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MITOCHONDRIA, OXIDATIVE STRESS AND NEURONAL APOPTOSIS: BIOCHEMICAL, CELLULAR AND PHARMACOLOGICAL APPROACHES
Funder
National Health and Medical Research Council
Funding Amount
$145,880.00
Summary
Our goal is to understand the detailed process whereby nerve cells die after various stresses and injury. We aim also to develop novel ways of protecting cells against such death. The death of nerve cells plays an important role in a series of neurodegenerative diseases, such as Parkinson's, Huntington's and Motor Neurone Diseases. One prevalent cause of cell death arises from the action of transmitters that normally signal between nerve cells but which, under conditions of stress and injury, ca ....Our goal is to understand the detailed process whereby nerve cells die after various stresses and injury. We aim also to develop novel ways of protecting cells against such death. The death of nerve cells plays an important role in a series of neurodegenerative diseases, such as Parkinson's, Huntington's and Motor Neurone Diseases. One prevalent cause of cell death arises from the action of transmitters that normally signal between nerve cells but which, under conditions of stress and injury, cause overstimulation of the nerve cells leading to death (excitotoxicity). Mitochondria are component of cells normally providing energy for the cell to carry out its various functions; but under stress conditions mitochondria act as controllers in cellular decision-making processes leading to cell death. Moreover, mitochondria are known to play an important role in neurodegenerative diseases, as they are a source of damaging oxygen derivatives called free radicals that cause cell injury. Mitochondria are also involved in death resulting from excitotoxicity. In order to understand the detailed mechanism of the nerve cell death process, we will use cultured nerve cells from the brains of laboratory mice, including both normal mice and those that are models of neurodegenerative disease. Injury leading to death will be induced by analogues of the transmitters that cause excitotoxicity. We will concentrate the those aspects of the death process that involve mitochondria, as this will enable us to test a range of antioxidants that can be expected to lead to new drug treatments for neuronal cell injury. Included in these compounds are novel antioxidants that are targeted to mitochondria. This project brings together the expertise in neuroscience and pharmacology of Professor Beart with the skills in biochemistry of Professor Nagley, particularly in mitochondrial and cell death research, to address this important medical research problem in a multidisciplinary manner.Read moreRead less
Characterisation Of Antioxidant Pathways Involving Gpx-1: Implications For Neural Ischemic Reperfusion Injury.
Funder
National Health and Medical Research Council
Funding Amount
$458,250.00
Summary
Neural damage following stroke can be grouped into two stages. The first occurs immediately following the ischemic insult and results in the rapid loss of neural cell viability; the second stage (which usually results in severe neural dysfunction) occurs over many hours following reperfusion. There is however, a window of opportunity shortly following the ischemia-reperfusion where damage to the brain can be minimized if appropriate therapeutic intervention was available. However, our ability to ....Neural damage following stroke can be grouped into two stages. The first occurs immediately following the ischemic insult and results in the rapid loss of neural cell viability; the second stage (which usually results in severe neural dysfunction) occurs over many hours following reperfusion. There is however, a window of opportunity shortly following the ischemia-reperfusion where damage to the brain can be minimized if appropriate therapeutic intervention was available. However, our ability to identify novel targets and devise strategies for the treatment of stroke relies on our understanding of (a) the molecular processes that are initiated following brain ischemia and (b) the delayed molecular events that follow reperfusion and hypoperfusion and result in extensive neuronal loss. A major component that accompanies stroke is the generation of oxidative stress. Reactive oxygen species (ROS) are thought to make a significant contribution to neuronal cell injury and death during both the early and late stages following ischemia. Therefore the molecular pathways that are involved in ROS generation are prime targets for the development of improved therapies. It has already been established by us that the antioxidant enzyme, glutathione peroxidase-1 (Gpx-1) is essential in protecting neurons from ischemic injury-death. A clearer understanding of how Gpx-1 confers this protection in vivo would make an important contribution towards the design of improved treatments. In this proposal, we plan to determine the role of Gpx-1 in an in vivo model of stroke to: (1) demonstrate in a broader sense the functional importance of this antioxidant enzyme in neuronal survival and (2) to demonstrate in a more specific manner, the impact of this enzyme on two signaling molecules, PI3kinase (PI3K) and NFkB (both of which are redox sensitive and play important roles in neuronal cell viability) and their relevance to ischemic cell injury and death.Read moreRead less
Understanding The Link Between Mitochondrial Biogenesis And Disease
Funder
National Health and Medical Research Council
Funding Amount
$421,055.00
Summary
As the predominate energy producers of our cells, mitochondria are implicated in a variety of diseases. To function properly, these dynamic organelles rely on protein components that regulate their structure and distribution throughout the cell. My work aims to expand our knowledge of the way these components control mitochondrial shape and trafficking. By understanding the correlation between mitochondrial morphology and function, we will gain insight into related diseases.
Mitochondria: Molecular And Cellular Insights Into Their Diverse Contributions To Neuronal Injury
Funder
National Health and Medical Research Council
Funding Amount
$747,927.00
Summary
Mitochondria are components of cells normally providing energy for essential functions and in the energy demanding brain, under stress conditions, mitochondria acts as controllers of cellular decision-making processes leading to neuronal death. Our goal is to understand mitochondrial mechanisms determining how neurones die after various stresses and injury. Using pathological insults relevant to neurological conditions, we shall analyse death molecules and how neurones adapt when threatened.
I have discovered particular factors produced by our white blood cells have the ability to shut down or boost protein production in the gut, pancreas and lung. My vision is to harness these to devise new strategies for treatments for infectious and non-infectious diseases (inflammatory bowel disease, diabetes) that have a high burden on our healthcare system.
Function Of FOR Gene Products In Normal And Cancer Cells
Funder
National Health and Medical Research Council
Funding Amount
$521,310.00
Summary
Cancer cells usually exhibit the loss of control of normal cell functions. This involves the increase of proteins which promote growth and cell division and the decrease in proteins which inhibit growth and cell division. Loss of function may also occur in proteins that are normally involved in killing the cell when growth becomes uncontrolled. Many of these proteins interact with one another and in so doing establish pathways and networks of control which must be perturbed and overridden in the ....Cancer cells usually exhibit the loss of control of normal cell functions. This involves the increase of proteins which promote growth and cell division and the decrease in proteins which inhibit growth and cell division. Loss of function may also occur in proteins that are normally involved in killing the cell when growth becomes uncontrolled. Many of these proteins interact with one another and in so doing establish pathways and networks of control which must be perturbed and overridden in the cancer cell. Sometimes this is because the role of the protein is altered in the cancer cell compared to what it normally is in a normal cell. The main aim of this study is to understand the role that is played by a set of proteins that are coded by a single gene. This gene (which we refer to as the FOR gene) spans a region of the human genome which is sensitive to a particular type of mutation. This mutation takes place early in tumour development and therefore we believe that it has important role to play in determining the fate of the cell - helping to cause it to become a tumour cell. We will find out which other proteins in the cell the FOR proteins interact with. Where these proteins are known then this will help determine the pathways in the cell in which the FOR proteins participate. In another approach we will establish animal models (in mice and flies) of mutations in the FOR genes of these species. The transgenic mice will help us find out whether the mutations that we have observed in the FOR gene in various human cancers cause increased sensitivity to mutagens and in so doing aid in transforming normal cells into cancer cells. The transgenic flies will help us identify the metabolic pathways in which the FOR proteins participate. These studies will help understand the roles of the FOR proteins and their significance in cancer.Read moreRead less
OCULAR PERFUSION PRESSURE: A MODIFIABLE RISK FACTOR FOR GLAUCOMA?
Funder
National Health and Medical Research Council
Funding Amount
$327,560.00
Summary
This project aims to study the mechanisms underlying glaucoma, the second leading cause of vision loss. Specifically it will provide proof for the idea that a person can develop vision loss without having high eye pressure, if their blood pressure cannot provide enough supply to the eye. It will achieve this by combining expertise from several disciplines; physiology, blood pressure control, anatomy and biochemistry. This project will help to improve glaucoma detection, monitoring and treatment.