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Targeting The Synaptic Actin Cytoskeleton In Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$840,741.00
Summary
Dementias have become one of the fastest growing sources of major disease burdens in developed countries with about one in fifteen Australians older than 65 being affected. We will study how pathological stimuli disrupt nerve cell connections in the brain by impacting on the cellular architecture at these connections. Findings from our study will provide profound new insights in how nerve cells communicate with each other and how this communication is breaking down in disease.
Modulating Cellular Copper Levels To Prevent The Effects Of Excitotoxicity In Neurodegenerative Diseases
Funder
National Health and Medical Research Council
Funding Amount
$434,652.00
Summary
Exitotoxicity has been implicated in many neurological disorders incluing Alzheimer's and Huntington's disesaes. This toxicity can be inhibited by modulated intracellular copper levels. Here we will ascertain the therapeutic potential of strategies designed to increase cellular copper levels.
The Role Of Excitotoxicity In Mediating Distal Axonal Degneration In ALS
Funder
National Health and Medical Research Council
Funding Amount
$392,952.00
Summary
Amyotrophic lateral sclerosis (ALS), the major cause of motor neuron disease, is a devastating diseasse for which there is no cure. There have been significant advances in understanding the pathology of ALS yet we still don’t know what causes the dying back of spinal motor neurons. We have new evidence that suggests that ALS may, in part, be caused by excitotoxcity - or over stimulation - of neurons in the spinal cord. We will follow this lead using a range of cutting edge experimental models.
Targeting Post-synaptic Tau To Treat Alzheimer's Disease
Funder
National Health and Medical Research Council
Funding Amount
$1,686,311.00
Summary
We have previously identified post-synaptic tau as being critical in mediating toxicity in Alzheimer's disease brains. This project aims at understanding the exact underlying molecular mechanisms and, more importantly, developing novel drugs to block early toxicity that initiates cascades that eventually lead to brain atrophy and dementia. To achieve this aim, this project will generate and utilize models of Alzheimer's disease in combination with a broad range of latest analytical tools.
Astrocytes, Mutant TDP-43 And Non-cell Autonomous Injury Of Motoneurons
Funder
National Health and Medical Research Council
Funding Amount
$626,492.00
Summary
Motor neuron disease (MND) leads to death of nerve cells, paralysis and death. There is no cure. Mutations in the protein TDP43 cause MND. In this study we will investigate the underlying mechanisms of which these mutations cause disease. We will also investigate how these mutations affect astrocytes, a cell type that maintains normal function and survival of nerve cells and determine if the mutations affect the important interactions that normally takes place between these cell types.
Aurora Kinase: Molecular, Cellular And Functional Studies Deciphering Its Role In Stroke Injury
Funder
National Health and Medical Research Council
Funding Amount
$580,993.00
Summary
In stroke patients, oxygen deprivation indirectly induces massive nerve cell death by activating an enzyme called aurora kinase A (AURKA). We aim at unravelling (i) how AURKA is activated by oxygen deprivation, (ii) where the activated AURKA is localised in cells, and (iii) how the activated AURKA induces nerve cell death.The study will benefit development of therapeutic strategies to protect against brain damage in stroke since this is novel and different target for drug targeting.
A New Function For An Old Enzyme: Src Protein Kinase Directs Excitotoxic Neuronal Death In Stroke
Funder
National Health and Medical Research Council
Funding Amount
$513,975.00
Summary
In our previous investigation of how brain cells die in patients suffering from stroke, we found that stroke causes aberrant activation of an enzyme called Src in the affected brain cells. Furthermore, this aberrantly activated Src directs the brain cells to undergo cell death. Our proposal, which aims to decipher this neurotoxic mechanism of the aberrantly activated Src will benefit development of new therapeutic strategies to reduce brain damage in stroke patients.