Targeted Nanoparticles To Deliver Combinations Of Calcium Channel Inhibitors To Prevent Myelin Damage During Secondary Degeneration After Neurotrauma
Funder
National Health and Medical Research Council
Funding Amount
$895,244.00
Summary
Following injury to the central nervous system the damage spreads into nearby areas, leading to worse outcomes for the patient. We will generate nanoparticle systems to deliver effective therapies directly to the most vulnerable cells, critical for function. We will modify the nanoparticles so that they can get to the injury site, both early after injury, and after longer periods of time have elapsed. We will then test the nanoparticle systems to see if they are effective at preserving function
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.
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
Using Non-invasive Magnetic Stimulation To Promote Remyelination
Funder
National Health and Medical Research Council
Funding Amount
$664,869.00
Summary
In patients with multiple sclerosis, brain insulation is lost from nerves. This leads to permanent and progressive disability. We have identified a non-invasive method of magnetic stimulation, and have shown that it increases the number of new insulating cells added to the brain. In this study we will determine whether this new treatment can promote insulation repair in a model of multiple sclerosis.
Optimising Myelin Repair And Restoring Neuronal Function In The Demyelinated Brain
Funder
National Health and Medical Research Council
Funding Amount
$1,009,933.00
Summary
Multiple sclerosis is a disease of the brain and spinal cord caused by damage to white matter. In healthy brains, a substance in white matter called myelin insulates the axons (cables) of nerve cells, which speeds up electrical conduction. In MS, myelin is destroyed which impairs conduction and can lead to permanent loss of axons and nerve cells. To prevent this, we will test whether increasing electrical activity in nerve cells helps restore myelin by activating myelin-forming stem cells.
Targeting The Canonical Wnt Signalling Pathway To Promote Central Nervous System Remyelination In Vivo
Funder
National Health and Medical Research Council
Funding Amount
$314,644.00
Summary
Multiple Sclerosis (MS) occurs when immune cells attack the sheaths, called myelin, that cover and protect nerve connections. If myelin is damaged nerve cells cannot function properly, leading to severe disability. The brain has a group of cells that could potentially replace damaged myelin, but as MS worsens these cells are blocked in a state where they cannot help in repair. I will remove a signal specifically from these cells and determine if this unblocks them resulting myelin repair.
New Projection Neurons Are Added To The Brain Throughout Life – Identifying Their Source And Function.
Funder
National Health and Medical Research Council
Funding Amount
$505,991.00
Summary
Scientists aim to use our body’s own stem cells to make new nerve cells for brain repair. There are two major types of nerve cell: long range and short range; and until now we did not know how to make new long range nerves. I recently discovered that a special type of brain stem cell, the OPC, makes new long range nerves throughout life. We are building on this discovery by trying to understand the signals that control this process in order to direct OPCs towards nerve regeneration.
Investigating A Role For TAM Receptor Signaling In Demyelination
Funder
National Health and Medical Research Council
Funding Amount
$444,318.00
Summary
In Multiple Sclerosis brain cells are damaged and myelin is lost in a process known as demyelination. Two proteins, called Gas6 and Protein S, can influence cells involved in MS, by signalling through proteins called TAMs. We have shown that Gas6 can affect the severity of demyelination in mice, and that TAMs can affect the response of cells to interferon-beta, a major MS treatment. We plan to further study the effects of these proteins during demyelination, and their interaction with interferon ....In Multiple Sclerosis brain cells are damaged and myelin is lost in a process known as demyelination. Two proteins, called Gas6 and Protein S, can influence cells involved in MS, by signalling through proteins called TAMs. We have shown that Gas6 can affect the severity of demyelination in mice, and that TAMs can affect the response of cells to interferon-beta, a major MS treatment. We plan to further study the effects of these proteins during demyelination, and their interaction with interferon-beta.Read moreRead less