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Prof Kenneth Smith
1 Wakefield Street
London
WC1N 1PJ
Appointment
  • Professor of Experimental Neuroinflammation
  • IoN - Neuroinflammation
  • Institute of Neurology
  • Faculty of Brain Sciences
Research Summary

The focus of our team is research into the mechanisms underlying the neurological deficits in disorders characterised by inflammation, demyelination and/or degeneration. Our main focus is the inflammatory demyelinating diseases such as multiple sclerosis (MS) and Guillain-Barré syndrome (GBS), but our research also includes projects on motor neuron disease and glaucoma. Particular current interests are the several roles of nitric oxide in neuropathology, hypoxia, and developing a novel therapeutic strategy for axonal protection in neuroinflammatory disease such as MS.


We are particularly interested in how inflammation disturbs the normal function of the nervous system, with particular reference to the suspected role of hypoxia and nitric oxide. We believe that understanding the mechanisms operating in neuroinflammatory lesions will indicate new potential therapeutic avenues. One such therapy arising directly from our research is currently under clinical trial in patients with secondary progressive MS (see below). New approaches to therapy are being explored under a programme grant from the European Union (NeuroproMiSe). Indeed, inflammation plays an important role in disorders as diverse as MS, the neurological complications of AIDS, spinal cord injury, glaucoma, Parkinson's disease and motor neuron disease, and it is not unreasonable to believe that research into neuroinflammation may benefit all of these disorders. Demyelination (i.e. loss of the insulating layer of myelin from nerve fibres) causes symptoms such as blindness, paralysis and numbness by blocking axonal conduction, and we are searching for ways to improve conduction so that symptoms are alleviated. Acting in different ways, demyelination can also contribute to the tingling sensations experienced by many MS patients because it can make nerve fibres hyperexcitable. We are exploring the changes in sodium channel expression believed to cause these changes, with the intention of developing therapies to treat the symptoms.


Axonal degeneration causes permanent loss of function, and we have identified a mechanism that we believe is responsible for at least some of the degeneration in MS. We have also developed a therapeutic strategy based on the partial blockade of sodium channels (and/or the sodium-calcium exchanger). The therapy is inexpensive, and safe for long term administration, and it is currently being assessed in a clinical trial in secondary progressive MS, under funding from the MS Society.


Another project, funded by the MRC and MS Society, explores the physiological properties of tissue affected by inflammation, with particular focus on mitochondrial physiology, and the ion concentrations of the affected cells (especially axons). Other research projects within the lab use histochemistry, immunohistochemistry and confocal microscopy to explore the role of hypoxia and disordered energy metabolism in neurological disease, and electrophysiological techniques to examine the effects of inflammation on the electrical properties of neurons.

Academic Background
1979 PhD Doctor of Philosophy – Physiology Institute of Neurology
1973 BSc Bachelor of Science – Zoology and Comparative Physiology Queen Mary College, University of London
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