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The Role Of Tau In Experimental Retinal And Optic Nerve Pathology: Relevance To Glaucoma
Funder
National Health and Medical Research Council
Funding Amount
$375,225.00
Summary
Aberrant processing of the axonal protein, tau, is believed to underlie key pathological events in Alzheimer's Disease (AD). Recent data have suggested a link between AD pathology and retinal neuron death in glaucoma. We have further evidence that changes in tau also occur in models of retinal damage. We thus aim to characterise the role of tau in retinal injury models and to relate these findings to glaucoma with a view to having a greater understanding of this disease process.
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
Mechanisms Of Cell Death In Focal Cerebral Ischaemia
Funder
National Health and Medical Research Council
Funding Amount
$229,624.00
Summary
Stroke most commonly results from interruption to a major artery in the brain. If not rapidly reversed the reduction in blood flow leads to the death of many cells in the brain tissue. There is currently considerable interest in developing treatments to be used in the early stages of stroke that can reduce cell death. As the extent of cell death is the major determinant of the long-term disabilities from stroke, such treatments are likely to provide considerable benenfits for affected individual ....Stroke most commonly results from interruption to a major artery in the brain. If not rapidly reversed the reduction in blood flow leads to the death of many cells in the brain tissue. There is currently considerable interest in developing treatments to be used in the early stages of stroke that can reduce cell death. As the extent of cell death is the major determinant of the long-term disabilities from stroke, such treatments are likely to provide considerable benenfits for affected individuals. Our study will investigate mechanisms underlying the death of brain cells in an animal model of stroke and in cells treated in culture. These studies will specifically focus on the role in cell death of alterations in mitochondria, a part of the cell that provides the energy needed for their normal function. The proposed investigations will identify molecular events that contribute to the mitochondrial dysfunction and examine the importance of these changes in brain tissue damage. The findings should contribute to the identication of new therapeutic approaches aimed at ameliorating the consequences of stroke.Read moreRead less
Cortical Spreading Depressions: Effects On Intracellular Ca2+ Concentration And Mechanisms Of Propagation
Funder
National Health and Medical Research Council
Funding Amount
$185,604.00
Summary
Human neuropathologies such as migraine, stroke, focal epilepsy and head injury all appear to involve an event called cortical spreading depression (CSD). This is characterised by a transient loss of excitability of cells that slowly spreads from a site of initiation out across the cortical surface. In normal brain tissue CSDs do not kill cells but in tissue with less than optimal energy supply CSDs do kill cells. This project is designed to understand the mechanisms contributing to CSD-induced ....Human neuropathologies such as migraine, stroke, focal epilepsy and head injury all appear to involve an event called cortical spreading depression (CSD). This is characterised by a transient loss of excitability of cells that slowly spreads from a site of initiation out across the cortical surface. In normal brain tissue CSDs do not kill cells but in tissue with less than optimal energy supply CSDs do kill cells. This project is designed to understand the mechanisms contributing to CSD-induced cell death. It is widely accepted that a high intracellular concentration of calcium ions is lethal to a cell. Thus, the proposed experiments are expected to show that a single episode of CSD in normal brain tissue induces only small changes in the intracellular calcium ion concentration but if repeated episodes of CSD occur, and if they take place in tissue with a compromised energy supply, then the calcium concentration rises to detrimental levels. Little is known about the mechanisms which underlie the propagation of CSD and therefore experiments will also be undertaken to investigate whether release of a messenger into the extracellular space is important or if there is a role for release of calcium from intracellular stores.Read moreRead less