Dr Simon McArthur, PhD FHEA
Senior Lecturer in Neuroscience & Pharmacology Clinical
Email: email@example.comTelephone: +44(0)20 7882 7133Room Number: Blizard Institute
I read Natural Sciences (Pharmacology) at the University of Cambridge, followed by a PhD in Neuropharmacology at Imperial College London in 2004. My thesis and postdoctoral work with Professor Glenda Gillies and Dr Egle Solito at Imperial College London examined the influence of peripheral stress and inflammation upon neuroinflammatory pathology in conditions including Parkinson’s disease, multiple sclerosis and Alzheimer’s disease.
In 2011 I moved to Queen Mary, University of London and undertook postdoctoral research with Professors Rod Flower and Mauro Perretti at the William Harvey Research Institute, studying mechanisms of inflammatory resolution and the roles of monocytes/macrophages in the termination of acute inflammation.
In 2014, I was appointed as a Lecturer in Physiology at the University of Westminster where I first developed my interest in the gut-brain axis, and the mechanism(s) linking the gut microbiota with the brain pathology in neurodegenerative disease, in collaboration with Dr Lesley Hoyles. In 2016 I took up my current position as a non-clinical Senior Lecturer in Neuroscience & Pharmacology at the Institute of Dentistry, QMUL, where I continues my research investigating the gut brain axis and its relevance to neurodegenerative disease
My principal teaching responsibilities are on the first year of the Bachelor of Dental Surgery course, where I am part of the team delivering the Basic Clinical Sciences module. I teach neuroscience and pharmacology as part of the essential background required for later clinical years. I also contribute to other courses in the School of Medicine & Dentistry, including the BSc in Pharmacology & Therapeutic Innovation and MSc in Translational Neuroscience.
A second branch of my research is into the mechanisms of neuroinflammatory resolution, focusing particularly on the role of the protein annexin A1 and its primary receptor FPR2. In peripheral inflammation, we have shown that annexin A1 via FPR2 acts to both recruit macrophages and promote their differentiation into a pro-resolving phenotype, a key step in the regulated termination of inflammation. We are now investigating the role of the annexin A1-FPR2 system in microglia, given their close relationship to macrophages, focussing on whether agonists for this receptor may have value as an approach to limit neuroinflammatory activity in Alzheimer’s disease.
Hoyles L, Snelling T, Umlai U-K, Nicholson JK, Carding SR, Glen RC, McArthur S (2018) Microbiome-host systems interactions: Protective effects of propionate upon the bloodbrain barrier. BMC Microbiome vol. 6, 55
Loiola RA, Wickstead ES, Solito E, McArthur S (2019) Estrogen Promotes Pro-resolving Microglial Behavior and Phagocytic Cell Clearance Through the Actions of Annexin A1. Frontiers in Endocrinology
Cooray SN, Gobbetti T, Montero-Melendez T, McArthur S, Thompson D, Clark AJL, Flower RJ, Perretti M (2013) Ligand-specific conformational change of the G-protein-coupled receptor ALX/FPR2 determines proresolving functional responses. PNAS 110, 18232-18237