In a groundbreaking advancement in Parkinson’s disease research, scientists from the University of Sydney have uncovered a malfunctioning form of the protein superoxide dismutase 1 (SOD1) that plays a critical role in the neurodegeneration associated with the disease. Typically responsible for protecting brain cells, SOD1 was found in a misfolded state in Parkinson ’s-affected brains, where it contributes to cell damage instead of preventing it.
This discovery, more than a decade in the making, was led by Professor Kay Double of the Brain and Mind Centre. Her team had previously identified the abnormal presence of SOD1 in Parkinson’s disease patients back in 2017. The current study builds on that foundation, focusing on how the protein’s faulty interaction with copper leads to its misfolding. By restoring proper copper coordination within SOD1, researchers hoped to revert it to its protective, functional state.
Copper Therapy Shows Dramatic Results in Mice
To test their hypothesis, the research team treated mice exhibiting Parkinson like symptoms with a targeted copper-based supplement over 12 weeks. Another group of mice received a placebo. The results were nothing short of astonishing: while the untreated group experienced the expected decline in motor abilities, the copper-treated mice not only resisted deterioration but also saw a reversal of tremor-like symptoms and significant improvement in mobility.
“We were astonished by the success,” said Professor Double in a statement quoted by the Good News Network. The study, now published in Acta Neuropathologica Communications, highlights that correcting copper imbalances in SOD1 effectively neutralizes its harmful misfolded form—potentially halting or even reversing the course of the disease, at least in animal models.
Toward Human Trials and Clinical Potential
Parkinson’s disease affects more than 10 million people worldwide and is marked by progressive loss of dopamine-producing neurons, leading to tremors, stiffness, and movement difficulties. Current treatments focus primarily on symptom management and do not address the root causes of neurodegeneration.
This copper-based approach could become a game-changing therapy, targeting a specific molecular trigger of the disease. The next phase of research involves translating these findings into human applications. Scientists are now exploring the safest and most effective delivery methods—whether oral supplements, injectables, or targeted drugs—and plan to initiate early-phase clinical trials shortly.
Professor Double, however, urges caution, noting that Parkinson’s is a multifactorial disease. “Just as we saw with HIV, a combination of therapies may be required. This discovery could be one critical piece of that puzzle,” she emphasized.
With symptoms reversed in mice and a clear biochemical target identified, this study marks one of the most hopeful developments in Parkinson’s research in years. As preparations for human trials begin, the scientific community watches closely, optimistic that a potential breakthrough treatment may finally be on the horizon.
Sources:
https://www.sciencedaily.com/releases/2025/07/250705083956.htm
