
Parkinson’s disease is one of the most common brain disorders affecting older adults.
It gradually damages the nervous system, causing symptoms such as shaking, muscle stiffness, slow movement, and problems with balance and walking.
As the disease progresses, many people also develop memory problems, changes in thinking, and dementia. Although treatments can help control symptoms, there is still no cure, and scientists have been searching for the underlying cause for many years.
A new study from the University of Copenhagen has revealed an important clue that could change how researchers understand Parkinson’s disease.
The scientists discovered that the disease may be driven by a blockage in the system that controls mitochondria, the tiny structures inside cells that produce the energy needed for normal cell function.
Mitochondria are often described as the cell’s power stations because they generate the energy that keeps cells alive. Healthy cells constantly remove old or damaged mitochondria and replace them with new ones. This natural cleaning process is essential because faulty mitochondria produce less energy and can release harmful substances that damage cells.
The new research suggests that this cleaning system becomes blocked in people with Parkinson’s disease. Instead of being removed, damaged mitochondria build up inside brain cells. As these unhealthy mitochondria accumulate, the cells produce less energy and become increasingly stressed. Eventually, many of these brain cells die, leading to the movement problems and other symptoms seen in Parkinson’s disease.
One of the most surprising findings was the role of the immune system. The researchers found that genes normally involved in protecting the body against viruses, including viruses such as COVID-19, also help control the system responsible for maintaining healthy mitochondria. In Parkinson’s disease, these immune-related genes appear to stop working properly, contributing to damage instead of protecting brain cells.
To better understand this process, the researchers analysed information from several previous studies and examined gene activity in brain cells from people with Parkinson’s disease. They identified unusually high levels of a protein called PIAS2. This protein may interfere with the normal recycling of damaged mitochondria, making it a possible contributor to the disease.
The discovery is important because PIAS2 could become a new target for future treatments. If scientists can develop medicines that reduce the harmful effects of this protein or restore the normal cleaning process inside cells, they may be able to protect brain cells from damage and slow the progression of Parkinson’s disease.
The researchers also believe this mitochondrial problem may not be limited to one form of Parkinson’s disease. It could play a role in inherited forms of the disease as well, suggesting that the findings may benefit a much wider group of patients than first expected.
The study was published in the journal Molecular Psychiatry. Although more research is needed before these findings lead to new treatments, the work represents a major step forward in understanding why Parkinson’s disease develops.
By uncovering the connection between mitochondria, the immune system, and the PIAS2 protein, scientists are moving closer to therapies that could slow the disease, protect memory, and improve the lives of millions of people worldwide.
If you care about brain health, please read studies that eating apples and tea could keep dementia at bay, and Olive oil: a daily dose for better brain health.
For more health information, please see recent studies what you eat together may affect your dementia risk, and time-restricted eating: a simple way to fight aging and cancer.
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