A R White

Summary

Affiliation: University of Melbourne
Country: Australia

Publications

  1. ncbi Contrasting, species-dependent modulation of copper-mediated neurotoxicity by the Alzheimer's disease amyloid precursor protein
    Anthony R White
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    J Neurosci 22:365-76. 2002
  2. pmc Neuroprotective copper bis(thiosemicarbazonato) complexes promote neurite elongation
    Laura Bica
    Department of Pathology, The University of Melbourne, Melbourne, Victoria, Australia
    PLoS ONE 9:e90070. 2014
  3. pmc Inhibition of TDP-43 accumulation by bis(thiosemicarbazonato)-copper complexes
    Sarah J Parker
    Department of Pathology, The University of Melbourne, Parkville, Victoria, Australia
    PLoS ONE 7:e42277. 2012
  4. pmc Kinase Inhibitor Screening Identifies Cyclin-Dependent Kinases and Glycogen Synthase Kinase 3 as Potential Modulators of TDP-43 Cytosolic Accumulation during Cell Stress
    Diane Moujalled
    Department of Pathology, The University of Melbourne, Victoria, Australia and Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia
    PLoS ONE 8:e67433. 2013
  5. pmc Altered biometal homeostasis is associated with CLN6 mRNA loss in mouse neuronal ceroid lipofuscinosis
    Katja M Kanninen
    Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia Present address AI Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio 70211, Finland
    Biol Open 2:635-46. 2013
  6. pmc Deregulation of subcellular biometal homeostasis through loss of the metal transporter, Zip7, in a childhood neurodegenerative disorder
    Alexandra Grubman
    Department of Pathology, The University of Melbourne, Parkville, VIC 3010, Australia
    Acta Neuropathol Commun 2:25. 2014
  7. doi Deregulation of biometal homeostasis: the missing link for neuronal ceroid lipofuscinoses?
    Alexandra Grubman
    Department of Pathology, The University of Melbourne, Victoria, 3010, Australia
    Metallomics 6:932-43. 2014
  8. doi Copper modulates the large dense core vesicle secretory pathway in PC12 cells
    Clare Duncan
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    Metallomics 5:700-14. 2013
  9. doi Copper complexes as therapeutic agents
    Clare Duncan
    Centre for Neuroscience and Department of Pathology, The University of Melbourne, Victoria, 3010, Australia
    Metallomics 4:127-38. 2012
  10. ncbi Clioquinol promotes cancer cell toxicity through tumor necrosis factor alpha release from macrophages
    Tai Du
    Centre for Neuroscience and Department of Pathology, University of Melbourne, Victoria, Australia 3010
    J Pharmacol Exp Ther 324:360-7. 2008

Collaborators

Detail Information

Publications67

  1. ncbi Contrasting, species-dependent modulation of copper-mediated neurotoxicity by the Alzheimer's disease amyloid precursor protein
    Anthony R White
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    J Neurosci 22:365-76. 2002
    ..Our findings also suggest that targeting of inhibitors to histidine residues at positions 147 and 151 of APP could significantly alter the oxidative potential of APP...
  2. pmc Neuroprotective copper bis(thiosemicarbazonato) complexes promote neurite elongation
    Laura Bica
    Department of Pathology, The University of Melbourne, Melbourne, Victoria, Australia
    PLoS ONE 9:e90070. 2014
    ....
  3. pmc Inhibition of TDP-43 accumulation by bis(thiosemicarbazonato)-copper complexes
    Sarah J Parker
    Department of Pathology, The University of Melbourne, Parkville, Victoria, Australia
    PLoS ONE 7:e42277. 2012
    ..These results demonstrate that Cu(II)(btsc) complexes could potentially be developed as a neuroprotective agent to modulate neuronal kinase function and inhibit TDP-43 aggregation. Further studies in TDP-43 animal models are warranted...
  4. pmc Kinase Inhibitor Screening Identifies Cyclin-Dependent Kinases and Glycogen Synthase Kinase 3 as Potential Modulators of TDP-43 Cytosolic Accumulation during Cell Stress
    Diane Moujalled
    Department of Pathology, The University of Melbourne, Victoria, Australia and Florey Institute of Neuroscience and Mental Health, Parkville, Victoria, Australia
    PLoS ONE 8:e67433. 2013
    ..This knowledge provides a valuable insight into the mechanisms controlling abnormal cytoplasmic TDP-43 accumulation and may herald new opportunities for kinase modulation-based therapeutic intervention in ALS and FTLD...
  5. pmc Altered biometal homeostasis is associated with CLN6 mRNA loss in mouse neuronal ceroid lipofuscinosis
    Katja M Kanninen
    Department of Pathology, The University of Melbourne, Parkville, Victoria 3010, Australia Present address AI Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio 70211, Finland
    Biol Open 2:635-46. 2013
    ..These data are consistent with a link between CLN6 expression and biometal homeostasis in CLN6 disease, and provide further support for altered cation transporter regulation as a key factor in neurodegeneration. ..
  6. pmc Deregulation of subcellular biometal homeostasis through loss of the metal transporter, Zip7, in a childhood neurodegenerative disorder
    Alexandra Grubman
    Department of Pathology, The University of Melbourne, Parkville, VIC 3010, Australia
    Acta Neuropathol Commun 2:25. 2014
    ..This study extended the concept that alteration of biometal functions is involved in pathology in these disorders, and investigated molecular mechanisms underlying impaired biometal trafficking in CLN6 disease...
  7. doi Deregulation of biometal homeostasis: the missing link for neuronal ceroid lipofuscinoses?
    Alexandra Grubman
    Department of Pathology, The University of Melbourne, Victoria, 3010, Australia
    Metallomics 6:932-43. 2014
    ..These results demonstrate that altered biometal homeostasis is a key feature of at least 4 genetically distinct forms of NCL disease. ..
  8. doi Copper modulates the large dense core vesicle secretory pathway in PC12 cells
    Clare Duncan
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    Metallomics 5:700-14. 2013
    ..Our findings demonstrate that elevated Cu can modulate LDCV metabolism potentially resulting in sequestration of Cu in this vesicle pool...
  9. doi Copper complexes as therapeutic agents
    Clare Duncan
    Centre for Neuroscience and Department of Pathology, The University of Melbourne, Victoria, 3010, Australia
    Metallomics 4:127-38. 2012
    ..This review seeks to provide a broad insight into some of the diverse actions of Cu complexes and demonstrate the strong future for these compounds as potential therapeutic agents...
  10. ncbi Clioquinol promotes cancer cell toxicity through tumor necrosis factor alpha release from macrophages
    Tai Du
    Centre for Neuroscience and Department of Pathology, University of Melbourne, Victoria, Australia 3010
    J Pharmacol Exp Ther 324:360-7. 2008
    ..These studies demonstrate that CQ can induce cancer cell toxicity through metal-dependent release of TNFalpha from macrophages. Our results may help to explain the targeted inhibition of tumor growth in vivo by CQ...
  11. pmc C-Jun N-terminal kinase controls TDP-43 accumulation in stress granules induced by oxidative stress
    Jodi Meyerowitz
    Department of Pathology, The University of Melbourne, Victoria, 3010, Australia
    Mol Neurodegener 6:57. 2011
    ..abstract:..
  12. ncbi Metal homeostasis in Alzheimer's disease
    Anthony R White
    The University of Melbourne, Department of Pathology, Victoria 3010, Australia
    Expert Rev Neurother 6:711-22. 2006
    ..This information will be vital for the development of safe and effective metal-based pharmaceuticals for the treatment of AD and, potentially, other neurodegenerative disorders...
  13. ncbi Degradation of the Alzheimer disease amyloid beta-peptide by metal-dependent up-regulation of metalloprotease activity
    Anthony R White
    Department of Pathology, University of Melbourne, Cnr Grattan Street and Royal Parade, Victoria 3010, Australia
    J Biol Chem 281:17670-80. 2006
    ..Our findings identify an alternative mechanism of action for CQ in the reduction of Abeta deposition in the brains of CQ-treated animals and potentially in Alzheimer disease patients...
  14. doi Subcellular localization of a fluorescent derivative of CuII(atsm) offers insight into the neuroprotective action of CuII(atsm)
    Katherine Ann Price
    Department of Pathology, The University of Melbourne, Victoria, Australia
    Metallomics 3:1280-90. 2011
    ....
  15. ncbi Homocysteine potentiates copper- and amyloid beta peptide-mediated toxicity in primary neuronal cultures: possible risk factors in the Alzheimer's-type neurodegenerative pathways
    A R White
    Department of Pathology, The University of Melbourne, Victoria, Australia
    J Neurochem 76:1509-20. 2001
    ....
  16. ncbi Sublethal concentrations of prion peptide PrP106-126 or the amyloid beta peptide of Alzheimer's disease activates expression of proapoptotic markers in primary cortical neurons
    A R White
    Department of Pathology, The University of Melbourne, Victoria, 3010 and The Mental Health Research Institute, Parkville, Victoria, 3052, Australia
    Neurobiol Dis 8:299-316. 2001
    ..If so, targeting of therapeutic strategies against neuronal caspase activation early in the disease course could be beneficial in AD and prion diseases...
  17. ncbi The Alzheimer's disease amyloid precursor protein modulates copper-induced toxicity and oxidative stress in primary neuronal cultures
    A R White
    Department of Pathology, The University of Melbourne, Parkville, 3052 Victoria, Australia
    J Neurosci 19:9170-9. 1999
    ..These data support a role for the APP copper-binding domain in APP-mediated copper (I) generation and toxicity in primary neurons, a process that has important implications for Alzheimer's disease and other neurodegenerative disorders...
  18. ncbi Involvement of the 5-lipoxygenase pathway in the neurotoxicity of the prion peptide PrP106-126
    L R Stewart
    Department of Pathology, The University of Melbourne, Victoria, Australia
    J Neurosci Res 65:565-72. 2001
    ..If this is so, therapeutic intervention with 5-LOX inhibitors may prove beneficial in the treatment of prion disorders...
  19. ncbi Familial prion disease mutation alters the secondary structure of recombinant mouse prion protein: implications for the mechanism of prion formation
    R Cappai
    Department of Pathology, The Mental Health Research Institute, The University of Melbourne, Parkville, Victoria, Australia
    Biochemistry 38:3280-4. 1999
    ..This suggests the mutation, while altering the secondary structure of PrP, is not sufficient to induce proteinase K resistance and could therefore represent an intermediate isoform along the pathway toward prion formation...
  20. ncbi Copper and zinc binding modulates the aggregation and neurotoxic properties of the prion peptide PrP106-126
    M F Jobling
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    Biochemistry 40:8073-84. 2001
    ..Mutagenesis of either His-111, Met-109, or Met-112 abolished PrP106-126 neurotoxicity and its ability to form fibrils. Therefore, Cu(2+) and/or Zn(2+) binding is critical for PrP106-126 aggregation and neurotoxicity...
  21. ncbi Copper levels are increased in the cerebral cortex and liver of APP and APLP2 knockout mice
    A R White
    Department of Pathology, The University of Melbourne, Parkville, Victoria, 3052, Australia
    Brain Res 842:439-44. 1999
    ..These data support a novel mechanism in the APP/Abeta pathway which leads to AD...
  22. pmc Prion protein-deficient neurons reveal lower glutathione reductase activity and increased susceptibility to hydrogen peroxide toxicity
    A R White
    Department of Pathology, University of Melbourne, Melbourne, Australia
    Am J Pathol 155:1723-30. 1999
    ..Our results suggest the pathophysiology of prion diseases may involve perturbed PrP(c) function with increased vulnerability to peroxidative stress...
  23. pmc Increasing Cu bioavailability inhibits Abeta oligomers and tau phosphorylation
    Peter J Crouch
    Department of Pathology, Centre for Neuroscience, School of Chemistry, and Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Victorial, 3010, Australia
    Proc Natl Acad Sci U S A 106:381-6. 2009
    ..This study demonstrates that increasing intracellular copper bioavailability can restore cognitive function by inhibiting the accumulation of neurotoxic Abeta trimers and phosphorylated tau...
  24. ncbi Therapeutic treatments for Alzheimer's disease based on metal bioavailability
    Peter J Crouch
    Department of Pathology, University of Melbourne, Victoria 3010, Australia
    Drug News Perspect 19:469-74. 2006
    ..The metal ligand clioquinol has been used successfully in vitro, as well as in animal models and small clinical trials, and a new generation of metal ligand-based therapeutics is under development...
  25. ncbi Diverse fibrillar peptides directly bind the Alzheimer's amyloid precursor protein and amyloid precursor-like protein 2 resulting in cellular accumulation
    Anthony R White
    Department of Pathology, The University of Melbourne, 3010, Victoria, Australia
    Brain Res 966:231-44. 2003
    ..These findings show that diverse fibrillogenic peptides can induce accumulation of APP and APLP2 and this mechanism could contribute to pathogenesis in neurodegenerative disorders...
  26. doi The role of metals in modulating metalloprotease activity in the AD brain
    Gulay Filiz
    Department of Pathology and the Centre for Neuroscience, The University of Melbourne, Melbourne, VIC 3010, Australia
    Eur Biophys J 37:315-21. 2008
    ..Elucidation of this pathway may have important implications for the development of metal ligand based therapeutics for treatment of AD and other neurodegenerative disorders...
  27. ncbi Overexpression of Alzheimer's disease amyloid-beta opposes the age-dependent elevations of brain copper and iron
    Christa J Maynard
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    J Biol Chem 277:44670-6. 2002
    ..These findings, complemented by our previous findings of elevated copper levels in APP knock-out mice, support roles for APP and Abeta in physiological metal regulation...
  28. doi Metallo-complex activation of neuroprotective signalling pathways as a therapeutic treatment for Alzheimer's disease
    Laura Bica
    Department of Pathology, The University of Melbourne, 3010, Victoria, Australia
    Mol Biosyst 5:134-42. 2009
    ..Further in vivo investigation is required to elucidate the mechanism of action of these metallo-complexes in vivo and determine their efficacy and safety as potential treatments of neurodegenerative diseases...
  29. ncbi Gene knockout of amyloid precursor protein and amyloid precursor-like protein-2 increases cellular copper levels in primary mouse cortical neurons and embryonic fibroblasts
    Shayne A Bellingham
    Department of Genetics, The University of Melbourne, Victoria, Australia
    J Neurochem 91:423-8. 2004
    ....
  30. ncbi In vitro gamma-secretase cleavage of the Alzheimer's amyloid precursor protein correlates to a subset of presenilin complexes and is inhibited by zinc
    David E Hoke
    Department of Pathology, The University of Melbourne and The Mental Health Research Institute, Parkville, Victoria, Australia
    FEBS J 272:5544-57. 2005
    ..These studies further refine our knowledge of the complexes and biochemical factors needed for gamma-secretase activity and suggest a mechanism by which zinc dysregulation may contribute to Alzheimer's disease pathogenesis...
  31. doi Sustained activation of glial cell epidermal growth factor receptor by bis(thiosemicarbazonato) metal complexes is associated with inhibition of protein tyrosine phosphatase activity
    Katherine Ann Price
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    J Med Chem 52:6606-20. 2009
    ..These studies provide an important insight into the mechanism of action of a neuroprotective M(II)(btsc) and provide a basis for future studies into this novel approach to AD therapy...
  32. doi Copper and zinc bis(thiosemicarbazonato) complexes with a fluorescent tag: synthesis, radiolabelling with copper-64, cell uptake and fluorescence studies
    SinChun Lim
    School of Chemistry, University of Melbourne, Parkville, Vic, 3010, Australia
    J Biol Inorg Chem 15:225-35. 2010
    ..In both cases, there was no evidence of uptake of the copper(II) bis(thiosemicarbazonato) complexes in the area of the cell nucleus...
  33. pmc Differential modulation of Alzheimer's disease amyloid beta-peptide accumulation by diverse classes of metal ligands
    Aphrodite Caragounis
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    Biochem J 407:435-50. 2007
    ..Given that a structurally diverse array of ligands was assessed, the results are consistent with the effects being due to metal transport rather than the chelating ligand interacting directly with a receptor...
  34. ncbi Clioquinol inhibits peroxide-mediated toxicity through up-regulation of phosphoinositol-3-kinase and inhibition of p53 activity
    Gulay Filiz
    Centre for Neuroscience and Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    Int J Biochem Cell Biol 40:1030-42. 2008
    ..These findings have important implications for the development of protective metal ligand-based therapies for treatment of disorders involving oxidative stress...
  35. doi Restored degradation of the Alzheimer's amyloid-beta peptide by targeting amyloid formation
    Peter J Crouch
    Department of Pathology, The University of Melbourne, Parkville, Victoria, Australia
    J Neurochem 108:1198-207. 2009
    ..This provides new data indicating that therapeutic compounds designed to modulate Abeta-metal interactions can inhibit Abeta accumulation by restoring the catalytic potential of Abeta-degrading proteases...
  36. doi Membrane-targeted strategies for modulating APP and Abeta-mediated toxicity
    Katherine A Price
    Department of Pathology, The University of Melbourne, Victoria, Australia
    J Cell Mol Med 13:249-61. 2009
    ..The putative role of copper (Cu) in AD is also discussed, and we highlight how targeting the cell membrane with Cu complexes has therapeutic potential in AD...
  37. doi A domain level interaction network of amyloid precursor protein and Abeta of Alzheimer's disease
    Victoria M Perreau
    Neuroproteomics and Neurogenomics Platform, National Neurosciences Facility, The University of Melbourne, Parkville, Vic, Australia
    Proteomics 10:2377-95. 2010
    ..Gene ontology and network analysis were used to identify potentially novel functional relationships among interacting proteins...
  38. doi Serum matrix metalloproteinase-9 activity is dysregulated with disease progression in the mutant SOD1 transgenic mice
    Cynthia P W Soon
    Department of Pathology, The University of Melbourne, Parkville, VIC 3010, Australia
    Neuromuscul Disord 20:260-6. 2010
    ..These data indicate that circulating MMP-9 is altered throughout the course of disease progression in mice. Further studies in human ALS may validate the suitability of serum MMP-9 activity as a biomarker for early stage disease...
  39. ncbi Mechanisms of A beta mediated neurodegeneration in Alzheimer's disease
    Peter J Crouch
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    Int J Biochem Cell Biol 40:181-98. 2008
    ..Further study of the mechanisms of A beta mediated neurodegeneration will considerably improve our understanding of AD, and may provide fundamental insights needed for the development of more effective therapeutic strategies...
  40. ncbi Alzheimer's disease amyloid beta and prion protein amyloidogenic peptides promote macrophage survival, DNA synthesis and enhanced proliferative response to CSF-1 (M-CSF)
    John A Hamilton
    Arthritis and Inflammation Research Centre, The University of Melbourne, Department of Medicine, The Royal Melbourne Hospital, Clinical Sciences Building, Royal Parade, Victoria 3050, Parkville, Australia
    Brain Res 940:49-54. 2002
    ..These fibrillogenic peptides join the list of aggregates having these effects on macrophages, indicating the generality of this type of response...
  41. ncbi Correlative studies support lipid peroxidation is linked to PrP(res) propagation as an early primary pathogenic event in prion disease
    Marcus W Brazier
    Department of Pathology, The University of Melbourne, VIC 3010, Australia
    Brain Res Bull 68:346-54. 2006
    ....
  42. pmc Platinum-based inhibitors of amyloid-beta as therapeutic agents for Alzheimer's disease
    Kevin J Barnham
    Department of Pathology, University of Melbourne, Parkville, Victoria, 3010, Australia
    Proc Natl Acad Sci U S A 105:6813-8. 2008
    ..The potent effect of the L-PtCl(2) complexes identifies this class of compounds as therapeutic agents for AD...
  43. ncbi Overexpression of Abeta is associated with acceleration of onset of motor impairment and superoxide dismutase 1 aggregation in an amyotrophic lateral sclerosis mouse model
    Qiao Xin Li
    Department of Pathology, The University of Melbourne, and The Mental Health Research Institute of Victoria, Parkville, VIC 3010, Australia
    Aging Cell 5:153-65. 2006
    ..SOD1(G93A) mice. This study supports abnormal SOD1 protein aggregation as the pathogenic mechanism in ALS, and implicates a potential role for Abeta in the development of ALS by exacerbating SOD1(G93A) aggregation...
  44. ncbi Activation of epidermal growth factor receptor by metal-ligand complexes decreases levels of extracellular amyloid beta peptide
    Katherine A Price
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    Int J Biochem Cell Biol 40:1901-17. 2008
    ..These findings provide the first evidence that metal-ligand complexes can activate the epidermal growth factor receptor with potentially neuroprotective effects...
  45. ncbi Iron inhibits neurotoxicity induced by trace copper and biological reductants
    Anthony R White
    Department of Pathology and Centre for Neuroscience, The University of Melbourne, 3010, Carlton South, Victoria, Australia
    J Biol Inorg Chem 9:269-80. 2004
    ..These findings have important implications for trace biometal interactions and free radical-mediated damage during neurodegenerative illnesses such as Alzheimer's disease and old-age dementia...
  46. ncbi Selective intracellular release of copper and zinc ions from bis(thiosemicarbazonato) complexes reduces levels of Alzheimer disease amyloid-beta peptide
    Paul S Donnelly
    School of Chemistry, The University of Melbourne, Parkville, Victoria 3010, Australia
    J Biol Chem 283:4568-77. 2008
    ..However, a role for alternative metal-induced Abeta metabolism has not been ruled out. These studies demonstrate that MII(btsc) complexes have potential for Alzheimer disease therapy...
  47. ncbi Immunotherapy as a therapeutic treatment for neurodegenerative disorders
    Anthony R White
    Neurochemistry Group, Howard Florey Institute of Experimental Physiology and Medicine, Victoria, Australia
    J Neurochem 87:801-8. 2003
    ....
  48. ncbi Amyloid beta
    R Cappai
    Department of Pathology, University of Melbourne, Parkville, Vic, Australia
    Int J Biochem Cell Biol 31:885-9. 1999
    ..Considerable activity is directed towards A beta as a therapeutic target. These strategies aim to inhibit A beta synthesis, A beta fibril formation, its toxic actions on cells or promote its clearance from the brain...
  49. ncbi The modulation of metal bio-availability as a therapeutic strategy for the treatment of Alzheimer's disease
    Peter J Crouch
    Department of Pathology and Centre for Neuroscience, The University of Melbourne, Australia
    FEBS J 274:3775-83. 2007
    ..In this review, we focus on copper dyshomeostasis in Alzheimer's disease, but we also discuss zinc and iron...
  50. ncbi Therapeutic treatment of Alzheimer's disease using metal complexing agents
    Katherine A Price
    Department of Pathology and the Centre for Neuroscience, The University of Melbourne, Victoria, Australia
    Recent Pat CNS Drug Discov 2:180-7. 2007
    ..Further research will be necessary to fully understand the complex pathways associated with efficacious metal-based pharmaceuticals for treatment of AD...
  51. ncbi Structure of the Alzheimer's disease amyloid precursor protein copper binding domain. A regulator of neuronal copper homeostasis
    Kevin J Barnham
    Department of Pathology, The University of Melbourne, Victoria 3010, Australia
    J Biol Chem 278:17401-7. 2003
    ..The surface location of this site, structural homology of CuBD to copper chaperones, and the role of APP in neuronal copper homeostasis are consistent with the CuBD acting as a neuronal metallotransporter...
  52. doi Bis(thiosemicarbazonato) Cu-64 complexes for positron emission tomography imaging of Alzheimer's disease
    Michelle T Fodero-Tavoletti
    Department of Pathology, University of Melbourne, Melbourne, Victoria, Australia
    J Alzheimers Dis 20:49-55. 2010
    ..This approach has the potential to offer complementary information to other diagnostic procedures that elucidate plaque burden...
  53. doi Zinc induces depletion and aggregation of endogenous TDP-43
    Aphrodite Caragounis
    Department of Pathology, The University of Melbourne, Melbourne, VIC 3010, Australia
    Free Radic Biol Med 48:1152-61. 2010
    ..These studies describe for the first time specific induction of endogenous TDP-43 aggregation in neuronal-like cells and suggest that specific Zn-associated processes could affect TDP-43 metabolism in neurodegenerative diseases...
  54. doi Neurotoxicity of prion peptides on cultured cerebellar neurons
    Giuseppe D Ciccotosto
    Department of Pathology and Mental Health Research Institute of Victoria, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Melbourne, Australia
    Methods Mol Biol 459:83-96. 2008
    ....
  55. doi Investigating copper-regulated protein expression in Menkes fibroblasts using antibody microarrays
    Tai Du
    Centre for Neuroscience, The University of Melbourne, Victoria, Australia
    Proteomics 8:1819-31. 2008
    ..Further analysis confirmed that expression of the DNA repair protein Ku80 was dependent on cellular Cu homeostasis and that Low-Cu levels in fibroblasts resulted in elevated susceptibility to DNA oxidation...
  56. ncbi Manganese chelation therapy extends survival in a mouse model of M1000 prion disease
    Marcus W Brazier
    Department of Pathology, The University of Melbourne, Melbourne, Victoria, Australia
    J Neurochem 114:440-51. 2010
    ..002). Although our findings support a role for Mn(2+) in prion disease, further studies are required to more precisely delineate the extent of pathogenic involvement...
  57. ncbi Neurotoxicity from glutathione depletion is mediated by Cu-dependent p53 activation
    Tai Du
    Department of Pathology, The University of Melbourne, Melbourne, VIC 3010, Australia
    Free Radic Biol Med 44:44-55. 2008
    ..These findings may have important implications for neurodegenerative disorders that involve GSH depletion and aberrant Cu metabolism...
  58. ncbi Neurotoxicity from glutathione depletion is dependent on extracellular trace copper
    Anthony R White
    Department of Pathology, The University of Melbourne, and The Mental Health Research Institute, Parkville, Victoria, Australia
    J Neurosci Res 71:889-97. 2003
    ..These studies demonstrate a critical role for extracellular trace copper in neuronal cell death caused by GSH depletion and may have important implications for the understanding of toxic processes in neurodegenerative diseases...
  59. doi Blood-borne amyloid-beta dimer correlates with clinical markers of Alzheimer's disease
    Victor L Villemagne
    Mental Health Research Institute, The University of Melbourne, Parkville, Melbourne, Victoria 3052, Australia
    J Neurosci 30:6315-22. 2010
    ..These results indicate that fundamental biochemical events relevant to AD can be monitored in blood, and that the species detected may be useful clinical biomarkers for AD...
  60. ncbi Metalloenzyme-like activity of Alzheimer's disease beta-amyloid. Cu-dependent catalytic conversion of dopamine, cholesterol, and biological reducing agents to neurotoxic H(2)O(2)
    Carlos Opazo
    Centro de Regulación Celular y Patología, Departamento de Biologia Celular y Molecular, Facultad de Ciencias Biologicas, Pontificia Universidad Catolica de Chile, Santiago 114 D, Chile
    J Biol Chem 277:40302-8. 2002
    ..Cu. Therefore, microregional catalytic H(2)O(2) production, combined with the exhaustion of reducing agents, may mediate the neurotoxicity of Abeta in Alzheimer's disease, and inhibitors of this novel activity may be of therapeutic value...
  61. ncbi Evidence for a copper-binding superfamily of the amyloid precursor protein
    Andreas Simons
    ZMBH Center for Molecular Biology, University of Heidelberg, Im Neuenheimer Feld 282, D 69120 Heidelberg, Germany
    Biochemistry 41:9310-20. 2002
    ..The more recently evolved homologues of human APP appear to take advantage of unique redox properties for yet unknown biological functions...
  62. ncbi Apurinic/apyrimidinic endonuclease 1 regulates endothelial NO production and vascular tone
    Byeong Hwa Jeon
    Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21214, USA
    Circ Res 95:902-10. 2004
    ..These findings uncover a novel physiological role for APE1/ref-1 in regulating vascular tone by governance of eNOS activity and bioavailable NO...
  63. ncbi Acetylcholinesterase is increased in mouse neuronal and astrocyte cultures after treatment with beta-amyloid peptides
    Javier Saez-Valero
    Instituto de Neurociencias, Universidad Miguel Hernandez CSIC, 03550, San Juan de Alicante, Spain
    Brain Res 965:283-6. 2003
    ....
  64. ncbi P66shc regulates endothelial NO production and endothelium-dependent vasorelaxation: implications for age-associated vascular dysfunction
    Tohru Yamamori
    Cardiovascular Institute, University of Pittsburgh Medical Center, Scaife 620, University of Pittsburgh School of Medicine, 3550 Terrace Street, Pittsburgh, PA 15213, USA
    J Mol Cell Cardiol 39:992-5. 2005
    ..These findings highlight a pivotal role for p66shc in inhibiting endothelial NO production, and endothelium-dependent vasorelaxation, that may provide important mechanistic information about endothelial dysfunction seen with aging...
  65. ncbi Knockdown of arginase I restores NO signaling in the vasculature of old rats
    Anthony R White
    Department of Anesthesiology and Critical Care Medicine, The Johns Hopkins Medical Institutions, Baltimore, MD, USA
    Hypertension 47:245-51. 2006
    ..AS oligonucleotides may, therefore, represent a novel therapeutic strategy against age-related vascular endothelial dysfunction...
  66. ncbi Monoclonal antibodies inhibit prion replication and delay the development of prion disease
    Anthony R White
    CNS Infection and Immunity Group, Department of Neurogenetics, Division of Neurosciences and Psychological Medicine, Faculty of Medicine, Imperial College, Norfolk Place, London W2 1PG, UK
    Nature 422:80-3. 2003
    ..These findings indicate that immunotherapeutic strategies for human prion diseases are worth pursuing...