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Preservation And Generation Of Beta Cells In Type 1 Diabetes With Novel Mimetic Peptides
Funder
National Health and Medical Research Council
Funding Amount
$1,096,055.00
Summary
Type 1 diabetes (T1D) is an autoimmune disease that destroys insulin producing beta cells in the pancreas. It can cause heart and kidney disease, and nerve damage. T1D is treated with insulin injections that can cause life-threatening low blood sugar levels. We have developed a new treatment that may stop beta cell loss, generate new beta cells and remove the need for insulin injections in T1D patients. A positive outcome will identify a completely new T1D treatment option.
Are Oligodendrocytes The Missing Link In Amyotrophic Lateral Sclerosis Pathogenesis?
Funder
National Health and Medical Research Council
Funding Amount
$1,054,405.00
Summary
Amyotrophic Lateral Sclerosis (ALS) is a debilitating and progressive neurodegenerative disease. Recent research suggests important cells of the central nervous system called glia play a role in disease onset and progression. We are interested in a type of glia called oligodendrocytes; they are crucial for supporting the survival of the cells that die in ALS. Only through understanding the underlying biology of ALS can we aim to identify effective therapies that will benefit patients.
Over 2 million Australians have diabetes and up to one in three adults will develop diabetes or pre-diabetes in their lifetime with the associated burden of complications. It is not simply genetics, as the genetic variability cannot explain why some individuals and indeed some families appear to be programmed to have an inordinate burden of complications. Over the last decade we have developed state of the art technologies to characterise epigenetic changes in human clinical cohorts.
Casting The Net: A New Approach To Identify Therapeutics To Treat Type-2 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$1,068,283.00
Summary
The discovery of treatments for type-2 diabetes (T2D) is a national health priority. In T2D, cells in the brain become 'insulin resistant' resulting in dangerously high blood sugar levels. There are no treatments for brain insulin resistance. The extracellular structures that surround brain cells undergo change in T2D, resulting in insulin resistance. By furthering understanding of these extracellular brain structures, this proposal will identify new drug targets to treat T2D.
Investigating The Consequences Of Dysregulated Lipogenesis In Cancer
Funder
National Health and Medical Research Council
Funding Amount
$600,647.00
Summary
Reprogramming of cellular metabolism is a hallmark of cancer. As such, there has been growing interest in developing strategies to exploit metabolism for therapeutic gain. Our ability to do this is dependent on a thorough understanding of the mechanisms by which dysregulation of cellular metabolism contributes to tumour progression. In this project, we seek to the investigate the fundamental mechanisms by which aberrant activation of lipid metabolism contributes to the tumourigenic process.
Tolerising Antigen-specific Immunotherapy For Type 1 Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$1,395,549.00
Summary
We have developed a new immunotherapy to treat the underlying causes of type 1 diabetes (T1D) while leaving the rest of the immune system intact. To use this in patients, we need better tests to know when immune therapy is working. We will develop new methods to design the therapy and tools to track the relevant immune cells in T1D that work in variable patient groups. The knowledge gained will speed the pace of development and increase the chance of success of immunotherapy in T1D.
Defining The Genes That Dictate The Cellular Response To Tumour Protein TP53 Activation
Funder
National Health and Medical Research Council
Funding Amount
$784,896.00
Summary
The tumour suppressor TP53 prevents the growth of abnormal cells by activating processes such as cell death and irreversible growth arrest. A cell will undergo only one of these possible responses, but it is not known why some cells die and others only stop growing. We will use innovative methods to define the genes that dictate the cellular response to TP53 activation. This research has implications for cancer, as many therapeutics aim to permanently kill cancer cells by activating TP53.
Oleoyl-ACP-hydrolase As An Early Predictive Biomarker For Severe And Fatal Influenza
Funder
National Health and Medical Research Council
Funding Amount
$866,807.00
Summary
Millions are hospitalized with severe influenza disease and ~500K die annually but the underlying mechanisms that drive disease are still not fully understood. We have identified a key role for an enzyme involved in fatty acid metabolism, which is profoundly elevated in patients who succumb to influenza and is thus a predictor for fatal outcomes. This research aims to investigate how this enzyme affects infection and impairs immune responses to drive severe respiratory viral disease.
The Interactive Effects Of Dietary Saturated Fat And Apolipoprotein-E Genotype On Peripheral Metabolism Of Lipoprotein-amyloid And Neurovascular Integrity.
Funder
National Health and Medical Research Council
Funding Amount
$637,536.00
Summary
This project is based on a remarkable discovery which suggests that in some individuals, Alzheimer's disease may be a consequence of corruption of microscopic blood vessels that supply brain, damaged as a consequence of exaggerated exposure in blood to a protein produced principally in liver. The project will explore this pathway further in subjects at heightened risk of Alzheimer's disease and in humanised animal models. The findings may provide new opportunities for prevention and treatment.
Preventing Diabetic Complications Using Anti-inflammatory Peptides
Funder
National Health and Medical Research Council
Funding Amount
$805,146.00
Summary
The Receptor for Advanced Glycation End-products (RAGE) triggers inflammation. It was thought that this receptor was only activated from outside the cell. However, we discovered that other receptors can activate it from the inside. This is called trans-activation. During this ideas grant, we will develop innovative ways to block trans-activation of RAGE and translate these findings to make new therapeutics that are highly-relevant to he development and progression of diabetes.