Brain immune cells may help protect nerve cells in Parkinson’s

Researchers at the University of Oxford, UK, have discovered a potentially important way the brain may protect itself against the harmful protein build-up linked to Parkinson’s disease. The study, led by Dr Hung-Ju Chueh and supervised by Professor George Tofaris, was published in Science Translational Medicine on 7 October 2026. The team found that specialised immune cells in the brain can remove harmful protein clumps from nerve cells without destroying the entire cell. The discovery could point towards new ways to protect the brain, although it is still early-stage research. A protein called alpha-synuclein normally helps nerve cells function. In Parkinson’s, it can fold into the wrong shape and form clumps inside neurons. These abnormal clumps are linked to the damage seen in the disease, particularly in dopamine-producing nerve cells, which are essential for controlling movement. The Oxford researchers focused on microglia, the brain’s own immune cells. These cells normally help keep the brain healthy by clearing away unwanted material. However, when they remain active for too long, they can also cause inflammation and damage nerve cells. Using models made from human stem cells, the team studied how microglia interact with dopamine-producing neurons containing abnormal alpha-synuclein. They found that the immune cells could remove small portions of the neurons containing the harmful protein, while leaving the rest of the cells intact. This process, called trogocytosis, is similar to one cell nibbling small pieces from another. It may allow the brain to remove harmful material without losing the entire neuron. The researchers also identified a protein called GPNMB that helps this clean-up process. When they reduced GPNMB in the microglia, the cells became less effective at removing the abnormal protein clumps. They also found increased levels of GPNMB in brain immune cells in tissue from people with Parkinson’s and people with early signs of abnormal alpha-synuclein build-up. Previous genetic studies have linked the GPNMB gene to Parkinson’s risk, making its role particularly interesting. The findings show that the brain’s immune response is not simply harmful or helpful. Microglia can contribute to damaging inflammation, but they can also protect neurons by removing unwanted material. The researchers now want to understand whether this protective activity could be strengthened without triggering harmful inflammation. For people with Parkinson’s, the research offers a promising new direction, but it does not yet suggest a new treatment is available. The experiments were mainly conducted in laboratory models made from human cells, alongside studies of human brain tissue. The team has not shown that boosting this process in people would slow the disease. The next step is to discover whether this natural clean-up system can be safely encouraged in the living brain. If scientists can help microglia remove harmful protein clumps while preserving nerve cells, it could eventually contribute to treatments designed to slow Parkinson’s progression rather than simply manage its symptoms.