D R Brown

Summary

Affiliation: University of Bath
Country: UK

Publications

  1. Angelova D, Brown D. Model Senescent Microglia Induce Disease Related Changes in ?-Synuclein Expression and Activity. Biomolecules. 2018;8: pubmed publisher
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    Brown D. Molecular advances in understanding inherited prion diseases. Mol Neurobiol. 2002;25:287-302 pubmed
    ..This review deals with the latest insights into how inherited mutations in the prion protein gene lead to neurodegenerative disease. ..
  3. Brown D. Prions and manganese: A maddening beast. Metallomics. 2011;3:229-38 pubmed publisher
    ..This article reviews the evidence for a link between prions and manganese. ..
  4. Pass R, Frudd K, Barnett J, Blindauer C, Brown D. Prion infection in cells is abolished by a mutated manganese transporter but shows no relation to zinc. Mol Cell Neurosci. 2015;68:186-93 pubmed publisher
    ..These studies strengthen the link between manganese and prion disease. ..
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    Brown D. BSE did not cause variant CJD: an alternative cause related to post-industrial environmental contamination. Med Hypotheses. 2001;57:555-60 pubmed
    ..Therefore it is quite possible that BSE and variant CJD have emerged as a result of manganese-rich industrial pollution that has only occurred in the last century. ..
  6. Brown D. Role of microglia in age-related changes to the nervous system. ScientificWorldJournal. 2009;9:1061-71 pubmed publisher
    ..This review provides illustrations of what is known about the role of microglia in neurodegeneration and makes suggestions about the role of microglia in age-related changes to the brain. ..
  7. Brown D. Oligomeric alpha-synuclein and its role in neuronal death. IUBMB Life. 2010;62:334-9 pubmed publisher
    ..Recent research has suggested that a unique oligomer associated with the copper binding capacity of the protein is the neurotoxic form of the protein. This review looks at the evidence for this possibility. ..
  8. McDowall J, Brown D. Alpha-synuclein: relating metals to structure, function and inhibition. Metallomics. 2016;8:385-97 pubmed publisher
    ..The recent proposal that alpha-synuclein is a ferrireductase is important as it can possibly catalyse the formation of such reactive species and as a result exacerbate neurodegeneration. ..
  9. Cichon A, Brown D. Nrf-2 regulation of prion protein expression is independent of oxidative stress. Mol Cell Neurosci. 2014;63:31-7 pubmed publisher
    ..Furthermore, Nrf-2 has no impact on PrP expression when cells are infected with scrapie. These findings highlight that Nrf-2 can regulate PrP expression, but that this regulation becomes uncoupled during cellular stress. ..

More Information

Publications12

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    Brown D. Prion protein expression modulates neuronal copper content. J Neurochem. 2003;87:377-85 pubmed
    ..Loss of normal Cu binding by the prion protein altered age-related increases in metals in the brain. This may explain why many forms of human prion disease do not develop until late in life. ..
  2. McDowall J, Ntai I, Honeychurch K, Hart J, Colin P, Schneider B, et al. Alpha-synuclein ferrireductase activity is detectible in vivo, is altered in Parkinson's disease and increases the neurotoxicity of DOPAL. Mol Cell Neurosci. 2017;85:1-11 pubmed publisher
    ..These findings demonstrate that ?-synuclein ferrireductase activity is present in vivo and its alteration may play a role in neuron loss in disease. ..
  3. Angelova D, Jones H, Brown D. Levels of ?- and ?-synuclein regulate cellular susceptibility to toxicity from ?-synuclein oligomers. FASEB J. 2017;: pubmed publisher
    ..Angelova, D. M., Jones, H. B. L., Brown, D. R. Levels of ?- and ?-synuclein regulate cellular susceptibility to toxicity from ?-synuclein oligomers...