MS is one of the most common, chronic neurologic diseases of adults worldwide, affecting more than 2.8 million people worldwide with 10,000 new diagnoses made each year. MS tends to strike early in adulthood, with women three times more likely than men to be diagnosed. The total direct cost to the US community of MS is just over $28 billion annually.
MS is caused by the body’s own immune system mistakenly attacking the brain, spinal cord or optic nerves. The primary target of this attack is myelin, the protective coating around the nerve fibres, which carry nerve impulses between nerve cells. These attacks cause active MS lesions, and the nerve cells themselves can also be damaged, leading to life-long disability.
The research team, headed by Dr Steven Petratos, has shown that a modified version of a specific protein is present within active MS lesions in a laboratory model of MS. This modified protein then interacts with another protein to cause nerve fibre damage.
The aim of Ms Danica Nheu’s project is to propose a new method to block either the modification or the interaction between the two proteins, to halt disease progression and provide recovery from disability.
Since the start of the project, Ms Nheu has made important progress in understanding how a new therapeutic approach may help protect and repair the brain and spinal cord in MS.
Her research has focused on a biological pathway involving a protein called Nogo Receptor 1, which plays a role in driving damage to nerve fibres. Using laboratory models of MS, she showed that blocking this pathway can protect nerve fibres from degeneration, confirming that it is an important contributor to nerve damage in MS.
Further studies have demonstrated how this pathway affects the movement of energy within cells. In MS, this process is impaired, contributing to damage in both nerve fibres and the cells responsible for producing myelin. By targeting this pathway with a therapeutic molecule, Ms Nheu was able to restore this energy transport process, helping support normal cell function and survival
Importantly, her work has also shown that this approach may promote repair. The treatment increased the number and activity of cells that produce myelin, suggesting it may help restore the protective coating around nerves that is lost in MS. These findings indicate that the therapy has the potential to support both protection of existing nerve fibres and regeneration of damaged tissue.
In addition, the research has shown that this therapeutic strategy may reduce harmful inflammation and create a more favourable environment for repair within the brain and spinal cord. Together, these results suggest that this approach may act through multiple mechanisms to slow damage and support recovery.
This project is now progressing towards more advanced testing of this therapeutic approach, including proof-of-concept studies using stem cell-based models. These studies are designed to better understand how this strategy could be translated into a future treatment for people living with MS.
Updated 31 March 2026Â
$105,000
2023
3 years
Current project
