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How Does Glucose Protect The Retina And Optic Nerve Against Ischaemia?
Funder
National Health and Medical Research Council
Funding Amount
$418,171.00
Summary
Raised blood sugar levels are generally considered to be bad for nerve cells, especially those in the eye. But we have made a groundbreaking discovery finding that in the short-term, sugar can rescue nerve cells in the eye from death caused by lack of blood flow. In this project we will investigate how this remarkable effect is achieved.
Functional Studies On A Neuroprotective Activity Of The Amyloid Precursor Protein Of Alzheimer S Disease.
Funder
National Health and Medical Research Council
Funding Amount
$160,475.00
Summary
Alzheimer's disease is a major health problem of the elderly. With our aging population living longer, this presents enormous economic and social pressures. Research into the mechanism of Alzheimer's disease is therefore of immediate importance. In this study we are trying to determine the relationship between proteins involved in the disease process. In particular we are studying the amyloid precursor protein (APP). APP has both therapeutic as well as disease causing actions. It gives rise to t ....Alzheimer's disease is a major health problem of the elderly. With our aging population living longer, this presents enormous economic and social pressures. Research into the mechanism of Alzheimer's disease is therefore of immediate importance. In this study we are trying to determine the relationship between proteins involved in the disease process. In particular we are studying the amyloid precursor protein (APP). APP has both therapeutic as well as disease causing actions. It gives rise to the toxic amyloid peptide Abeta which is responsible for disease. However APP can also inhibit Abeta toxicity thus controlling cell death. We are studying how APP is able to modulate the neurotoxic activity of Abeta. These studies will identify key aspects of the disease pathway and hopefully lead to treatment strategies.Read moreRead less
The Effects Of Maternal Glucocorticoid Administration In Growth Restricted Fetuses.
Funder
National Health and Medical Research Council
Funding Amount
$513,946.00
Summary
Antenatal administration of glucocorticoids to pregnant women at risk of preterm delivery has been shown to enhance fetal lung maturation. However, glucocorticoids such as betamethasone have a range of potentially deleterious non-pulmonary effects, which include significant alterations in fetal cardiovascular function. This is important because intrauterine growth restricted (IUGR) fetuses constitute a significant proportion of pregnancies in Australia, are at risk of preterm delivery and are th ....Antenatal administration of glucocorticoids to pregnant women at risk of preterm delivery has been shown to enhance fetal lung maturation. However, glucocorticoids such as betamethasone have a range of potentially deleterious non-pulmonary effects, which include significant alterations in fetal cardiovascular function. This is important because intrauterine growth restricted (IUGR) fetuses constitute a significant proportion of pregnancies in Australia, are at risk of preterm delivery and are therefore likely to receive maternal betamethasone. From both human observations and animal studies, it is well documented that IUGR fetuses demonstrate a range of cardiovascular adaptations that ensure maintenance of oxygen delivery to vital organs despite reduced placental perfusion. However, in recent clinical and experimental studies we have demonstrated that administration of betamethasone to IUGR fetuses induces changes in fetal blood flow that may be detrimental to the IUGR fetus. Specifically, we believe that glucocorticoids may increase the risk of both cardivascular and cerebral damage in the growth restricted fetus. The significance of these findings and the mechanisms regulating these changes remain unclear but they have clear implications for future clinical management. This proposal represents the further development of preliminary experimental studies to examine the effects of betamethasone in the ovine IUGR fetus with future clinical care in mind.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.
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.
Role Of Osteopontin In Ischemic-like Injury To The Retina
Funder
National Health and Medical Research Council
Funding Amount
$357,862.00
Summary
The molecule osteopontin (OPN) is implicated in the response of certain tissues to disease. We have new evidence that the level of OPN in the visual retina increases markedly following injury. We hypothesise that OPN is produced by specialised retinal cells in response to injury and functions to promote the survival of nerve cells. The proposed research seeks to investigate this hypothesis and the results will contribute to a greater understanding of the role of OPN in retinal diseases.
Neuroprotection In A Model Of Chronic Ocular Hypertension
Funder
National Health and Medical Research Council
Funding Amount
$264,221.00
Summary
Damage can occur to nervous tissues like the retina and brain when there is a reduction in the blood supply. This can occur in the eye disease, glaucoma, in which the pressure inside the eye is elevated. This serious condition often results in blindness. Much of the neuronal damage is thought to be due to the release of an excess of glutamate. Glutamate is a chemical (neurotransmitter) that nerves use to communicate with each other, but it is toxic to nerves when present at high concentrations. ....Damage can occur to nervous tissues like the retina and brain when there is a reduction in the blood supply. This can occur in the eye disease, glaucoma, in which the pressure inside the eye is elevated. This serious condition often results in blindness. Much of the neuronal damage is thought to be due to the release of an excess of glutamate. Glutamate is a chemical (neurotransmitter) that nerves use to communicate with each other, but it is toxic to nerves when present at high concentrations. This project will utilise a new model of glaucoma to investigate the mechanisms that regulate the concentration of glutamate in the retina. If these mechanisms could be made to work more efficiently, they may prevent the build-up of the glutamate and therefore prevent damage to the nerve cells. Understanding these mechanisms will aid in the development of an effective treatment to prevent visual loss in the 150,000 Australians who suffer from glaucoma.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.