Parkinson’s disease is a long-term brain disorder that slowly worsens over time. It affects movement, balance, and coordination, and it often begins with symptoms such as tremors, muscle stiffness, and slowed movement.
As the disease progresses, it can also affect thinking, mood, and sleep. Parkinson’s disease is caused mainly by the gradual loss of special brain cells called dopaminergic neurons. These neurons produce dopamine, a chemical that helps control smooth and coordinated muscle movements.
For many years, scientists believed that these neurons died mainly because they became damaged or worn out. More recently, research has shown that inflammation in the brain plays an important role in this process. Inflammation is the body’s natural defense response, but when it becomes excessive or poorly controlled, it can cause harm.
In the brain, inflammation is largely controlled by microglia, which are the immune cells of the central nervous system. Microglia normally protect the brain by removing dead cells, fighting infections, and cleaning up waste. However, when they become overactive, they may start damaging healthy tissue.
A new study from the Institut de Neurociències of the Universitat Autònoma de Barcelona provides important insight into how this harmful process may occur in Parkinson’s disease.
By examining brain tissue from people with Parkinson’s disease, as well as animal and cell models, the researchers discovered that microglia behave abnormally even when dopaminergic neurons are still alive and functioning.
The team found that in the brains of people with Parkinson’s disease, there is a much higher number of reactive microglia. These are microglial cells that are in an alert state, ready to respond aggressively.
More importantly, these reactive microglia produce unusually high levels of structures on their surface called Fc gamma receptors. Under normal conditions, these receptors help microglia recognize harmful substances or damaged cells that need to be removed.
In Parkinson’s disease, however, the study suggests that these receptors begin to make mistakes. Instead of identifying only damaged or dying neurons, the overexpressed Fc gamma receptors appear to tag healthy dopaminergic neurons as targets.
Once this happens, the microglia treat these neurons as if they are dangerous or useless, even though they are still doing their job.
When Fc gamma receptors are activated in this way, they trigger changes inside the microglial cell. One key step involves a protein called Cdc42, which controls the shape and movement of cells.
Activation of Cdc42 allows the microglia to change shape, surround the neuron, and engulf it. This process, known as phagocytosis, is normally used to remove dead cells. In Parkinson’s disease, it appears to be wrongly directed at living neurons.
The researchers found encouraging evidence that this process can be slowed or stopped. In animal and cell experiments, blocking Fc gamma receptors with targeted immunotherapy significantly reduced the loss of dopaminergic neurons.
Similarly, stopping the activity of the Cdc42 protein also protected neurons, even when inflammation in the brain was high. This suggests that microglia-driven neuron loss is not inevitable and may be controlled with the right treatments.
These findings point to a possible new approach for treating Parkinson’s disease. Current therapies mainly focus on replacing dopamine or improving symptoms, but they do not stop neurons from dying.
By targeting the immune system in the brain and preventing microglia from mistakenly destroying healthy neurons, future treatments may help slow disease progression and preserve brain function for longer.
In reviewing and analyzing this study, its importance lies in shifting the focus from neurons alone to the immune environment surrounding them. The research suggests that dopaminergic neurons may not always die because they are damaged beyond repair, but because the brain’s immune system wrongly marks them for removal.
This opens the door to immunotherapy strategies that protect neurons rather than replacing dopamine after neurons are already lost. While further studies in humans are needed, this work provides strong evidence that controlling microglial behavior could become a powerful tool in the fight against Parkinson’s disease.
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