Parkinson's Disease (PD) is one of the most common neurodegenerative disorders. Its incidence increases steadily with age affecting approximately one per cent of the population at age 65 and up to five per cent by the age of 85. At the time of diagnosis, patients suffer from a range of motor impairments that worsen over time. Pathologically these patients are characterised by the accumulation of a protein known as alpha-synuclein in specific types of nerve cells in their brain. However, the function of this protein is unknown. This research aims to clarify the role of alpha-synuclein in PD and normal CNS function and provide new potential therapeutic targets for the treatment of PD and other neurodegenerative disorders in which oxidative stress, excitotoxicity and central nervous system trauma have been implicated.

Our studies found that the protein alpha-synuclein is upregulated in neurones in response to chronic oxidative stress and is associated with neuroprotection. Furthermore, we have determined that a similar response occurs in response to neuronal physical trauma, which is a risk factor for PD and also occurs across a range of nerve cell types including those that are selectively vulnerable to PD. We have established two colonies of transgenic mice, one that models a genetic mutation in alpha-synuclein that is present in some cases of PD and another that doesn't produce the protein at all, therefore introducing a range of experimental possibilities for these investigations.