Daniel C Anthony
Professor of Experimental Neuropathology
- Fellow of Somerville College
- Honorary Professor, University of Southern Denmark
The focus of the work of my lab is to identify how inflammation contributes to the outcome of acute and chronic brain injury or infection and the identification of novel biomarkers to diagnosis disease and predict progression. We are particularly interested in the role played by circulating extracellular vesicles in the pathogenesis of CNS disease and the way in which their presence impacts on behaviour.
I have published extensively on the neurobiology of inflammation with the help of creative friends and colleagues in Oxford and throughout the world. The lab is well equipped for in vivo biology, molecular biology, immunohistochemistry and metabolomics.
Following the completion of my PhD in 1994 at UCL, I joined Professor Hugh Perry, then in Oxford, on a British Biotech Fellowship investigating metalloproteinase expression in the CNS. It was during this period that I became interested in the leukocyte-mediated mechanisms of neurodegeneration. In 1998, I moved to a faculty position at the University of Southampton, where I was a Lecturer in Neurobiology before returning to Oxford in 2004. I am also a Fellow of Somerville College and hold an honorary Professorial position at the University of Southern Denmark.
Dimethyl fumarate decreases short-term but not long-term inflammation in a focal EAE model of neuroinflammation
Vainio SK. et al, (2022), EJNMMI Research, 12
The Sedentary Lifestyle and Masticatory Dysfunction: Time to Review the Contribution to Age-Associated Cognitive Decline and Astrocyte Morphotypes in the Dentate Gyrus
Siqueira Mendes FDCCD. et al, (2022), International Journal of Molecular Sciences, 23, 6342 - 6342
Assessing the effect of anesthetic gas mixtures on hyperpolarized 13 C pyruvate metabolism in the rat brain.
Healicon R. et al, (2022), Magn Reson Med
Correction to: SPIKE-1: A Randomised Phase II/III trial in a community setting, assessing use of camostat in reducing the clinical progression of COVID-19 by blocking SARS-CoV-2 Spike protein-initiated membrane fusion.
Halford S. et al, (2022), Trials, 23
Reductive site-selective atypical C,Z-type/N2-C2 cleavage allows C-terminal protein amidation.
Mollner TA. et al, (2022), Sci Adv, 8