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Glaucoma is a progressive, poorly understood blinding disease with limited treatment options. It is characterised by the death of the nerve cells in the eye whose fibres form the optic nerve. Results obtained in the current proposal will lead to a better understanding of key features of the early stages of the disease and, additionally, will explore the potential of a novel therapeutic approach based on regeneration of damaged nerve fibres within the optic nerve.
Axonal Regeneration And Degeneration: Cellular And Molecular Mechanisms
Funder
National Health and Medical Research Council
Funding Amount
$2,088,220.00
Summary
The ability to surgically repair an injured axon and restore neuronal function is still a significant challenge in neurosurgery. However, a spontaneous repair mechanism, axonal fusion, by which the two separated ends of a transected axon are fused back together, has been observed in invertebrates. Understanding the molecular mechanisms of this biological event will allow us to determine its potential as a novel therapeutic approach to repair injured and damaged neurons.
Nerve cells communicate with each other through nerve processes or neurites. The dysfunction of neurites results in the clinical symptoms of dementia such as cognitive decline. Currently we cannot directly monitor degeneration of neurites in the living brain and therefore it is difficult to determine whether therapeutic agents are protective. My goal is to develop a detection system in the blood that will allow us to monitor these changes during disease progression and therapeutic intervention.
Identification And Study Of Novel Conserved Molecule With An Axonal Protective Function
Funder
National Health and Medical Research Council
Funding Amount
$625,005.00
Summary
Axonal degeneration is a common feature of a number of neurodegenerative conditions, such as motor neuron, Parkinson’s, Alzheimer’s and Huntington’s diseases. However, the genetic causes that regulate this biological event are poorly understood. We have identified a novel, conserved axonal protective molecule. We will study how it functions, and if it can be exploited to protect diseased neurons.
Investigating Mechanisms Of Axonal Pathology Following Oligodendrocyte Apoptosis: Avenues For Neuroprotection In Early MS
Funder
National Health and Medical Research Council
Funding Amount
$678,138.00
Summary
Recent research suggests that Multiple Sclerosis could first be triggered by the death of a type of brain cell called an oligodendrocyte. These cells insulate nerve cells in the brain which help them function normally. We will test the idea that death of oligodendrocytes impairs nerve cell function by causing inflammation and by depriving nerve cells of energy. We will determine whether preventing inflammation and feeding the nerve cells an alternative source of energy can restore normal functio ....Recent research suggests that Multiple Sclerosis could first be triggered by the death of a type of brain cell called an oligodendrocyte. These cells insulate nerve cells in the brain which help them function normally. We will test the idea that death of oligodendrocytes impairs nerve cell function by causing inflammation and by depriving nerve cells of energy. We will determine whether preventing inflammation and feeding the nerve cells an alternative source of energy can restore normal function.Read moreRead less
Multiple sclerosis is a particularly devastating disease that affects people early in their lives. This chronic disabling condition is characterized by inflammation and loss or damage to the myelin sheath that surrounds axons. There is preliminary evidence suggesting that certain cell signals may prevent the cells that produce myelin from death in multiple sclerosis. This study will seek to determine how and which signals prevent cell death and whether this may be a potential therapeutic interve ....Multiple sclerosis is a particularly devastating disease that affects people early in their lives. This chronic disabling condition is characterized by inflammation and loss or damage to the myelin sheath that surrounds axons. There is preliminary evidence suggesting that certain cell signals may prevent the cells that produce myelin from death in multiple sclerosis. This study will seek to determine how and which signals prevent cell death and whether this may be a potential therapeutic intervention.Read moreRead less
There are escalating numbers of Alzheimer�s disease sufferers. This Project aims to provide a better understanding of the fundamental process underlying the damage to brain circuitry in this condition. This proposal may provide key information regarding the relationship between the major pathological changes of Alzheimer�s disease, identifying the cellular mechanisms that are crucial to this process, and providing new avenues for therapeutic agents targeted at the earliest stage of AD.
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.
Structural Biology And Therapeutic Targeting Of Axon Degeneration
Funder
National Health and Medical Research Council
Funding Amount
$1,512,250.00
Summary
The molecular mechanisms underlying SARM1 (sterile alpha and TIR 1) function will be investigated, which will allow design of inhibitors of axon degeneration, which can be developed into therapeutic agents for neurodegenerative disease. Outcomes are not only anticipated to support excellence in basic research, but have potential of assisting health sectors and the economy, by reducing the burden of prevalent neurodegenerative diseases such as peripheral neuropathies and traumatic brain injury.
Discovering Novel Molecules That Regulate Axonal Degeneration.
Funder
National Health and Medical Research Council
Funding Amount
$588,622.00
Summary
The axon is the primary signaling component of every neuron and is essential for normal function. Axonal degeneration is a key early pathological hallmark of Alzheimer’s disease. We lack a basic understanding of molecules that regulate this process. Such knowledge is essential for the development of treatments and therapies for dementia and the preservation of healthy ageing. I aim to discover the molecules that regulate axonal degeneration and study their function.