MS is a chronic neurological disease that causes the body’s immune system to attack the protective coating around nerve fibres (myelin) in the brain and spinal cord. This leads to communication problems between the brain and the rest of the body, resulting in a wide range of disabling symptoms.
As MS progresses from the initial relapsing remitting phase to the secondary progressive phase, the damage becomes more widespread and severe. This is characterised by increased demyelination (loss of myelin) and neurodegeneration (damage to nerve cells) in the brain and spinal cord. This progressive nerve damage causes significant cognitive impairments for people living with MS.
Interestingly, researchers have found that levels of a protein in the brain called tau are significantly elevated in people with progressive MS. Tau is also implicated in other neurodegenerative diseases like Alzheimer’s disease. This suggests there may be a link between tau abnormalities and the nerve damage that occurs as MS worsens.
One potential explanation is the role of a protein called BIN1, which is selectively expressed in myelin-producing cells. Studies have shown that BIN1 may play a key part in regulating tau processing, but little is known about this process in MS.
Dr Kai-He Tse’s project will investigate the relationship between tauopathy (abnormal tau), demyelination, and neurodegeneration in progressive MS. By closely examining the patterns of tau, BIN1, and immune system activity, he hopes to uncover the underlying biological mechanisms driving nerve damage in later-stage MS.
These insights could pave the way for new therapies that target tau or BIN1. Such therapies could potentially slow down or even halt the neurodegeneration seen in secondary progressive MS.
The first part of this study is using a new state-of-the-art microscope to examine post-mortem brain tissue from the MS Australia Brain Bank.
Dr Tse and his team will map where tauopathy, myelin loss and nerve loss are happening in different connected or distant regions in the brain in MS.
By using samples from people with relapsing remitting MS and people with secondary progressive MS, this work will shed light on how problems with tau protein might spread during the transition to progressive MS.
In addition, examining MS lesions gives information about the timing of demyelination and how tau is involved at each of these stages – for example, comparing new lesions where the immune system is actively attacking the myelin, with older lesions that have much less immune activity.
The researchers will also examine where BIN1 and tau are found at these different stages – for example, within nerves or myelin-producing cells – and whether they interact. This will help uncover the role of BIN in tauopathy during myelin loss in MS.
Towards these aims, Dr Tse has obtained all required ethics and access approvals for brain bank tissue and has scanned 60% of all approved tissue slides. Analysis is now underway, including samples from relapsing remitting MS, primary progressive MS and secondary progressive MS, as proposed.
In the second part of the study, the researchers are examining BIN1 expression in human myelin-producing cells grown in the laboratory under stresses mimicking MS.
The team has found that tau and different forms of BIN1 are present in these cells and tend to group together. They also observed that BIN1 production increases when the cells are under stress. These findings support the hypothesis that BIN1 may act as a regulator of tau in myelin-producing cells.
These findings were presented in the 43rd Australasian Neuroscience Society annual meeting in Hobart in December 2025.
The next step for this part of the study is to examine BIN1 in the brain using laboratory models of MS, alongside hundreds of other genes involved in brain cell function and nerve degeneration. This will help us understand the role of BIN1 in tauopathy, myelin loss and MS.
A MPhil student has been recruited at UTS to support the research project.
Updated 31 Mar 2026
MSWA
$225,000
2025
3 years
Current project
