A major breakthrough from researchers at the University of Copenhagen may finally explain why Parkinson’s Disease develops—and why it often leads to dementia in some patients. The findings offer new hope for understanding and eventually treating this serious brain condition, which affects millions of people around the world.
Parkinson’s Disease (PD) is a neurodegenerative disorder that damages brain cells over time. It causes problems with movement, speech, balance, and, in many cases, memory and thinking.
Until now, scientists have not fully understood what triggers this condition in its most common form. But this new study has identified a surprising culprit: a blocked system that affects the energy supply in brain cells.
At the center of this discovery are mitochondria, the parts of cells that produce energy. In healthy brain cells, damaged mitochondria are regularly cleared out and replaced. But the study found that in people with Parkinson’s, this clean-up process is blocked.
As a result, old and damaged mitochondria build up in nerve cells, reducing their energy supply and eventually causing them to die. This cell death leads to the familiar symptoms of Parkinson’s and may also explain why some patients later develop dementia.
This energy crisis in the brain doesn’t happen randomly—it’s driven by a breakdown in a specific biological pathway that normally keeps mitochondria in check. And this blocked pathway appears to be caused by problems with immune genes.
Usually, immune genes are known for protecting the body from infections like viruses. But in this study, researchers discovered that some of these genes also play a key role in the brain’s energy management. When they’re not working properly, they disrupt the mitochondrial pathway, leading to energy shortages in brain cells.
Interestingly, mutations in these same genes have also been linked to severe COVID-19 infections. This suggests a deeper connection between the immune system and the health of the brain than scientists previously thought.
The researchers didn’t rely on just one experiment—they analyzed data from multiple studies and compared gene activity in the neurons of people with Parkinson’s, especially those who had also developed dementia.
They discovered that a protein called PIAS2 was highly active in these patients. This protein may be involved in the breakdown of the mitochondrial clean-up process, making it a new target for future treatments.
This study represents a major shift in how we understand Parkinson’s Disease. Instead of focusing only on brain inflammation or the build-up of abnormal proteins (like alpha-synuclein), it shows that energy failure in brain cells—caused by blocked immune and mitochondrial pathways—could be the root problem.
By pinpointing the exact process that leads to neuron damage, scientists now have a clearer path toward developing drugs that could stop or slow down the disease. If future treatments can unblock this pathway or support the mitochondria, they might prevent or delay both Parkinson’s symptoms and the onset of dementia.
The University of Copenhagen’s findings, published in Molecular Psychiatry, offer a fresh direction for Parkinson’s research. This discovery could lead to treatments that don’t just manage the symptoms, but actually address the cause of the disease at the cellular level.
For now, more research is needed—especially to understand how this pathway functions in different types of Parkinson’s, including genetic or inherited cases. But this is a big step forward in the quest to protect brain health and improve the lives of people with Parkinson’s 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 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..
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