A small protein known for its role in brain diseases like Parkinson’s may also play a surprising role in skin cancer, according to new research from Oregon Health & Science University (OHSU).
Published in the journal Science Advances, the study reveals that this protein, called alpha-synuclein, could be a key player in both conditions—but in very different ways.
Alpha-synuclein has long been studied in relation to Parkinson’s disease, where it is known to form harmful clumps inside brain cells.
These clumps, called Lewy bodies, damage neurons and contribute to the symptoms of Parkinson’s and Lewy body dementia.
But what this new study shows is that the same protein may also drive the growth of melanoma, a serious form of skin cancer.
Dr. Vivek Unni, a neurologist and lead author of the study, has been studying alpha-synuclein for years. In 2019, he and his team discovered that the protein has an important job inside brain cells—it helps repair breaks in DNA.
When this function fails, neurons can die, contributing to neurodegeneration. But in the new study, conducted in melanoma cells, alpha-synuclein was doing its job too well.
Normally, skin cells grow and die in a constant cycle. That’s part of how our skin renews itself. But in cancer, this cycle goes wrong. In melanoma, the researchers found that alpha-synuclein stays in the cell’s nucleus—the control center of the cell—where it continues to help repair DNA damage.
The problem is, it becomes too effective at this job, helping damaged cells survive and divide when they should be dying. This, in turn, leads to uncontrolled cell growth—a hallmark of cancer.
In skin cancer cells, alpha-synuclein stays active in the nucleus and works in the nucleolus, a structure inside the nucleus where it spots DNA damage and brings in another protein called 53BP1 to help with repairs. By fixing these breaks too effectively, the protein may allow skin cells that would normally die to keep multiplying, leading to melanoma.
Interestingly, in neurons affected by Parkinson’s, too much alpha-synuclein seems to cause the opposite effect. Instead of staying in the nucleus where it can repair DNA, the protein moves out into the rest of the cell and forms harmful clusters. This shift means the DNA repair job doesn’t get done, and the neuron eventually dies.
Dr. Unni explained that neurons are meant to live for a person’s entire lifetime. So when they lose alpha-synuclein from their nucleus, they lose their ability to maintain DNA stability over time, which is vital to their survival. Once the protein reaches a certain level in these brain cells, it starts to cause harm instead of help.
This new understanding of alpha-synuclein’s dual role opens the door for future treatments. One idea is to develop drugs that reduce alpha-synuclein levels or adjust how it behaves in different types of cells.
For melanoma, that might mean limiting the protein’s activity to stop cancer cells from multiplying. For Parkinson’s, the opposite approach might help—finding a way to boost the DNA repair function or replace it with other proteins like 53BP1.
The researchers now aim to explore whether increasing 53BP1 alone, without depending on alpha-synuclein, could help protect neurons in Parkinson’s disease. If successful, this could lead to new treatments that avoid the side effects of targeting alpha-synuclein directly.
In the end, this research offers a powerful insight into why Parkinson’s disease and melanoma sometimes appear together in patients—and how a single protein, depending on the cell type, can either drive cancer or cause brain cells to die. Understanding this unusual connection could lead to promising new ways to treat both diseases in the future.
If you care about Parkinson’s disease, please read studies that Vitamin B may slow down cognitive decline, and Mediterranean diet could help lower risk of Parkinson’s.
For more health information, please see recent studies about how wheat gluten might be influencing our brain health, and Olive oil: a daily dose for better brain health..
The research findings can be found in Science Advances.
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