Iron, Ferritin and Dopamine: a model system study

Disrupted dopamine signalling is a feature of multiple psychiatric and age-related neurodegenerative disorders, including Parkinson's disease. Iron is essential for both the normal function of neurons and the regulation of dopamine. Brain iron significantly increases during ageing and may disturb dopamine signalling. In young, healthy individuals, iron in excess of metabolic needs is safely stored in the protein ferritin. However, during normal ageing the function of ferritin appears to fail.
Understanding of the molecular basis for how iron, ferritin and dopamine homeostasis interact in vivo and why dopaminergic neurons die in Parkinson’s disease is limited. In response, my lab has developed Caenorhabditis elegans models of ageing, disturbed iron and dopamine homeostasis to look at neuronal function and neurodegeneration in vivo.
I will discuss our efforts to understand why and how ageing, iron and dopamine interact to increase neuronal dysfunction and vulnerability to cell death.

I graduated with a PhD in Genetics from Monash University in 1999. From1999 to 2001 I was a postdoctoral fellow at the University of Manchester. I moved to the Buck Institute for Age Research (USA) in 2001, where I studied the genetics of ageing in C. elegans at with a Glenn Foundation/AFAR Fellowship awarded in 2003. In late 2007 I returned to Australia as a Research Fellow at the Mental Health Research Institute (MHRI). In 2011, the MHRI moved to the University of Melbourne, where it merged with the Florey Neuroscience Institute to become the new Florey Institute of Neuroscience and Mental Health (Florey). I joined the Florey Faculty in 2013, where I am now Head of the Molecular Gerontology laboratory in the Neurodegeneration Division. My research activities include investigating the genetics of ageing, dopamine function and iron metallobiology using the nematode Caenorhabditis elegans.