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In Vivo Tau Imaging In Alzheimer’s Disease And Other Dementias
Funder
National Health and Medical Research Council
Funding Amount
$538,998.00
Summary
Alteration of the normal protein tau leads to its deposition inside the brain cells leading to their death. These deposits have been well characterized and they are associated with cognitive impairment. We propose to study tau deposits in vivo in humans using positron emission tomography (PET) and assess its association with cognition and other signs of neurodegeneration
Apathy In Dementia: Identifying Mechanisms For Targeted Interventions
Funder
National Health and Medical Research Council
Funding Amount
$514,404.00
Summary
One of the most common symptoms in dementia is apathy - a reduction in concern, motivation or interest. Apathy impacts on a person’s ability to engage in necessary daily activities (e.g., cooking, washing, visiting friends) and often leads to people being placed in aged care facilities. This project will investigate the mechanisms which give rise to apathy in dementia. Understanding these mechanisms is the first step in developing new interventions to treat this challenging symptom.
Mutations In Ubiquitin Proteasome Pathway Genes As A Cause Of Frontotemporal Dementia And Motor Neuron Disease
Funder
National Health and Medical Research Council
Funding Amount
$639,860.00
Summary
This project aims to identify genes that are mutated in families affected with dementia and motor neuron disease, and to determine whether the same genes are responsible for disease in large collections of patients with similar disorders. Identifying these genes will reveal what biological processes can lead to brain and nerve cell degeneration, providing knowledge important for development of new treatments for the many people worldwide affected with these disorders.
SELECTIVE VULNERABILITY IN ALZHEIMER’S DISEASE AND RELATED DISORDERS: MECHANISM OF TAU PATHOLOGY
Funder
National Health and Medical Research Council
Funding Amount
$1,072,324.00
Summary
Alzheimer’s disease and related dementias affect 230,000 people in Australia, with numbers expected to grow to 730,000 by 2050. The direct costs for health and residential care alone exceed $6.6 billion per annum. By identifying genes that protect degenerating neurons in the Alzheimer brain, a deeper understanding of the underlying processes will be gained and therapeutic targets will be defined that will assist in developing a therapy for a yet uncurable disease.
NOVEL MECHANISMS UNDERLYING THE SPREADING OF TAU PATHOLOGY IN ALZHEIMER’S DISEASE AND OTHER TAUOPATHIES
Funder
National Health and Medical Research Council
Funding Amount
$640,106.00
Summary
Alzheimer’s disease and related dementias affect 230,000 people in Australia, with numbers expected to grow to three times that by 2050. The direct costs for health and residential care alone already exceed $6.6 billion per annum. The underlying pathomechanisms and the processes that drive the progression of neurodegeneration in these devastating disorders remain largely unknown. Here, we will identify novel therapeutic targets and assist in developing therapies for yet incurable diseases.
Investigating The Propagation Of Protein Aggregation In Amyotrophic Lateral Sclerosis
Funder
National Health and Medical Research Council
Funding Amount
$406,217.00
Summary
Motor Neurone Disease is a rapidly progressive disease that attacks neurones responsible for controlling voluntary muscles, leading invariably to death. Currently there is no effective treatment. Recent work in humans suggests that degeneration begins focally and spreads through the three dimensional anatomy of the nervous system. This project will address the important question of how the toxicity is spread amongst adjacent neurones by characterising the propagation of protein aggregates.
Understanding The Early Disease Mechanisms Of Motor Neuron Disease And Frontotemporal Dementia
Funder
National Health and Medical Research Council
Funding Amount
$692,487.00
Summary
Motor neuron disease (MND) and frontotemporal dementia (FTD) are incurable, fatal neurodegenerative diseases. MND and FTD patients have similar brain and spinal cord pathology, but the causes of disease remain unclear. Using new genetically modified mice that for the first time recapitulate key features of the human diseases, this project will define the biochemical processes that contribute to disease onset and progression and will test potential disease-modifying therapeutics.
The Role Of Mutant CYLD In Frontotemporal Dementia And Motor Neuron Disease
Funder
National Health and Medical Research Council
Funding Amount
$963,216.00
Summary
We have identified a new gene that when mutated causes dementia and motor neuron disease (MND), diseases that are currently incurable. This project will examine how this mutated gene affects cell functions to cause nerve cell death, using cutting-edge cell and mouse models of disease, and find out whether people who have more common variants of this gene are at greater risk of developing dementia or MND. This knowledge is crucial for diagnosing and developing therapies for these disorders.
RNA-based Expanded Repeat Pathogenic Pathway In Neurodegenerative Diseases
Funder
National Health and Medical Research Council
Funding Amount
$595,153.00
Summary
Many important human genetic diseases (incl Huntington’s Disease) are due to a common mutation mechanism with some similarities in clinical outcome (late in life nerve cell loss). For these diseases it is still not known what mechanism is responsible for causing the disease. This is essential in order to delay onset, slow progression or effect cure. We will test a mechanism for disease pathology that we have identified in a simple model organism and seen evidence of its activity in human disease
The Role Of Beta-Amyloid Precursor Protein And Tau In The Regulation Of Neuronal Iron
Funder
National Health and Medical Research Council
Funding Amount
$650,226.00
Summary
We have recently discovered a novel relationship between amyloid precursor protein (APP) and tau in regulating neuronal iron balance. This project will establish how tau aids APP transport to the cell surface where it assists cellular iron release. A commonality in some neurodegenerative diseases are disruptions in either proteinsÍ function and iron-related excitotoxicity. Understanding the iron role of APP and tau will lead to a therapeutic mechanism of action and better future drug design.