David R. Brown (neuroscientist)

Source: Wikipedia, the free encyclopedia.

David R. Brown
prion diseases
Scientific career
FieldsNeuroscience
Doctoral advisorMax Bennett (scientist)[1]

Professor David Ronald Brown (born 7 September 1964,

vCJD. His most notable research relates to the metal binding of the protein central to these diseases, the prion
protein, and its possible cellular role as an antioxidant.

Brown was a member of the Spongiform Encephalopathy Advisory Committee (SEAC), a British government advisory board on BSE and related diseases.[3] Since then he has pursued research related to other neurodegenerative diseases.[4]

Career

Brown completed his studies at the University of Sydney at the age of 25 and gained the degrees B.Sc. M.Sc. and Ph.D. His doctoral studies were carried out in the Neurobiology Research Centre under Professor Max Bennett and involved research on nerve regeneration.

After completing his Ph.D. he worked for several more years in Australia before moving to the US in 1993 where he worked at the Albert Einstein College of Medicine. He moved to Germany and worked at the University of Göttingen where he first began work on the study of prion diseases in the Department of Neuropathology with Hans Kretzschmar. In 1997 he moved to the University of Cambridge and in 2001 to the University of Bath, where he is currently Professor of Biochemistry.[4] He consults in this capacity with the media.[5] He is the author of several textbooks and a number of research papers on prion diseases, and has served on the boards of four scientific journals,[6][7][8] including the Journal of Neurochemistry.[9]

Prion research

Brown advanced research related to the role of metals in the cause of prion diseases such as vCJD. Media attention focused on this work when it became associated with that of the farmer Mark Purdey, who argued that human cases of vCJD might be caused by exposure to manganese rather than eating beef from BSE-infected cattle (the medical consensus).[10][11] Both Purdey and Brown agreed that exposure to elevated levels of manganese in the environment could increase the incidence of BSE.[12]

Brown's research showed that manganese causes the protein to change conformation, similar to that seen in prion diseases such as BSE.

Charles, Prince of Wales.[11]

Select bibliography

Books

Articles

References

  1. ^ "Discipline of Physiology". Archived from the original on 21 March 2012. Retrieved 25 April 2012.
  2. ^ http://www.euchems2008.unito.it/download/WBioL-III.3DRBrown.pdf Archived 22 July 2011 at the Wayback Machine [bare URL PDF]
  3. ^ see http://www.seac.gov.uk/papers/papers.htm Archived 2009-10-10 at the Wayback Machine where he is listed as being in attendance between the 81st meeting (http://www.seac.gov.uk/minutes/final81.pdf Archived 2009-10-10 at the Wayback Machine) and then thanked for completing two terms in the 100th meeting (http://www.seac.gov.uk/minutes/final100.pdf Archived 2009-10-10 at the Wayback Machine)
  4. ^ a b c Research Profile, University of Bath
  5. ^ "'Human remains link' to BSE cases". September 2005.
  6. ^ "Biochemistry Research International - an Open Access Journal".
  7. ^ "Covering Addiction News from a Evidence-Based & Scientific View". Archived from the original on 25 June 2009. Retrieved 25 November 2009.
  8. ^ "BioMed Research International - an Open Access Journal".
  9. ^ "Wolters Kluwer Ovid is the world's most trusted medical research platform".
  10. ^ The metal detector, Anjana Ahuja, The Times, February 4, 2002
  11. ^ a b Charles backs controversial CJD research, Lorraine Fraser, The Telegraph, 13 Jan 2002
  12. ^ p4, CJD is caused by BSE Archived 8 October 2008 at the Wayback Machine, David R Brown, Body & Mind, BBC/Open University, Open2.net
  13. ^ Brown, D. R. et al. (2000) Consequences of manganese replacement of copper for prion protein function and proteinase resistance. EMBO J. 19, 1180-1186.
  14. ^ "BBC NEWS | Programmes | Correspondent | Europe | Solidarity: Mad cows and an Englishman". news.bbc.co.uk. Archived from the original on 6 February 2007.