D R Brown

Summary

Affiliation: University of Cambridge
Country: UK

Publications

  1. pmc PrPSc-like prion protein peptide inhibits the function of cellular prion protein
    D R Brown
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, U K
    Biochem J 352:511-8. 2000
  2. ncbi Antioxidant activity related to copper binding of native prion protein
    D R Brown
    Department of Biochemistry, Cambridge University, Cambridge, UK
    J Neurochem 76:69-76. 2001
  3. ncbi Microglia and prion disease
    D R Brown
    Department of Biochemistry, Cambridge University, Cambridge, CB2 1QW, United Kingdom
    Microsc Res Tech 54:71-80. 2001
  4. ncbi Neuronal release of vasoactive intestinal peptide is important to astrocytic protection of neurons from glutamate toxicity
    D R Brown
    Department of Biochemistry, Cambridge University, United Kingdom
    Mol Cell Neurosci 15:465-75. 2000
  5. ncbi Functional and structural differences between the prion protein from two alleles prnp(a) and prnp(b) of mouse
    D R Brown
    Department of Biochemistry, Cambridge University, UK NERC Institute of Virology, Oxford, UK
    Eur J Biochem 267:2452-9. 2000
  6. pmc Consequences of manganese replacement of copper for prion protein function and proteinase resistance
    D R Brown
    Department of Biochemistry, Tennis Court Road, Cambridge University, Cambridge CB2 1QW
    EMBO J 19:1180-6. 2000
  7. pmc Altered toxicity of the prion protein peptide PrP106-126 carrying the Ala(117)-->Val mutation
    D R Brown
    Department of Biochemistry, Cambridge University, Tennis Court Road, Cambridge CB2 1QW, U K
    Biochem J 346:785-91. 2000
  8. ncbi Copper and prion disease
    D R Brown
    Department of Biochemistry, Cambridge University, Cambridge, UK
    Brain Res Bull 55:165-73. 2001
  9. pmc Normal prion protein has an activity like that of superoxide dismutase
    D R Brown
    Department of Biochemistry, Tennis Court Road, University of Cambridge, Cambridge CB2 1QW, U K
    Biochem J 344:1-5. 1999
  10. ncbi Astrocytic glutamate uptake and prion protein expression
    D R Brown
    MRC Cambridge Centre for Brain Repair, Cambridge University, United Kingdom
    Glia 25:282-92. 1999

Collaborators

Detail Information

Publications27

  1. pmc PrPSc-like prion protein peptide inhibits the function of cellular prion protein
    D R Brown
    Department of Biochemistry, University of Cambridge, Cambridge CB2 1QW, U K
    Biochem J 352:511-8. 2000
    ..Direct inhibition of prion protein function by PrP(Sc) may be necessary for neurodegeneration in prion disease...
  2. ncbi Antioxidant activity related to copper binding of native prion protein
    D R Brown
    Department of Biochemistry, Cambridge University, Cambridge, UK
    J Neurochem 76:69-76. 2001
    ..These results suggest that PrP(c) is a copper-binding protein which can incorporate varying amounts of copper and exhibit protective antioxidant activity...
  3. ncbi Microglia and prion disease
    D R Brown
    Department of Biochemistry, Cambridge University, Cambridge, CB2 1QW, United Kingdom
    Microsc Res Tech 54:71-80. 2001
    ..The implication of this is that microglia may play a major role in initiating the pathological changes in prion disease. This review discusses the role of microglia in these changes...
  4. ncbi Neuronal release of vasoactive intestinal peptide is important to astrocytic protection of neurons from glutamate toxicity
    D R Brown
    Department of Biochemistry, Cambridge University, United Kingdom
    Mol Cell Neurosci 15:465-75. 2000
    ..These results indicate that VIP is essential to the molecular interaction of neurons and astrocytes and is involved in the regulation of the protective effects of astrocytes for neurons...
  5. ncbi Functional and structural differences between the prion protein from two alleles prnp(a) and prnp(b) of mouse
    D R Brown
    Department of Biochemistry, Cambridge University, UK NERC Institute of Virology, Oxford, UK
    Eur J Biochem 267:2452-9. 2000
    ..The findings provide insight into the differences between the two alleles and might have consequences for understanding differences in susceptibility to prion disease...
  6. pmc Consequences of manganese replacement of copper for prion protein function and proteinase resistance
    D R Brown
    Department of Biochemistry, Tennis Court Road, Cambridge University, Cambridge CB2 1QW
    EMBO J 19:1180-6. 2000
    ..These results show that it is possible to generate proteinase-resistant PrP from cells and suggest a possible mechanism for the formation of the scrapie isoform of the PrP as generated in sporadic prion disease...
  7. pmc Altered toxicity of the prion protein peptide PrP106-126 carrying the Ala(117)-->Val mutation
    D R Brown
    Department of Biochemistry, Cambridge University, Tennis Court Road, Cambridge CB2 1QW, U K
    Biochem J 346:785-91. 2000
    ..These results suggest a possible mechanism of toxicity for protein carrying this mutation via destabilization of the cytoskeleton and deposition of tau in filaments, as observed in GSS...
  8. ncbi Copper and prion disease
    D R Brown
    Department of Biochemistry, Cambridge University, Cambridge, UK
    Brain Res Bull 55:165-73. 2001
    ..This conversion may alter the function of the prion protein or abolish it. These results suggest that prion disease may involve disturbance to brain copper homeostasis...
  9. pmc Normal prion protein has an activity like that of superoxide dismutase
    D R Brown
    Department of Biochemistry, Tennis Court Road, University of Cambridge, Cambridge CB2 1QW, U K
    Biochem J 344:1-5. 1999
    ..These results describe an enzymic function for PrP(C) consistent with its cellular distribution and suggest it has a direct role in cellular resistance to oxidative stress...
  10. ncbi Astrocytic glutamate uptake and prion protein expression
    D R Brown
    MRC Cambridge Centre for Brain Repair, Cambridge University, United Kingdom
    Glia 25:282-92. 1999
    ..These results show that glutamate uptake from astrocytes is dependent on PrPc expression which in turn may be related to copper metabolism...
  11. ncbi Prion protein-overexpressing cells show altered response to a neurotoxic prion protein peptide
    D R Brown
    MRC Cambridge Centre for Brain Repair, England
    J Neurosci Res 54:331-40. 1998
    ..This may explain the increased PrP106-126 toxicity to Tg35 PrPc-overexpressing cerebellar cells. These results suggest that the toxicity of PrP106-126 may depend on the level of expression of PrPc by microglia as well as by neurones...
  12. pmc Prion protein expression and superoxide dismutase activity
    D R Brown
    MRC Cambridge Centre for Brain Repair, E D Adrian Building, Forvie Site, Robinson Way, Cambridge CB2 2PY, UK
    Biochem J 334:423-9. 1998
    ..As recent studies have suggested that PrPc may regulate some aspect of copper metabolism, it is suggested that PrPc expression may regulate Cu,Zn SOD activity by influencing copper incorporation into the molecule...
  13. ncbi Effects of oxidative stress on prion protein expression in PC12 cells
    D R Brown
    Institut für Neuropathologie, Universitat Gottingen, Germany
    Int J Dev Neurosci 15:961-72. 1997
    ..Prion protein expression may be involved in both the metabolism of copper and resistance to oxidative stress. Increased cellular resistance to copper toxicity may be partly related to increased activity of anti-oxidant enzymes...
  14. ncbi Prion protein fragment interacts with PrP-deficient cells
    D R Brown
    Institut für Neuropathologie, Universitat Gottingen, Germany
    J Neurosci Res 52:260-7. 1998
    ..This indicates that PrP106-126 is nontoxic to PrPo/o cells, not because of an inability to interact with these cells but because of the loss of some aspect of a PrP expression-dependent phenotype...
  15. ncbi Prion and prejudice: normal protein and the synapse
    D R Brown
    Department of Biochemistry, Tennis Court Road, Cambridge University, Cambridge, UK CB2 1QW
    Trends Neurosci 24:85-90. 2001
    ..There is increasing evidence that the normal prion protein binds copper and the resulting complex possesses anti-oxidant activity, and that this, in turn, might have vital implications for synaptic homeostasis...
  16. ncbi Toxicity of novel C-terminal prion protein fragments and peptides harbouring disease-related C-terminal mutations
    M Daniels
    Department of Biochemistry, Cambridge University, UK
    Eur J Biochem 268:6155-64. 2001
    ..Point mutations in the inherited forms of disease might have their effects by diminishing this inhibition...
  17. ncbi Effects of copper on survival of prion protein knockout neurons and glia
    D R Brown
    Institut für Neuropathologie, Biochemie II, Universitat Gottingen, Germany
    J Neurochem 70:1686-93. 1998
    ..The survival-promoting effects of PrPOcta on neurons may be due to its ability to effectively chelate copper. The octameric repeat region of PrP may represent a functional domain of the native protein...
  18. ncbi Inhibition of tumour necrosis factor-alpha (TNFalpha)-induced NF-kappaB p52 converts the metabolic effects of microglial-derived TNFalpha on mouse cerebellar neurones to neurotoxicity
    R S Nicholas
    University of Cambridge Neurology Unit, Addenbrooke's Hospital, Hills Road, Cambridge, UK
    J Neurochem 76:1431-8. 2001
    ..Characterizing and manipulating these events in vivo theoretically provides an opportunity for neuroprotection in selected diseases affecting the central nervous system...
  19. ncbi Prion protein peptide neurotoxicity can be mediated by astrocytes
    D R Brown
    Department of Biochemistry, Cambridge University, England
    J Neurochem 73:1105-13. 1999
    ..This new model provides a possible mechanism by which the gliosis in prion disease may accelerate the neurodegeneration seen in the later stages of the disease...
  20. ncbi Astrocytes regulate N-methyl-D-aspartate receptor subunit composition increasing neuronal sensitivity to excitotoxicity
    M Daniels
    Department of Biochemistry, Cambridge University, Cambridge CB2 1QW, United Kingdom
    J Biol Chem 276:22446-52. 2001
    ..This result implies that astrocytes regulate the expression of NMDA receptor subunit subtypes which influence neuronal sensitivity to glutamate toxicity...
  21. ncbi Prion protein expression aids cellular uptake and veratridine-induced release of copper
    D R Brown
    Department of Biochemistry and MRC Cambridge Centre for Brain Repair, Cambridge University, Cambridge, United Kingdom
    J Neurosci Res 58:717-25. 1999
    ..These results suggest that PrP(c) aids cellular copper uptake and may have a function at the synapse related to release of copper during transmission...
  22. ncbi Doppel expression is regulated by the Brn-3a and Brn-3b transcription factors
    M Calissano
    MMBU, Institute of Child Health, University College London 30 Guilford Street, London WC1N 1EH, UK
    Neuroreport 15:483-6. 2004
    ....
  23. ncbi Aberrant metal binding by prion protein in human prion disease
    B S Wong
    National Prion Disease Pathology Surveillance Center, Institute of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA
    J Neurochem 78:1400-8. 2001
    ....
  24. ncbi Opioid, cannabinoid and vanilloid receptor localization on porcine cultured myenteric neurons
    A Kulkarni-Narla
    Department of Veterinary Pathobiology, University of Minnesota, 1988 Fitch Avenue, St. Paul, MN 55108-6010, USA
    Neurosci Lett 308:153-6. 2001
    ..These observations indicate that receptors for cannabinoids or vanilloids are co-localized in opioid receptor-expressing myenteric neurons which modulate intestinal sensorimotor function...
  25. ncbi Increased levels of oxidative stress markers detected in the brains of mice devoid of prion protein
    B S Wong
    Institute of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106, USA
    J Neurochem 76:565-72. 2001
    ..Taken together, these findings are indicative of a role for PrP in oxidative homeostasis in vivo...
  26. ncbi Induction of HO-1 and NOS in doppel-expressing mice devoid of PrP: implications for doppel function
    B S Wong
    Institute of Pathology, Case Western Reserve University School of Medicine, Cleveland, Ohio
    Mol Cell Neurosci 17:768-75. 2001
    ..No induction was observed with Hsp-60, indicating a specific response by the HO/NOS system. We proposed that Dpl expression exacerbates oxidative damage that is antagonistic to the protective function of wild-type PrP...
  27. ncbi Therapeutics and prion disease: can immunisation or drugs be effective?
    J Sassoon
    Department of Biology and Biochemistry, University of Bath, Bath BA2 7AY, UK
    Mini Rev Med Chem 5:361-6. 2005
    ..This review examines research on possible therapeutic strategies that might have potential benefits if applied before neurodegeneration has occurred...