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.
The Sulphate Anion Protects Against Stroke: Characterisation Of Neuroprotective Potential And Mechanism Of Action.
Funder
National Health and Medical Research Council
Funding Amount
$189,170.00
Summary
Stroke-cerebral ischaemia affects approximately 40,000 - 50,000 Australians every year and is Australia's leading single cause of disability and second greatest cause of death after heart disease. About 25% of people who suffer a stroke die within one month while most survivors are disabled because of impaired speech, memory, thought processes, vision, balance, or motor control of the limbs (paralysis). The direct and indirect cost of stroke to the Australian community is over $2 billion annuall ....Stroke-cerebral ischaemia affects approximately 40,000 - 50,000 Australians every year and is Australia's leading single cause of disability and second greatest cause of death after heart disease. About 25% of people who suffer a stroke die within one month while most survivors are disabled because of impaired speech, memory, thought processes, vision, balance, or motor control of the limbs (paralysis). The direct and indirect cost of stroke to the Australian community is over $2 billion annually. Hence preventing or reducing brain damage following stroke is of fundamental clinical, social and economic significance. A stroke occurs when there is a reduced blood supply to the entire brain (Global ischaemia; eg. cardiac arrest, heart bypass surgery, closed head injury) or when there is a reduced blood supply to a specific region of the brain, usually as a result of a blockage in a brain artery (thrombo-embolic stroke or focal ischaemia). Despite decades of research, there is no totally satisfactory clinical treatment to reduce brain damage following stroke; the search for new treatments is paramount. We have shown that sodium sulphate can prevent brain damage in rat models of focal and global ischaemia. Importantly we demonstrated that sodium sulphate could prevent brain damage when given up to 8 hours after the stroke was induced in the global model. Delayed treatment following stroke is of clinical significance, since most patients do not receive medical attention until several hours after initial stroke symptoms. It is not known how sodium sulphate protects the brain from stroke. This project has three main aims: 1. To determine the how well sodium sulphate treatment protects the brain in rats following stroke. 2. To determine if sodium sulphate treatment can reduce brain damage in the rat model of focal ischaemia when given 4 - 8 hours after the stroke. 3. To determine how sodium sulphate protects the brain from stroke.Read moreRead less
Role Of Insulin-regulated Aminopeptidase In Ischemic Stroke Damage
Funder
National Health and Medical Research Council
Funding Amount
$499,219.00
Summary
Stroke is a neurovascular disease which is the leading cause of adult disability. A focus of our research group is to investigate the role of a protein called insulin-regulated aminopeptidase (IRAP) in ischemic stroke. We have shown a dramatic protection from ischemic brain damage in mice with deletion of the IRAP gene. The aims of this study are to explore the potential use of the newly developed IRAP inhibitors in protecting brain damage following ischemic stroke and to determine the role of I ....Stroke is a neurovascular disease which is the leading cause of adult disability. A focus of our research group is to investigate the role of a protein called insulin-regulated aminopeptidase (IRAP) in ischemic stroke. We have shown a dramatic protection from ischemic brain damage in mice with deletion of the IRAP gene. The aims of this study are to explore the potential use of the newly developed IRAP inhibitors in protecting brain damage following ischemic stroke and to determine the role of IRAP in the pathophysiology of cerebral ischemia.Read moreRead less
ROLE OF A DOWN SYNDROME-RELATED PROTEIN IN STROKE OUTCOME
Funder
National Health and Medical Research Council
Funding Amount
$931,302.00
Summary
This project will test whether a gene called DSCR1, which is present at a higher level in Down Syndrome individuals, might play a protective role in the outcome after stroke. We will identify the cells and molecular pathways that are involved in this protective effect in mice, with a longer term view of applying this information to the development of new types of targeted therapies for clinical stroke.
Enhancing The Neuroprotective Benefit Of Hypothermia With Melatonin In The Asphyxiated Neonate
Funder
National Health and Medical Research Council
Funding Amount
$785,331.00
Summary
During labour, asphyxic episodes which cause a severe reduction in oxygen supply can become prolonged and result in perinatal brain injury, termed Hypoxic Ischemic Encephalopathy, which may underlie cerebral palsy. Presently, newborn infants with suspected encephalopathy are cooled, which modestly protects the brain against cellular injury. We propose that the administration of melatonin to the newborn, in addition to cooling, will decrease the post-asphyxic formation of oxygen free radicals, th ....During labour, asphyxic episodes which cause a severe reduction in oxygen supply can become prolonged and result in perinatal brain injury, termed Hypoxic Ischemic Encephalopathy, which may underlie cerebral palsy. Presently, newborn infants with suspected encephalopathy are cooled, which modestly protects the brain against cellular injury. We propose that the administration of melatonin to the newborn, in addition to cooling, will decrease the post-asphyxic formation of oxygen free radicals, thereby reducing the progression of brain damage.Read moreRead less
Stroke is Australia's second single greatest killer and a leading cause of disability, with high blood pressure associated with a greater risk of stroke occurring. We have evidence of a possible new target, the angiotensin type 2 receptor that is protective in stroke. This proposal involves elucidating the mechanisms underlying this protective effect which may lead to new therapeutic strategies in treating stroke.
Evaluation Of Combined Mild Hypothermia And Magnesium As A Neuroprotective Therapy Following Cerebral Ischaemia/stroke
Funder
National Health and Medical Research Council
Funding Amount
$310,286.00
Summary
Stroke-cerebral ischaemia affects over 50,000 Australians every year and is Australia's leading single cause of disability and third greatest cause of death after heart disease. About 25% of people who suffer a stroke die within one month while most survivors are disabled because of impaired speech, memory, thought processes, vision, balance, or motor control of the limbs (paralysis). The direct and indirect cost of stroke-cerebral ischaemia to the Australian community is over $2 billion annuall ....Stroke-cerebral ischaemia affects over 50,000 Australians every year and is Australia's leading single cause of disability and third greatest cause of death after heart disease. About 25% of people who suffer a stroke die within one month while most survivors are disabled because of impaired speech, memory, thought processes, vision, balance, or motor control of the limbs (paralysis). The direct and indirect cost of stroke-cerebral ischaemia to the Australian community is over $2 billion annually. The ability to inhibit or limit brain damage once a stroke has occurred will reduce the devastating effects of stroke to patients and the Australian community. Despite decades of research, there is no totally satisfactory drug that directly inhibits brain damage following stroke; the search for new treatments is paramount. A stroke occurs when there is a reduced blood supply to the entire brain (global cerebral ischaemia; eg. cardiac arrest, closed head injury) or to a specific region of the brain, usually as a result of a blockage in a brain artery (focal cerebral ischaemia or thrombo-embolic stroke). This project will evaluate the efficacy of combined magnesium and mild hypothermia (35) treatment protocols to reduce brain damage in animal models of focal and global cerebral ischaemia. This work stems from our recent data showing for the first time that magnesium is only neuroprotective in animals following cerebral ischaemia when present with hypothermia. Thus our data indicates that magnesium, when combined with hypothermia is an effective stroke therapy. Moreover treatment with magnesium-mild hypothermia has several attractions. Both are likely to have multiple mechanisms of action, are cheap to administer and safe. Importantly, the experimental findings from this project will enable better design of future clinical trials to test the efficacy of combined magnesium-modest hypothermia to improve patient outcome following stroke.Read moreRead less
Neuroprotection By Ndfip1 In Brain Injury - Identifying Targets And Understanding Mechanisms
Funder
National Health and Medical Research Council
Funding Amount
$836,225.00
Summary
Brain injury from trauma and motor vehicle accidents is a serious health issue, affecting approximately 30,000 Australians per year. About 10% of the victims suffer serious long term consequences, including mental, physical and behavioural impairment. We have discovered a new brain protein capable of preventing neurons from dying following injury. This grant will improve our understanding of how this protein works, and provide a scientific foundation for devising therapies.
Brain Repair Following Stroke: The Role Of Npas4, A Neural-specific Transcription Factor
Funder
National Health and Medical Research Council
Funding Amount
$611,053.00
Summary
Stroke is the #1 cause of adult disability in Australia and #2 cause of death. About 60,000 Australians suffer a stroke each year while about 250,000 live with the disabilities of stroke, costing over $2B/year. The Queen Elizabeth Hospital and University of Adelaide will study why the Npas4 gene switches on after stroke and the role it plays in brain repair. Future health benefits may be tests to help improve stroke outcome in patients and therapy to decrease loss of brain cells after stroke.
Substance P Antagonists As A Novel Therapeutic Intervention In Stroke
Funder
National Health and Medical Research Council
Funding Amount
$318,267.00
Summary
Stroke is the major cause of disability in adults over 45 years of age in Australia. The economic and social cost of stroke is enormous with billions of dollars spent each year on the management and rehabilitation of stroke patients. Despite the enormity of this public health problem, no effective treatment currently exists. A number of studies have now demonstrated that much of the morbidity following stroke is associated with the breakdown of the blood brain barrier, development of oedema, and ....Stroke is the major cause of disability in adults over 45 years of age in Australia. The economic and social cost of stroke is enormous with billions of dollars spent each year on the management and rehabilitation of stroke patients. Despite the enormity of this public health problem, no effective treatment currently exists. A number of studies have now demonstrated that much of the morbidity following stroke is associated with the breakdown of the blood brain barrier, development of oedema, and subsequent brain damage in areas surrounding the central region of the stroke. These events develop over hours to days following the stroke and are known as secondary injury. This delayed progression of injury suggests that appropriate pharmacologic intervention can prevent, or at least attenuate, this secondary injury process with a resultant improvement in outcome. Nonetheless, few interventions are available that can limit this development. Our own recent studies have demonstrated that regions in brains which demonstrate the presence of stroke also exhibit signs of neurogenic inflammation, which has been associated with oedema formation, oxidative damage and cell death in other tissues. Although a number of neuropeptides have been implicated in this process, it is thought that substance P release is closely associated with these pathophysiological processes. Thus, inhibiting substance P binding may offer a novel therapeutic approach to attenuating oedema formation and the development of neurologic deficits following stroke. This proposal will utilise a combined biochemical, pharmacologic and behavioural approach to characterize the role of neurogenic inflammation in the development of oedema and neurologic deficits following stroke. Moreover, we will develop a novel pharmacotherapy that can potentially be used in the treatment of clinical stroke.Read moreRead less