David R. Brown mainly focuses on Biochemistry, Cell biology, Oxidative stress, Gene isoform and Neurodegeneration. David R. Brown specializes in Biochemistry, namely Superoxide dismutase. He combines subjects such as Scrapie, Neuroglia, Virology, Astrocyte and Glycoprotein with his study of Cell biology.
His Oxidative stress research is multidisciplinary, incorporating perspectives in Oxidative phosphorylation, Gene, Antioxidant and Methionine. His biological study spans a wide range of topics, including Cell culture and Immunology, Ratón. His Neurodegeneration research integrates issues from Glutamate receptor, Protein aggregation and Mutation.
Biochemistry, Inorganic chemistry, Cell biology, Catalysis and Scrapie are his primary areas of study. His Biochemistry research includes themes of Prion protein and Copper. His study looks at the intersection of Inorganic chemistry and topics like Uranium with Crystallography.
His Cell biology study incorporates themes from Neuroglia, Glutamate receptor, Astrocyte, Toxicity and Programmed cell death. His Scrapie study combines topics in areas such as Recombinant DNA and Virology. His studies in Virology integrate themes in fields like Bovine spongiform encephalopathy and Disease, Neurodegeneration.
His primary areas of investigation include Cancer research, Cancer, Biochemistry, Cell biology and Catalysis. His Cancer research study also includes
His Cell biology course of study focuses on Synuclein and Neuroscience. In his research on the topic of Catalysis, Adsorption, Metal, Reactive oxygen species and Zinc is strongly related with Inorganic chemistry. His study explores the link between Protein aggregation and topics such as Mutation that cross with problems in Neurodegeneration.
His scientific interests lie mostly in Biochemistry, Catalysis, Organic chemistry, Neurodegeneration and Cell biology. David R. Brown combines subjects such as Biophysics, Function, Alpha-synuclein and Amyloid with his study of Biochemistry. His Biophysics research includes elements of Protein structure, Scrapie, Alzheimer's disease and Protein folding.
His Catalysis study integrates concerns from other disciplines, such as Inorganic chemistry, Adsorption, Molecule, Sugar and Radical. His study in Neurodegeneration is interdisciplinary in nature, drawing from both Quinolinic acid and Glial cell line-derived neurotrophic factor, Neurotrophic factors. His biological study spans a wide range of topics, including Cell, Glutamate receptor, Secretion, Transfection and Wild type.
This overview was generated by a machine learning system which analysed the scientist’s body of work. If you have any feedback, you can contact us here.
The cellular prion protein binds copper in vivo
D R Brown;K Qin;J W Herms;A Madlung.
Normal prion protein has an activity like that of superoxide dismutase.
David R. Brown;Boon-Seng Wong;Farida Hafiz;Christine Clive.
Biochemical Journal (1999)
Role of microglia and host prion protein in neurotoxicity of a prion protein fragment
David R. Brown;Bernhard Schmidt;Hans A. Kretzschmar.
Prion protein-deficient cells show altered response to oxidative stress due to decreased SOD-1 activity
David R. Brown;Walter J. Schulz-Schaeffer;Bernhard Schmidt;Hans A. Kretzschmar.
Experimental Neurology (1997)
Prion protein expression and superoxide dismutase activity.
David R. Brown;Andreas Besinger.
Biochemical Journal (1998)
Biological inorganic and bioinorganic chemistry of neurodegeneration based on prion and Alzheimer diseases.
David R. Brown;Henryk Kozlowski.
Dalton Transactions (2004)
Consequences of manganese replacement of copper for prion protein function and proteinase resistance
David R. Brown;Farida Hafiz;Leslie L. Glasssmith;Boon-Seng Wong.
The EMBO Journal (2000)
Role of Microglia in Neuronal Cell Death in Prion Disease
Armin Giese;David R. Brown;Martin H. Groschup;Claudia Feldmann.
Brain Pathology (2006)
Structure-activity relations in Cs-doped heteropolyacid catalysts for biodiesel production
K. Narasimharao;D.R. Brown;Adam Lee;A.D. Newman.
Journal of Catalysis (2007)
Preferential Cu2+ Coordination by His96 and His111 Induces β-Sheet Formation in the Unstructured Amyloidogenic Region of the Prion Protein
Christopher E. Jones;Salama R. Abdelraheim;David R. Brown;John H. Viles.
Journal of Biological Chemistry (2004)
If you think any of the details on this page are incorrect, let us know.
We appreciate your kind effort to assist us to improve this page, it would be helpful providing us with as much detail as possible in the text box below: