205 Sanders-Brown Center on Aging, 800 S. Limestone, University of Kentucky, Lexington, Kentucky 40536-0230, USA
    FASEB J 20:1055-63. 2006
    ..Together these findings have important implications for understanding proteasome inhibition as a potential contributor to aging and age-related disease...
  51. ncbi Analysis of Werner's expression within the brain and primary neuronal culture
    Jillian Gee
    Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536 0230, USA
    Brain Res 940:44-8. 2002
    ..Taken together, these data indicate that WRN is present in the cells of the brain, expressed throughout primary neuronal cells in culture, possibly playing a developmental role in the central nervous system...
  52. ncbi Effects of aging and dietary restriction on ubiquitination, sumoylation, and the proteasome in the spleen
    Le Zhang
    Sanders Brown Center on Aging, 205 Sanders Brown, 800 South Limestone, University of Kentucky, Lexington, KY 40536 0230, USA
    FEBS Lett 581:5543-7. 2007
    ..Together, these data demonstrate for the first time the multiple effects of aging and DR on ubiquitination, sumoylation, and the proteasome in the spleen...
  53. ncbi Cytochrome c release and caspase activation after traumatic brain injury
    Patrick G Sullivan
    229 Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536-0230, USA
    Brain Res 949:88-96. 2002
    ..Our data suggest that several pro-apoptotic events occur following TBI, however the translocation of cytochrome c itself and/or other events upstream of caspase activation/inhibition may be sufficient to induce neuronal cell death...
  54. ncbi Enhanced toxicity to the catecholamine tyramine in polyglutamine transfected SH-SY5Y cells
    Rebecca R Smith
    Department of Neurology, University of Kentucky, Lexington, KY 40536-0284, USA
    Neurochem Res 30:527-31. 2005
    ..These observations support the notion that the metabolism of dopamine plays a role in neuron death in Huntington's disease...
  55. ncbi Astrocytes: regulation of brain homeostasis via apolipoprotein E
    Jillian R Gee
    Department of Anatomy and Neurobiology, University of Kentucky, 205 Sanders-Brown, 800 S. Limestone, Lexington, KY 40536-0230, USA
    Int J Biochem Cell Biol 37:1145-50. 2005
    ..This review highlights many of the diverse roles played by astrocytes in regulating brain homeostasis and discusses their potential role in a variety of disorders...
  56. ncbi Interplay between protein synthesis and degradation in the CNS: physiological and pathological implications
    Qunxing Ding
    Department of Anatomy and Neurobiology, and Sanders Brown Center on Aging, University of Kentucky, Lexington, KY 40536 0230, USA
    Trends Neurosci 30:31-6. 2007
    ..In this review, we discuss evidence for interplay between the UPS and protein-synthesis machinery, and outline the implications of this crosstalk for physiological and pathological processes in the CNS...
  57. ncbi 4-Hydroxynonenal oxidatively modifies histones: implications for Alzheimer's disease
    Jennifer Drake
    Department of Chemistry, University of Kentucky, Lexington, KY 40506, USA
    Neurosci Lett 356:155-8. 2004
    ..Conceivably, altered DNA-histone interactions, subsequent to oxidative modification of histones by the lipid peroxidation product HNE, may contribute to the vulnerability of DNA to oxidation in AD brain...
  58. ncbi Modulation of apolipoprotein E and interleukin-1beta in the aging liver
    Jillian R Gee
    Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA
    Exp Gerontol 40:409-15. 2005
    ..Taken together, these studies demonstrate that ApoE expression is altered during normal aging, and indicates that there is no correlation between ApoE and IL-1beta expression in the aging liver...