The Australian Research Data Commons (ARDC) invites you to participate in a short survey about your
interaction with the ARDC and use of our national research infrastructure and services. The survey will take
approximately 5 minutes and is anonymous. It’s open to anyone who uses our digital research infrastructure
services including Reasearch Link Australia.
We will use the information you provide to improve the national research infrastructure and services we
deliver and to report on user satisfaction to the Australian Government’s National Collaborative Research
Infrastructure Strategy (NCRIS) program.
Please take a few minutes to provide your input. The survey closes COB Friday 29 May 2026.
Complete the 5 min survey now by clicking on the link below.
Studies On Induction Of Antigen Specific T Regulatory Cells To Control Autoimmunity
Funder
National Health and Medical Research Council
Funding Amount
$353,033.00
Summary
The immune system has natural control mechanisms, called regulatory cells. Our group was the first in the world to correctly identify these cells. There is now a world-wide interest in these cells as they can prevent unwanted immune mediated injury. In autoimmune diseases such as multiple sclerosis, regulatory cells can prevent relapse and progression. This project will identify ways of producing potent specific regulatory cells to control multiple sclerosis and other debilitating neurological d ....The immune system has natural control mechanisms, called regulatory cells. Our group was the first in the world to correctly identify these cells. There is now a world-wide interest in these cells as they can prevent unwanted immune mediated injury. In autoimmune diseases such as multiple sclerosis, regulatory cells can prevent relapse and progression. This project will identify ways of producing potent specific regulatory cells to control multiple sclerosis and other debilitating neurological diseases.Read moreRead less
Gene Discovery And Functional Insights For Neurological And Retinal Disorders
Funder
National Health and Medical Research Council
Funding Amount
$2,163,220.00
Summary
Understanding the genetic drivers of disease is key for the development of disease therapies. Determination of the causal genetic variants in a disorder can be used for future diagnosis, prognostication, and personalised treatment. We have previously identified ~20 novel genes and developed new methods providing genomic diagnoses for 1000s of individuals. In the next five years I will make significant advances in our understanding of what causes diseases such as epilepsy, ataxia and dementia.
Hereditary Motor Neuronopathies And Neuropathies: Mechanisms Of Neurodegeneration And Potential Modification.
Funder
National Health and Medical Research Council
Funding Amount
$104,664.00
Summary
The aim of the study is to investigate the pathophysiology of motor neuron degeneration in its various acquired and inherited forms. Nerve function will be determined by clinical and neurophysiological assessments in patients. The findings of the study will reveal further insights into the cause and progression of disorders of the motor neuron. This data may function to monitor disease progression, response to potential therapies and lead to the development of further therapeutic strategies.
How Do Glycosaminoglycans Promote The Propagation Of Prions?
Funder
National Health and Medical Research Council
Funding Amount
$512,270.00
Summary
The prion diseases are a group of transmissible, neurodegenerative disorders affecting both humans and animals. The most common form in humans is sporadic Creutzfeldt-Jakob disease (CJD), although acquired (variant CJD) and inherited (familial CJD) forms are recognised. Prion diseases are transmissible to the same species by inoculation with, or dietary exposure to, infected tissues. The infectious agent, referred to as a prion , has not been identified at the molecular level. However, a major c ....The prion diseases are a group of transmissible, neurodegenerative disorders affecting both humans and animals. The most common form in humans is sporadic Creutzfeldt-Jakob disease (CJD), although acquired (variant CJD) and inherited (familial CJD) forms are recognised. Prion diseases are transmissible to the same species by inoculation with, or dietary exposure to, infected tissues. The infectious agent, referred to as a prion , has not been identified at the molecular level. However, a major component of purified prions is an abnormal disease associated form of the host encoded prion protein. Understanding how the disease associated form of the prion protein is generated and how host-derived cofactors contribute to its formation will help in our understanding of the infectious nature of these diseases and in the development of effective therapeutic and prophylactic strategies. Glycosaminoglycans are host-derived components of the extracellular matrix that are associated with prion protein plaques found in the brain tissue of patients with prion diseases. Glycosaminoglycans are believed to influence the transmission of prions and the ongoing propagation of infectivity. In this study the importance of glycosaminoglycans in the formation of the disease associated prion protein and the generation of infectivity will be investigated using both cell-free and cell-based models of prion propagation. The understanding gained from this study will be used to develop a high throughput assay that can be used to detect prion infection prior to the development of clinical disease and within a time frame whereby therapeutic intervention may be effective.Read moreRead less
Investigation Into The Roles Of A Novel Vertebrate Gene, S52, In CNS Development And Pathogenesis
Funder
National Health and Medical Research Council
Funding Amount
$272,389.00
Summary
Developmentally regulated genes when mutated or deleted can cause a variety of diseases including neurological diseases in humans. It is therefore important to understand the fundamental molecular genetics of development. We have discovered a novel human gene, termed S52, and its equivalent gene in the mouse. The predicted protein derived from these genes would indicate that S52 protein may interact with other proteins, possibly nerve growth factors, in the body to regulate normal development an ....Developmentally regulated genes when mutated or deleted can cause a variety of diseases including neurological diseases in humans. It is therefore important to understand the fundamental molecular genetics of development. We have discovered a novel human gene, termed S52, and its equivalent gene in the mouse. The predicted protein derived from these genes would indicate that S52 protein may interact with other proteins, possibly nerve growth factors, in the body to regulate normal development and possibly facilitate the survival of nerve cells in embryos. Strikingly, the worm C. elegans, an evoluationary very distant animal, also has a very similar gene to human. The fact that the protein has been so conserved throughout evolution supports the idea that S52 function is important in development. S52 mRNA is expressed in the developing brain, particularly in a special group of cells called the floor plate. Floor plate is a tissue that has ability to organize the patterning and differentiation of cells within the developing brain. S52 is also expressed in motor neurons in early stages of development and later in a subset of dorsal spinal cord neurons. We have mapped S52 to the short arm of human chromosome 2 (2p15-22). This region of chromosome 2 is linked to several human genetic diseases with neurological defects. Based on our preliminary data, we think S52 is not only important for normal brain development but may be mutated in a human neurological disease called Spastic Paraplegia Type 4 (SPG4) which is characterized by a degeneration of nerve cells in the spinal cord. The aim of this project is to further our understanding of the function of this gene and investigate its role in disease. This knowledge will contribute to an overall increase in our understanding of the molecular basis of brain development and neurological disease in humans.Read moreRead less
The Physiological And Pathophysiological Roles Of Melanotransferrin
Funder
National Health and Medical Research Council
Funding Amount
$227,485.00
Summary
Melanotransferrin (MTf) is a membrane bound molecule that was originally identified in the malignant melanoma skin cancer and other tumours. Interestingly, MTf has many similarities to the serum iron-binding protein, transferrin, and initially MTf was thought to play a role in iron uptake by these cells. However, a series of studies by the applicant demonstrated that MTf did not play a major role in iron uptake by melanoma cells (Richardson et al. 1990, 1991a,b). In fact, most iron taken up by t ....Melanotransferrin (MTf) is a membrane bound molecule that was originally identified in the malignant melanoma skin cancer and other tumours. Interestingly, MTf has many similarities to the serum iron-binding protein, transferrin, and initially MTf was thought to play a role in iron uptake by these cells. However, a series of studies by the applicant demonstrated that MTf did not play a major role in iron uptake by melanoma cells (Richardson et al. 1990, 1991a,b). In fact, most iron taken up by these cells was via the binding of transferrin to the transferrin receptor. More recently, under the current NHMRC grant, we have been able to confirm and signficantly extend our previous studies to convincingly show that MTf is not involved in iron uptake by melanoma cells where it is expressed at very high levels (Richardson 2000 Eur. J. Biochem. 267 (in press). In addition, we showed that the expression of MTf in 50 human tissues was very different to transferrin and the transferrin receptor (TfR) that are well known to be involved in iron transport. For example, the TfR is expressed at high levels in tissues that require large amounts of iron eg. the placenta and bone marrow. In contrast, MTf was not expressed at high levels in these tissues, but was found in large amounts in unexpected locations such as the salivary gland. Furthermore, the expression of MTf was widespread through a variety of tissues, and in contrast to expectations, was found at higher levels in normal rather than fetal tissues. It is also intesting that MTf is found in the blood and brain of Alzheimer's disease patients. Our results suggest that MTf may play other unexpected roles apart from iron uptake. The present proposal will assess the roles of MTf in cellular functioning. This information will be very important in understanding the function of MTf in cancer cells, Alzheimer's disease and also in other tissues (eg. the salivary gland) where it is expressed at very high levels.Read moreRead less
Dendritic Cells And CCAAT/enhancer Binding Protein-delta (CEBP?) In Neuroinflammation And Autoimmunity
Funder
National Health and Medical Research Council
Funding Amount
$576,538.00
Summary
This projects aims to develop new treatments by finding the cells and chemicals that naturally stop inflammation in the central nervous system in diseases like MS. It also aims to test new treatments by delivering them to where this inflammation takes place. This targeted delivery should mean fewer side effects because the rest of the body is not exposed to the treatment. Hopefully this will reduce the impact of these diseases on the community, and reduce side effects for the patient.
Nix Mediated Mitophagy: A New Therapeutic Approach To Parkinson's Disease
Funder
National Health and Medical Research Council
Funding Amount
$674,428.00
Summary
Parkinson’s disease (PD) is the most common neurodegenerative movement disorder in the world. A key problem in PD is that affected neurons lose energy and then die. We have discovered that by recycling mitochondria (the parts of the cell that produce energy), we can protect neurons from dying and restore function. This project will determine whether mitochondrial recycling mediated by Nix can restore energy and prevent neuronal loss. This would represent a new therapeutic approach to treat PD.