Scientists from the University of Copenhagen have uncovered a critical clue about what causes Parkinson’s disease, offering hope for new treatments. Their study reveals that the most common form of Parkinson’s may be driven by a blockage in a cellular pathway that helps manage mitochondria—the tiny structures inside cells that produce energy.
This finding shines a light on how nerve cells gradually lose function and die, leading to the symptoms of Parkinson’s and, in many cases, dementia.
Parkinson’s disease affects between 7 to 10 million people worldwide. It is the second most common neurodegenerative disease in older adults, and the leading cause of movement disorders. Until now, the exact cause of most cases remained unclear.
The new research shows that when a key signaling pathway is blocked, mitochondria in nerve cells can’t properly clean up damaged parts. Over time, damaged mitochondria build up, reducing the cell’s ability to generate energy. This energy shortage is especially harmful in the brain, where neurons rely heavily on a constant supply of energy to function and survive.
This breakdown in mitochondrial function is linked to the abnormal activity of immune-related genes. These genes are normally involved in defending the body against viruses and bacteria, but they also help regulate energy use in nerve cells. When this balance is thrown off, it contributes to the gradual death of neurons in people with Parkinson’s.
Interestingly, this immune pathway is also part of the body’s response to infections like COVID-19. In fact, mutations in related genes have been connected to more severe outcomes in COVID-19 patients, showing that these immune-energy connections play a bigger role in health than previously thought.
To reach their conclusions, the researchers analyzed brain cell data from four separate studies, focusing on gene activity in neurons from people with Parkinson’s disease, especially those who also had dementia.
They found that these cells had disrupted gene expression, and a build-up of both damaged mitochondria and harmful proteins. One protein in particular, called PIAS2, was found at much higher levels in the brains of Parkinson’s patients than in healthy people of the same age.
The study suggests that PIAS2 may be a key piece of the puzzle and could be involved in why the disease worsens over time. Blocking or reversing this pathway dysfunction might offer a way to slow or prevent the loss of brain function in Parkinson’s patients.
The team also believes this discovery could help explain other inherited forms of Parkinson’s disease and open new doors to treating or preventing dementia in those affected.
Led by Professor Shohreh Issazadeh-Navikas, the study was published in Molecular Psychiatry and is being hailed as a breakthrough in understanding how Parkinson’s develops at the cellular level.
By revealing how problems in energy production and immune regulation combine to damage neurons, the study offers new targets for future treatments—giving fresh hope to millions of people living with this challenging disease.
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 information about brain health, please see recent studies that blueberry supplements may prevent cognitive decline, and results showing Plant-based diets could protect cognitive health from air pollution.
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