on leave July 1, 2012 to December 30, 2012
My research interests are focused on understanding the cell and molecular mechanisms underlying Parkinson’s disease. The aims of my research are to understand the events responsible for neurodegeneration in Parkinson’s disease, as well as elucidate the molecular mechanisms responsible for generation of parkinsonian symptoms, and side effects related to current treatments. The ultimate goal of this research is to develop more effective treatments for Parkinson’s disease.
Keywords:
Many different cell mechanisms have been implicated in neurogeneration in Parkinson’s disease, all of which appear to converge at the level of the mitochondria. We are characterising the role of mitochondria dynamics in cell death linked with Parkinson’s disease using real-time imaging in mesencephalic primary cell cultures and nigro-striatal co-cultures. The aim of these studies is to reveal novel targets for neuroprotective treatments.
Changes in synaptic plasticity within the striatum play a major role in generation of parkinsonian symptoms, and are also responsible for side effects associated with the current treatments for Parkinson’s disease. Re-organisation of molecules and proteins within striatal synapses probably underpins these abnormalities in synaptic plasticity. Using whole-cell patch clamp recording techniques in striatal slices prepared from transgenic mouse models, we are currently delineating the changes in synaptic plasticity that underpin symptoms and side-effects of Parkinson’s disease. We are using pharmacological and molecular biology tools to reverse these abnormalities, so that better symptomatic control of Parkinson’s disease may ultimately be achieved.