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Solving the Parkinson’s Puzzle with Professor Kay Double
Thursday, 9th April 2026
Over 200,000 Australians are currently living with Parkinson’s disease, with a further 38 diagnosed every day. It’s the fastest growing neurological disorder in the world, and there is still no cure. In our ‘Solving the Parkinson’s Puzzle’ series, we speak to leading Australian researchers to find out how their work is helping to slow, stop and ultimately cure Parkinson’s disease.
Researchers at the University of Sydney, funded by Shake It Up Australia, have made a groundbreaking discovery that could pave the way for new treatments to slow or stop the progression of Parkinson’s disease. The team, led by Professor Kay Double, have identified a fault in a protein called SOD1, which normally protects brain cells but becomes dysfunctional in Parkinson’s disease. We spoke to Professor Double about the findings, what’s next for this research, and what it means for people living with Parkinson’s disease.
What did this research project involve?
As a research team, we were looking to see why some people develop Parkinson’s, and others don’t. We know that one of the important things that happens in Parkinson’s disease, is that there is something wrong with some of the proteins in the brain. Instead of doing what they’re supposed to, they change and can become toxic. This can affect the survival of brain cells. There is one protein in the brain, alpha-synuclein, that is known to be involved in Parkinson’s. There has been a lot of research into this protein and whether we can treat Parkinson’s by modifying this protein.
Even though we have learned a lot about alpha-synuclein, and how it forms clumps called Lewy Bodies in the brain, research is still ongoing into a treatment that slows down or stops Parkinson’s. We believe that Parkinson’s is such a complex disease, that we probably need to be treating several things at once, rather than just one.
Our research project was based on the idea that looking at multiple proteins in the brain and treating multiple things at once is likely to be helpful for people with Parkinson’s.
What is the SOD1 protein and what did you discover about it?
One of the things that we discovered in our group is that another protein called Superoxide Dismutase 1, or SOD1, goes wrong in the brain. This has not been previously studied in Parkinson’s disease but SOD1 has been studied in some forms of motor neurone disease, particularly the type commonly known as ALS. We know that changes in SOD1 can cause people to develop ALS.
When we studied the brains of people who had lived with Parkinson’s, we saw similar changes in the SOD1 protein. This made us consider, is SOD1 also contributing to the death of brain cells in Parkinson’s disease?
Then, we had a hypothesis that was a very different construct for looking at Parkinson’s disease. We recreated what we see in the brain of people with Parkinson’s disease in a mouse model. In the brains of these mice we saw the same abnormal changes in the protein, and the death of the dopamine cells that control movement. When SOD1 malfunctions, it clumps together and damages dopamine-producing neurons, causing the hallmark symptoms of Parkinson’s, including tremors, stiffness, slow movement, and poor balance.
This demonstrated that if the SOD1 protein goes wrong, it is enough to damage the dopamine cells in the brain. So, we thought, maybe we can treat Parkinson’s by decreasing the amount of the faulty SOD1 protein.
We targeted the faulty protein in the brain with a treatment containing a special copper-containing compound. We saw a significant improvement in the mouse models that received the treatment; the treated mice had hardly any brain cell death or movement problems.
What do these findings reveal about potential future treatments for Parkinson’s?
This was a hugely exciting discovery, as it indicated an opportunity to prevent Parkinson’s disease from progressing.
Ultimately, we need to find a treatment that is even more effective, so we are planning to trial a combination treatment, where a two-pronged approach will try and correct the SOD1 protein with two different mechanisms.
It’s important to understand that the abnormal SOD1 protein is toxic, but the protein in its normal form is actually a very important, protective protein in the brain. It can help us as we age. So, what we’re aiming to do with this treatment is restore the protein back to its normal form.
This is a brand-new mechanism of disease, and a brand-new way of looking at Parkinson’s, what causes it, and how we could treat it.
What is the potential impact of this research 10 years from now?
This new mechanism might provide us with a new way of treating patients, to either slow or stop the death of the dopamine cells.
For people already diagnosed with Parkinson’s, it’s a way of slowing down the disease.
If we were able to identify people at risk of Parkinson’s, before the cell death starts, and treat those people, we could potentially even prevent them from getting it at all. That’s the ultimate goal.
First, we need to work out how to identify people in that stage. There is a lot more research happening into risk factors for Parkinson’s, as well as modifying disease progression, so the two types of research happening in parallel is extremely important.
In 10 years, my hope is that we will be able to reliably identify people who are in early or pre-clinical stages of the disease. This treatment of the SOD1 protein could be part of treating people at that stage, preventing them from developing Parkinson’s completely, or delaying the onset of the disease for a significant period of time. This would give people back a lot of functional years, which has a huge impact on quality of life.
What’s next for your research?
The exciting thing about the combination treatment we are planning to test is that the two treatments are already being used safely and effectively in other diseases. We already know that they are safe – not just in healthy populations but also vulnerable groups such as older people. Depending on the results of our initial tests, we are aiming to go into clinical trials with Parkinson’s disease patients and be able to move through the early trial stages faster, with a view to get this into the clinic where people with Parkinson’s can be prescribed with the treatment.
Ultimately, our research identifies faulty SOD1 as a critical target for Parkinson’s therapies. By restoring the normal function of this protein, we may be able to slow, or even halt, the progression of the disease. While further studies are needed, these findings open an exciting new avenue for treatment development.
Your support this Parkinson’s Awareness Month can help us fund research studies just like this one, which are making groundbreaking discoveries to slow, stop and cure Parkinson’s disease. By making a donation during April, you become part of a global community joining forces to change the future for people with Parkinson’s.
