Dr Elizabeth Bradbury
Dr Katalin Bartus/ Post-Doc
Dr Athanasios Didangelos/Post-Doc
Dr Nick James/Post-Doc
Ms Michaela Iberl/Research Assistant
Ms Emily Burnside/PhD Student
Mr Merrick Strotton/PhD Student
News - MRC Senior Non-Clinical Fellowship awarded to Liz Bradbury
Spinal Cord Injury Repair Strategies
It is an exciting time for spinal cord injury research with many recent advances being made in identifying key factors that prevent repair after injury. Proteoglycans have been identified as important inhibitors of growth and the manipulation of these molecules can result in plastic changes and restoration of lost function. Understanding the mechanisms underlying such repair may ultimately lead to the development of therapeutic targets.
Spinal cord injury
The complex anatomical arrangement of the projections that transmit sensory and motor information between the brain and the spinal cord means that even minor injury to the spinal cord can have devastating consequences. There are currently no adequate treatments for spinal cord injury with the focus being on rehabilitation and reducing secondary inflammatory events. However, in recent years spinal cord injury research has progressed at a rapid pace, with great advances being made in understanding why this severely debilitating condition is so unresponsive to repair. This has led to a real hope for more ambitious therapies in the future, which are aimed at promoting regeneration, optimizing intact systems and restoring lost function.
Manipulating proteoglycans to promote repair after spinal cord injury
Chondroitin sulphate proteoglycans (CSPGs) have been identified as important inhibitory molecules that are present in the extracellular matrix and are associated with the glial scar that forms around injury sites. Recent work from my laboratory has shown that degrading CSPGs can result in the re-establishment of synaptic connections and a recovery of lost sensorimotor function in adult spinal injured rats. Degrading CSPGs has also recently been demonstrated to induce plasticity in the visual system, to an extent normally only seen during development. Thus, CSPGs may function in the adult CNS to inhibit intact systems from sprouting as well as damaged systems from regenerating. Thus, a major goal of the research in my lab is to determine whether exploiting sprouting and plasticity responses may be a key to regaining lost function after spinal cord injury.
Modeling human spinal cord injury
A second goal of the research in my lab is to establish an experimental model that closely resembles the trauma characteristic of human spinal cord injuries. This would be an optimal model in which to test whether various treatment strategies have the potential to be used therapeutically. Thus, in a collaboration with the Ohio State University we are establishing a controlled contusion injury device in my lab which can produce graded spinal cord contusion injuries with reproducible effects on behavioural and anatomical outcome measures. This will provide a valuable tool with which to assess the therapeutic potential of interventions aimed at targeting CSPG-mediated inhibition and other treatment strategies.
Combination approaches to promoting repair after spinal cord injury
A third goal of the research in my lab is to test the hypothesis that combining CSPG-degrading treatments with neurotrophic factor delivery, and other treatment strategies, will have synergistic effects in enhancing functional recovery following spinal cord injury. Thus, we are using multiple outcome measures to assess the functional effects of novel treatment strategies, aimed at optimising regeneration and compensatory sprouting responses.