The brain is the most important organ in the human body and controls everything we do or think. The brain consists of billions of tiny cells and it links to all other systems in the body, including the immune system. The immune system helps us to fight off infection and to repair the body after an injury. This is done by special cells in the blood, the white blood cells, which can release different chemicals. For many years people believed that this so-called 'inflammatory' response had little to do with the brain. However, inflammatory responses can occur in the brain but, rather than being a good thing, this brain inflammation can be involved in diseases of the brain, including stroke and dementia. Stroke is when the blood supply to the brain is stopped, which kills brain cells, leading to death of the patient or severe disability. In my research I am trying to understand how it is that inflammation causes brain cells to die. By doing this one day we hope to be able to design treatments that can stop the inflammation and hence the brain cells from dying. This will lead to a better outcome for patients who have a stroke.

2012 - present
Professor of Neuroscience, Faculty of Life Sciences, University of Manchester, UK

2008-2012
Senior Lecturer, Faculty of Life Sciences, University of Manchester, UK.

2002-2008
Lecturer, Faculty of Life Sciences, University of Manchester, UK.

1993-2002
Postdoctoral Research Associate, School of Biological Sciences, University of Manchester, UK.

1990-1993
PhD Biomedical Sciences, University of Aberdeen, Scotland.

1986-1990
BSc Pharmacology (Upper 2nd Class Honours), University of Dundee, Scotland.

Inflammation in the brain

At one time the brain was considered an `immune-privileged' organ but it has become increasingly apparent that it is capable of producing key mediators of inflammation in response to injury and/or infection. Research over the last decade has implicated these inflammatory mediators in both acute and chronic neurodegenerative conditions, such as stroke, Alzheimer's disease, Parkinson's disease and epilepsy. Each of these conditions involves neuronal injury and death which translates to severe disability in the patient. 

Cytokines and neuronal injury

Cytokines are a group of key inflammatory molecules which have both beneficial and detrimental effects on CNS injury. Interleukin-1 (IL-1), often referred to as the "prototypical" pro-inflammatory cytokine, is the most extensively studied in neurodegeneration and has been the focus of our research. We have demonstrated that, in response to experimental brain injury, IL-1 contributes to cell death in the brain. Several possible mechanisms of IL-1 action have been proposed and our recent data indicate that effects of IL-1 on CNS injury are mediated via peripheral effects. We have also shown that IL-1 has marked effects on seizure activity and studies to identify the underlying mechanisms are currently ongoing, as are studies on the role of IL-1, as well as inflammation in general, in Alzheimer's disease.

Overall therefore our research is focused on elucidating the role of both central and peripheral cytokines (particularly IL-1) in neuronal injury, using appropriate experimental paradigms both in vitro and in vivo. Together with future clinical studies this work should enable us to determine the potential therapeutic benefit of targeting the IL-1 system in neurodegenerative disease.

Public engagement in science

I have developed and run a diverse range of innovative projects to communicate science to the public. A significant achievement is that these projects have reached a very wide audience from different backgrounds, and that they have focused not just on scientific fact but the scientific process itself. The latter is very important in both the attitude of the public to scientists and in attracting the scientists of the future. Our approach to public engagement has been disseminated to other scientists through posters at scientific meetings and articles in professional newsletters (including the British Neuroscience Association and Physiological Society).