Quick Project Snapshot

Support Cells and Dopaminergic Neurons

Brain iron increases significantly during ageing and is even further elevated in Parkinson’s disease. The death of dopaminergic neurons contributes to motor deficits characteristic of this disease. While iron is essential for normal function of these neurons, increased levels within these cells may be a trigger a newly identified form of cell death that drives neurodegeneration. The health of dopaminergic neurons is also supported by closely associated glial cells. However, the details of how glial dysfunction affects dopaminergic cell viability need further examination.

We will explore early life changes to the dopaminergic system through to neuronal death in late life. Understanding how the interactions between iron, glia and dopamine change through lifespan will provide new avenues for interventions to prevent cell death in Parkinson’s disease.


The project: To use Caenorhabditis elegans, a model organism with powerful genetics, to understand how losing control of iron homeostasis in glial cells contributes to the loss of dopaminergic neurons.


·      Using transgenic manipulation of iron homeostasis and dopamine.

·      Model dopaminergic cell loss through cell specific (including glia) genetic manipulations










Figure: Cephalic sheath glia in C. elegans: CEPsh cells (Blue), CEP dopaminergic neurons (Pink), Nerve ring (Red)



Suitable for PhD or MSc

Dr Gawain Mccoll

Molecular Gerontology Laboratory

Ageing is universal in multicellular organisms. How ageing and lifespan can be modulated is an area of significant scientific interest. By reducing complexity and time scale, the study of simple organisms has provided a wealth of information about the biochemical systems that contribute to the ageing process. The nematode, Caenorhabditis elegans has numerous advantages for the study of the biology of ageing.

These nematodes are microscopic (~1 mm), self-fertilizing, free living, and easily cultured in the laboratory. Benefits of this model system include: a short three-day life cycle, 14-day natural lifespan, highly developed genetic tools, fully characterised cell lineage, and an open research community. Despite its simplicity, conservation of genetic and disease pathways between C. elegans and higher eukaryotes make it an effective in vivo model for study ageing and disease pathogenesis and the preeminent model system for genetic manipulation of ageing.

Work using this model first demonstrated that single genes and compounds could dramatically modulate life span and the rate of ageing.

All Projects by this Lab

Rapid animal models of Parkinson’s diseaseNew animal models of Alzheimer’s diseaseIron and Biological AgeingSupport Cells and Dopaminergic Neurons


Scientists in the Neurodegeneration division interrogate how neurones live, die and can be rescued to improve brain function in degenerative conditions such as Parkinson’s and Motor Neuron Diseases. There is no effective treatment for Motor Neurone Disease and the incidence of Parkinson’s Disease is rising alarmingly in our aging community. Gene abnormalities, energy deprivation, toxic rubbish accumulation and inflammation all contribute to a toxic environment for brain cells. Our teams study these events in animal models and cultured cells, with a view to translating knowledge into new therapies for human patients.

All Labs that operate in this Division

Atomic Pathology LaboratoryCreutzfeldt Jakob Disease Clinical Research GroupMolecular Gerontology LaboratoryMotor Neurone Disease LaboratoryNational Dementia Diagnostics LaboratoryNeurochemistry of Metal IonsNeurogenesis and Neural Transplantation LaboratoryNeuropathology and Neurodegeneration LaboratoryNeuroproteomics and Metalloproteomics LaboratoryNeurotherapeutics LaboratoryParkinson's Disease LaboratoryPre-clinical Parkinson’s Disease Research LaboratoryPresynaptic Physiology Stem Cells and Neural Development LaboratorySteroid Neurobiology LaboratorySynaptic Neurobiology LaboratoryThe Australian Imaging Biomarker and Lifestyle Study (AIBL)