My laboratory is interested in the molecular mechanisms of molecular degeneration and axonal repair. We employ a variety of modern molecular techniques such as lentiviral vectors, microRNA analyses, individual-nucleotide resolution Cross-Linking and ImmunoPrecipitation (iCLIP) and Translating Ribosome Affinity Purification (TRAP) techniques to study how specific genes can affect cellular pathways to alter function and phenotype of neural cells. The overall aim is to further our understanding of the molecular and cellular pathways that underlie neuronal degeneration in disorders such as Parkinson's disease, Alzheimer's disease, stroke, traumatic brain injury and nerve injury. This information can help us identify new targets that can be manipulated, either using druggable or gene therapy approaches, in order to devise new treatments for these diseases. Current projects include:

1) investigating the role of microRNAs in adult neurogenesis and axonal regrowth. We have previously identified a microRNA - miR-21 - that is significantly increased in injured nerves and encourages neurite outgrowth in neurons. We are currently trying to understand how this occurs and how we can manipulate this to develop treatment strategies to encourage nerves to regrow. Interestingly, miR-21 is also significantly increased in traumatic brain injuries and may have roles in regulating brain function and repair. We are currently conducting studies to understand how miR-21 can affect neurogenesis in the brain and spinal cord.

2) We are interested in developing new treatment strategies for treating spinal cord injury. In collaboration with Dr Nicolas Granger (University of Bristol), we are exploring combination strategies that will enhance the function of olfactory ensheathing cells in the treatment of canine spinal cord injury. These include genetic manipulation of olfactory ensheathing cells to secrete an enzyme chondroitinase in a regulatable manner, or manipulating olfactory ensheathing cells to produce growth factors to encourage injured nerves (axons) to regrow.

3) Using cell models of Parkinson's disease, we are looking at how specific proteins can affect gene expression and function of dopaminergic neurons. In particular, we are interested in how normal and mutant synuclein can affect gene expression in dopaminergic neurons derived from normal and Parkinson's patients.