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Field of Research : Cellular Nervous System
Research Topic : VESTIBULAR DISEASE
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  • Funded Activity

    Axon Degeneration And Axon Protection In CNS Disease And Injury

    Funder
    National Health and Medical Research Council
    Funding Amount
    $389,120.00
    Summary
    One of the major reasons for the clinical symptoms of neurological diseases such as Alzheimer’s disease and Motor Neuron Disease is the loss of connections between the nerve cells. Nerve cells are connected by specialized processes called axons. In disease these processes can breakdown. This project specifically looks at how axons break down in disease and tests therapeutic strategies to protect them.
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    Funded Activity

    Research Fellowship - Grant ID:401101

    Funder
    National Health and Medical Research Council
    Funding Amount
    $665,060.00
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    Funded Activity

    Uncovering The Molecular Mechanisms Behind Charcot-Marie-Tooth Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $320,967.00
    Summary
    Charcot-Marie-Tooth disease (or CMT) is one of the most common disorders of the nervous system, affecting the normal function of the limbs and causing lifelong disabilities. There is currently no cure for CMT. The aim of this research is to develop a new model of CMT, which will allow us to uncover novel information about how the disease develops. This research will provide a better understanding of the disease and therefore provide valuable insight for the future generation of therapeutics.
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    Funded Activity

    A Novel Intracellular Roadblock To Cobalamin Utilization In Ageing And Alzheimer�s Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $11,304.00
    Summary
    Vitamin B12 is required for red blood cell formation, DNA synthesis and normal neurological function. B12 deficiency contributes to age-related cognitive decline and Alzheimer�s disease. This research will provide important new information regarding the ageing process and the impact that brain changes associated with ageing and Alzheimer's disease have on B12 metabolism. It will provide important information related to the therapeutic potential of B12.
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    Funded Activity

    Role Of The Microglial Adaptor Molecule TYROBP In Alzheimer’s Disease Pathology

    Funder
    National Health and Medical Research Council
    Funding Amount
    $469,433.00
    Summary
    Immune activation characterizes Alzheimer’s disease (AD) brains; however, how it impacts AD progression is not understood. Our previous studies in AD brains identified the immune molecule TYROBP, pointing at both beneficial and detrimental effects triggered by this molecule. Here, we aim to understand in detail how TYROBP is involved in AD and how we can enhance its beneficial effects and decrease its unintended actions.
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    Funded Activity

    Defining The Function Of Apolipoprotein-D In Alzheimer's Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $457,231.00
    Summary
    Alzheimer's disease (AD) prevalence is rising and there is no curative treatment. Neurotoxic amyloid-beta peptide and concomitant lipid oxidation in the brain contribute to the cause of AD. We have identified a new pathway by which a protein called apoD may inhibit lipid oxidation in the AD brain. We will test the impact that changing apoD levels in neurons and in genetically modified mice has on neuron stress and AD-like characteristics. This may reveal new avenues to prevent or treat AD.
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    Funded Activity

    Anti-inflammatory Copper Complexes For Treatment Of Alzheimer's Disease

    Funder
    National Health and Medical Research Council
    Funding Amount
    $603,622.00
    Summary
    Brain inflammation and disrupted metabolism of the biologically important metal, copper, play key roles in Alzheimer’s disease (AD) progression. Our team has developed new copper-based therapeutics, but limited knowledge of how they work impedes clinical trials. My recent findings indicate that these drugs potently prevent inflammation. My proposal seeks to understand how copper-complexes reduce damaging inflammatory responses in novel human cell models of AD.
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    Funded Activity

    Investigation Of The Molecular Mechanisms Underlying Alpha Synuclein Function At The Presynapse

    Funder
    National Health and Medical Research Council
    Funding Amount
    $419,180.00
    Summary
    Parkinson’s Disease (PD) is a common brain disease affecting 7 million people worldwide. It is caused by the death of brain cells. ?-synuclein is a protein in that brain that is likely to contribute to the cell death in PD, but the normal role of the protein remains unknown. This study will investigate the function of ?-synuclein in maintaining normal healthy brain activity. In addition, this work will help us understand how normal brain processes are affected in diseases such as PD.
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    Funded Activity

    Lysosomal Dysfunction As An Inhibitor Of Vitamin B12 Utilisation In Neurodegenerative Diseases

    Funder
    National Health and Medical Research Council
    Funding Amount
    $554,901.00
    Summary
    Vitamin B12 is required for red blood cell formation, DNA synthesis and normal neurological function. B12 deficiency contributes to age-related cognitive decline and Alzheimer’s disease. This research will provide important new information regarding the ageing process and the impact that brain changes associated with ageing and Alzheimer's disease have on B12 metabolism. It will provide important information related to the therapeutic potential of B12.
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    Funded Activity

    Developing Insight Into The Molecular Origins Of Familial And Sporadic Frontotemporal Dementia And Amyotrophic Lateral Sclerosis

    Funder
    National Health and Medical Research Council
    Funding Amount
    $6,377,279.00
    Summary
    There is strong evidence that frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) represent a spectrum of neurodegenerative disease with common origins. A combined study of FTD/ALS patient cohorts will provide greater power to identify these shared molecular origins. We aim to discover gene variants that cause, predispose, or modify onset and progression of inherited and sporadic FTD/ALS, and validate and study our discoveries in new cell and animal models of these disorders.
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