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Search for a cause: the role of astrocytes in the early pathology of Parkinson's disease


The projects in our lab are directed towards finding the cause of Parkinson’s Disease.  In particular we want to know what is the nature of the mechanism that sets the neuronal degeneration into motion.


Dr Haydn Allbutt.

Research location

Camperdown - School of Medical Sciences - Bosch Institute

Program type



The laboratory of Motor and Sensory Systems is located in the historic Anderson Stuart Building on the main Camperdown campus of the University of Sydney.

Parkinson’s Disease (PD) is the second most common neurodegenerative disease after Alzheimer’s disease affecting an estimated 1% of people over the age of 65.  The disease is characterized by the loss of dopamine producing cells in the substantia nigra of the mid brain, in addition to the degeneration of a number of other nuclei in the brain stem, thalamus and cortex.  The result of these degenerations is that a range of motor, sensory, cognitive and autonomic symptoms develop.  There is currently no way of preventing the disease or stopping it once it has started and the only treatments we have to date are directed towards the relieving the symptoms.  The principal reason for this is that despite being first described more than 190 years ago we still don’t know what causes the disease.  There has been a genetic link found to 5-10% of cases but the cause of the other 90-95% is unknown.  Virtually all research is directed towards either developing new treatments, the pathology of the degenerations, the early detection of PD, the anatomy of the structures disrupted or new methods of visualizing dopamine disruption in the living brain.  There is very little if any work directed towards discovering what might cause Parkinson’s Disease.

It is therefore the primary aim of this lab to investigate possible causes of Parkinson’s disease.  We do this by modelling the condition based on our understanding of the pathologies associated with PD in an effort to work out which cell type must be involved in the development of these pathologies. The projects currently underway in the lab are examining whether the mechanisms predicted by our model may give rise to the human condition.  These projects have the potential to greatly expand our knowledge of not only PD but other neurodegenerative diseases such as Alzheimer’s disease and amyotrophic lateral sclerosis, a form of motoneuron disease, as the data we produce brings us a step closer to the ultimate goal of finding out what actually causes them.

Additional information

Possible projects that we have available in the lab are:

1. Examine the new model of Parkinson’s disease that we have developed to see if the same characteristic pathologies associated with the disease in humans also develop.  To date we have examined loss of dopaminergic neurons in the nigra and dopamine in the striatum, metabolic changes generally in the nigra and striatum, as well as for deficits specifically in complex I of the mitochondrial transport chain, changes in the levels of early and late apoptosis and glial cell changes.  Our next aim is to examine our model for changes in glutathione and iron levels in the substantia nigra to see if it accurately reproduces these pathologies.

2. To develop a blood test based on our model of Parkinson’s disease that can detect characteristic changes that occur prior to any neuronal loss.  If successful this test may form the basis of a cheap and easy screening test for pre-Parkinson’s disease which would allow preventative treatments to be initiated prior to any neuronal loss occurring thus effectively preventing the disease.

3. To use gene chip technologies to examine both our rat model of Parkinson’s disease as well as human tissue taken from presumptive pre-clinical Parkinsonian brain as well as late stage Parkinsonian brains.  Gene chips allow us to examine changes in expression in up to 28,000 genes at once.  The aims of this project would be to first of all examine whether our new rat model of Parkinson’s disease causes a similar change in gene expression as occurs in the human condition, and secondly to be the first to compare the pattern of gene expression in pre-clinical cases of PD with the pattern of gene expression observed in the late stage brain.  By doing this we hope to identify a series of genes involved with the pathological changes that occur as PD runs its course and could perhaps use this to “fingerprint” these gene changes at various stages of the disease.

4. To further develop our rat model of Parkinson’s disease to make it more accurately model the human condition.

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Opportunity ID

The opportunity ID for this research opportunity is 86