David Baker Professor of Neuroimmunology

 

David Baker spent his academic career based at different places of the University of London. He was awarded a BSc (Hons) in Zoology from Bedford College in 1983 and was awarded a PhD from London University in Immunology/Pathology in 1987 on immunological tolerance induction. He then spent six years as the Angela Limerick lecturer, for multiple sclerosis research at the Hunterian Institute, The Royal College of Surgeons of England working, where he developed an active research interest in multiple sclerosis. He took a 5 year Principal Fellowship to the Institute of Ophthalmology, University College London in 1994 and became the first Senior Fellow of the Multiple Sclerosis Society and moved to the Institute of Neurology, University College London in 1999. He became a senior lecturer in 2003 and got a personal chair in 2004 as Professor of Neuroimmunology. He moved to Queen Mary in the autumn of 2006. The research of the laboratory focuses notably on experimental models of multiple sclerosis. This provides a basic science arm to complement the clinical arm of the laboratory lead by Professor Gavin Giovannoni.

The initially focus of the laboratory centred on neuroimmunological aspects of the disease process. Recently however, this has broadened to examination of novel therapeutics and disease pathways in the control of immune function, neuroprotection and symptom control. We are investigating a number of pathways that can prevent nerve loss from the damaging effects of disease. There has been a recent focus on the role of the cannabinoid system in control of multiple sclerosis and the identification of novel cannabinoid-related receptors for disease control. We have been investigating how we can prevent cannabis-like drugs from entering certain bits of the brain, such that we can keep the therapeutic benefit, whilst limiting the mind-altering side-effects.

The group and collaborators have synthesised and developed new therapeutics, which they are moving from the bench towards the clinic.

 

Lesion in Multiple Sclerosis

 

Recent publications:

Pryce G and Baker D. Control of Spasticity in a Multiple Sclerosis Model is CB1, not CB2, cannabinoid receptor mediated. Brit J Pharmacol. 2007;150:519-525.

Maresz K et al. Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T Cells.  Nat Medicine 2007;13:492-497.

Croxford JL et al. Cannabinoid-mediated neuroprotection, not immunosuppression, may be relevant to multiple sclerosis. J. Neuroimmunol. 2008; 193:120-129