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Taurine Transporters And Brain Taurine Homeostasis
Funder
National Health and Medical Research Council
Funding Amount
$226,034.00
Summary
Taurine is a very abundant amino acid in the brains of all mammals. Some animals such as cats gain almost all their taurine from their diet; others such as rats make significant amounts of taurine themselves; humans lie somewhere between these two extremes. Despite the variation in sources of taurine it has been standard practise for well over a decade to include taurine in human infant milk formulae because lack of dietary taurine in kittens leads to epileptic fits and abnormalities in brain de ....Taurine is a very abundant amino acid in the brains of all mammals. Some animals such as cats gain almost all their taurine from their diet; others such as rats make significant amounts of taurine themselves; humans lie somewhere between these two extremes. Despite the variation in sources of taurine it has been standard practise for well over a decade to include taurine in human infant milk formulae because lack of dietary taurine in kittens leads to epileptic fits and abnormalities in brain development, whilst in adult cats death of cells such as photoreceptors (in the eye) is also observed. Despite these observations we have very little knowledge as to what taurine does in the brain because we have no selective drugs to examine the site or sites of taurine action. We hypothesise that taurine might mediate its actions by modifying the intracellular and extracellular levels of other neurotransmiters, especially glutamate. We plan to examine the brains and retinas of adult cats and kittens which have been given a diet deficient in taurine. We will determine the levels of each of the main neurotransmitters in the brain, both as global assays of whole tissues and at the cellular level by immunocytochemistry. We will examine whether there are any compensatory changes in levels of expression of taurine transporters as the body becomes depleted of taurine (since taurine content of nerve cells will be regulated by uptake of taurine in the absence of endogenous synthesis). Expression of glutamate transporters will also be examined. By understanding the way that the major neurotransmiter systems respond to a reduction in taurine levels we hope to generate both descriptive and predictive models that define the roles of taurine in the mammalian nervous system and which may give insights into mechanisms of significant human disease processes including epilepsy and a series of conditions involving degeneration of photoreceptors.Read moreRead less
Regulation Of The Beta-secretase (BACE1) By Glycosaminoglycans
Funder
National Health and Medical Research Council
Funding Amount
$561,212.00
Summary
Alzheimer's disease is the leading cause of dementia in the elderly. Because of the prolonged institutionalisation of patients, it is a major health care burden. This project aims to develop novel drugs which can treat Alzheimer's disease by inhibiting production of the protein which causes the neurodegeneration.
The Receptor-associated Protein (RAP) As A Molecular Chaperone For The Amyloid Protein (Abeta) Of Alzheimers Disease
Funder
National Health and Medical Research Council
Funding Amount
$402,403.00
Summary
Our research will examine the role of a protein known as the receptor-associated protein (RAP) in Alzheimer's disease. We will determine whether the protein contributes to the progression of Alzheimer's disease and we will examine the possiblity that that RAP may be used as a drug to treat the disease. The project could potentially have direct benefit for patients by leading to an effective treatment for dementia associated with Alzheimer's disease.
Extracellular Matrix, Cell-surface Receptors And Alzheimer's Disease: A Novel Glycoform Of Acetylcholinesterase
Funder
National Health and Medical Research Council
Funding Amount
$265,074.00
Summary
Alzheimer's disease is the leading cause of dementia in the elderly, affecting approximately 5-10% of the population over the age of 65. With an increasingly ageing population, Alzheimer's disease will be a major health problem in the next century unless effective treatments (probably in combination with early diagnosis) are found. We have identified a novel form of a protein acetylcholinesterase (AChE-AD), which is present in high levels in the brains of patients with Alzheimer's disease. Our w ....Alzheimer's disease is the leading cause of dementia in the elderly, affecting approximately 5-10% of the population over the age of 65. With an increasingly ageing population, Alzheimer's disease will be a major health problem in the next century unless effective treatments (probably in combination with early diagnosis) are found. We have identified a novel form of a protein acetylcholinesterase (AChE-AD), which is present in high levels in the brains of patients with Alzheimer's disease. Our work has shown that the accumulation of another protein in the brains of Alzheimer patients, known as the amyloid protein, is the cause of the increase in AChE-AD. This finding is important for two reasons: 1) Identification of the mechanism by which the amyloid protein causes an increase in AChE-AD will tell us about some of the basic causes of Alzheimer's disease. 2) AChE-AD may be a useful diagnostic marker of Alzheimer's disease. At present, diagnosis is performed by clinical examination. This is a time consuming and inaccurate process. A biochemical diagnostic marker will provide an objective criterion with which to diagnose Alzheimer's disease. Therefore, our research is aimed at: Aim 1: Evaluating AChE-AD as a diagnostic marker. Aim 2: Developing tools with which we can more easily measure AChE-AD. Aim 3: Understanding the basic biochemical mechanisms which cause the increase in AChE-AD in the brains of patients. Aim 4: Examining whether AChE-AD may contribute to the cause of Alzheimer's disease.Read moreRead less
Targetting Nogo A As A Means To Promote CNS Axonal Regrowth
Funder
National Health and Medical Research Council
Funding Amount
$325,911.00
Summary
Unlike the peripheral nervous system, regenerative nerve fiber growth and structural plasticity are limited in the adult mammalian central nervous system (CNS), following injury. Although lesioned axons can sprout spontaneously, this regeneration attempt is transitory and no significant re-growth occurs over long distances. Consequently, injury to the CNS often leads to permanent disability. In many cases, it has been shown that it is not the absence of growth-promoting molecules in the CNS but ....Unlike the peripheral nervous system, regenerative nerve fiber growth and structural plasticity are limited in the adult mammalian central nervous system (CNS), following injury. Although lesioned axons can sprout spontaneously, this regeneration attempt is transitory and no significant re-growth occurs over long distances. Consequently, injury to the CNS often leads to permanent disability. In many cases, it has been shown that it is not the absence of growth-promoting molecules in the CNS but rather the presence of axon outgrowth inhibitors, including components of both CNS myelin and astroglial scars that limit regeneration. Given that axonal injury is an important pathological determinant of permanent disability in multiple sclerosis (MS), we have recently investigated the role of the CNS neurite outgrowth inhibitor, Nogo A in the development of a chronic form of murine MS-like disease. We showed that targeting Nogo A by active and passive immunization blunts clinical signs, demyelination and axonal damage associated with this model of MS. These results identify Nogo A as an important determinant of the development of autoimmune-mediated demyelination and suggest that its blockage may help to maintain and-or to restore the neuronal integrity of the CNS after autoimmune insult in disease such as MS. The principal goal of this application is to study the mechanism by which blockade of Nogo A improves clinical outcome in disease like MS and to determine whether neurite sprouting accounts for such an improvement. Targeting Nogo A and-or its receptor, has the potential to not only regulate-modulate the process of autoimmune mediated demyelination but could lead to the first therapy ever offered to patients that helps damaged nerves regenerate after axonal injury following neurodegeneration due to insult or disease.Read moreRead less
Cholinergic Abnormalities In Alzheimer's Disease: Identification Of Novel Therapeutic Targets
Funder
National Health and Medical Research Council
Funding Amount
$478,500.00
Summary
The aim of this project is to develop new drugs for the treatment of Alzheimer's disease. Alzheimer's disease is a disease of ageing commonly associated with memory loss. The disease is caused by the build up of amyloid protein in the brain. However, it is not known how amyloid protein causes degeneration of normal brain function. Our previous studies have shown that amyloid protein targets two components which are important for normal brain function. These components are 1) acetylcholinesterase ....The aim of this project is to develop new drugs for the treatment of Alzheimer's disease. Alzheimer's disease is a disease of ageing commonly associated with memory loss. The disease is caused by the build up of amyloid protein in the brain. However, it is not known how amyloid protein causes degeneration of normal brain function. Our previous studies have shown that amyloid protein targets two components which are important for normal brain function. These components are 1) acetylcholinesterase and 2) nicotinic receptors, which are known to be important for memory. The aim of this application is to identify the mechanisms by which amyloid protein targets acetylcholinesterase and nicotinic receptors and to design inhibitors of this interaction which may ultimately provide a platform for future drug development.Read moreRead less
Discovery Early Career Researcher Award - Grant ID: DE170101514
Funder
Australian Research Council
Funding Amount
$372,000.00
Summary
The control of neuroplasticity in the brain. This project aims to determine how neuroplasticity – the brain’s ability to remodel and make new circuits – is controlled in both excitatory and inhibitory neurons. This capacity, vital for all cognitive functions, diminishes as people age. It is imperative to determine neuroplasticity’s mechanisms and how and why they change, but it is not known how both excitatory and inhibitory neurons contribute to neuroplasticity and how these dynamic alterations ....The control of neuroplasticity in the brain. This project aims to determine how neuroplasticity – the brain’s ability to remodel and make new circuits – is controlled in both excitatory and inhibitory neurons. This capacity, vital for all cognitive functions, diminishes as people age. It is imperative to determine neuroplasticity’s mechanisms and how and why they change, but it is not known how both excitatory and inhibitory neurons contribute to neuroplasticity and how these dynamic alterations are controlled. Understanding neuroplasticity is vital for learning, memory and healthy ageing throughout life.Read moreRead less
The role of actin in driving bulk endocytosis in neurons and neurosecretory cells. Synaptic release of neurotransmitter is essential for neuronal communication. Following fusion, synaptic vesicle membrane is incorporated into the plasma membrane and retrieved by endocytosis to recover both lipids and essential vesicular proteins. The project will characterise how the actin cytoskeleton perform this function.
Investigating the neuroprotective actions of metallo-complexes. Metal-based drugs offer an exciting new approach to treatment of neurodegeneration. However, little is known about how cells metabolise these drugs: information that is critical for further drug development. This project will determine how metal-based drugs are metabolized by neuronal cells and how this may result in therapeutic benefit.
Identifying the specific structural features of metallothionein that regulate its ability to modulate astrogliosis. This project contributes directly to the Designated National Research Priority 2 and could potentially have a significant impact upon the broader Australian Community by identifying a novel and powerful therapeutic agent based upon metallothionein proteins with the ultimate aim of helping patients who have a brain injury or a neurodegenerative disease. It is important to note that ....Identifying the specific structural features of metallothionein that regulate its ability to modulate astrogliosis. This project contributes directly to the Designated National Research Priority 2 and could potentially have a significant impact upon the broader Australian Community by identifying a novel and powerful therapeutic agent based upon metallothionein proteins with the ultimate aim of helping patients who have a brain injury or a neurodegenerative disease. It is important to note that the partnership between UTAS and Bestenbalt LLC is a critical step in the development of these exciting research discoveries into commercially viable outcomes for the Australian Biotechnology Industry and the broader Australian community.Read moreRead less