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.
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.
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
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