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.
Live or heat-killed probiotic administration reduces anxiety and central cytokine expression in BALB/c mice, but differentially alters brain neurotransmitter gene expression.
Chan KW. et al, (2023), Neuropharmacology
HDL and LDL have distinct, opposing effects on LPS-induced brain inflammation.
Radford-Smith DE. et al, (2023), Lipids Health Dis, 22
cFOS expression in the prefrontal cortex correlates with altered cerebral metabolism in developing germ-free mice.
Pate T. et al, (2023), Front Mol Neurosci, 16
In FUS[1−359]‐tg mice O,S-dibenzoyl thiamine reduces muscle atrophy, decreases glycogen synthase kinase 3 beta, and normalizes the metabolome
Probert F. et al, (2022), Biomedicine and Pharmacotherapy, 156
Metabolomics detects clinically silent neuroinflammatory lesions earlier than neurofilament-light chain in a focal multiple sclerosis animal model.
Yeo T. et al, (2022), J Neuroinflammation, 19