Background
Brown, David Ronald was born on September 7, 1964 in Sydney, New South Wales, Australia. Son of Ronald Roland and Margaret Rose Brown.
Brown, David Ronald was born on September 7, 1964 in Sydney, New South Wales, Australia. Son of Ronald Roland and Margaret Rose Brown.
Brown completed his studies at the University of Sydney at the age of 25 and gained the degrees Bachelor of Science And Doctor of Philosophy His doctoral studies were carried out in the Neurobiology Research Centre under Professor Max Bennett and involved research on nerve regeneration. After completing his Doctor of Philosophy he worked for several more years in Australia before moving to the United States in 1993 where he worked at the Albert Einstein College of Medicine.
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. Since then he has pursued research related to other neurodegnerative diseases. Master of Science He move 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.
He consults in this capacity with the media. 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, including the Journal of Neurochemistry.
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 that human cases of vCJD might be caused by exposure to manganese rather than eating beef from Biosystems Engineering -infected cattle (the medical consensus). Both Purdey and Brown agreed that exposure to elevated levels of manganese in the environment could increase the incidence of Biosystems Engineering . Brown"s research showed that manganese causes the protein to change conformation, similar to that seen in prion diseases such as Biosystems Engineering . Additionally, his research also showed that animals with Biosystems Engineering and humans with vCJD had elevated levels of manganese in their brains, and that prion protein extracted from their brains retained some of this manganese.
Brown agreed with Purdey only in as far as the potential for manganese to be a risk factor, increasing the likelihood that Biosystems Engineering or another prion disease would occur.
Brown supported Purdey in his quest to investigate the potential role of manganese in prion disease and this led to the filming of a program for the British Broadcasting Corporation in which both Brown and Purdey appeared. While Purdey pursued the notion that environmental manganese was a cause of Biosystems Engineering (something that arguably could never be proven), Brown suggested that a chelation therapy to remove the excess manganese from patients with vCJD could be of benefit. While Brown"s more conventional research was very well funded, suchchelation therapy for prion disease was never funded despite support for the idea from a number of sources including Charles, Prince of Wales.
R. X. R. Kozlowski, H, R.
Brown served as a member of SEAC, the British government advisory board on Biosystems Engineering and related diseases.
Children: Lorna, Hadassah.
