A recent study from the University of Copenhagen, led by Professor Shohreh Issazadeh-Navikas, has provided new insights into the underlying causes of Parkinson’s disease, the second most common neurodegenerative disorder affecting aging populations worldwide.
This research, published in Molecular Psychiatry, focuses on the blockage of a crucial cellular pathway that manages the mitochondria, often referred to as the cell’s powerhouse.
Parkinson’s disease affects approximately seven to ten million people globally and is the most prevalent movement disorder among older adults.
Despite its widespread impact, the root causes of Parkinson’s have largely remained a mystery. This study sheds light on a critical aspect of cellular dysfunction that contributes to the disease’s progression.
The research centers on how neurons, or nerve cells, manage their mitochondria. Mitochondria are essential for energy production in cells, but they can become damaged over time.
Typically, cells can clean up and recycle damaged mitochondria, a process akin to how people consume food and expel waste. However, the study found that in Parkinson’s disease, this cleanup process is disrupted due to a blockage in a specific signaling pathway.
This blockage is particularly problematic because it leads to the accumulation of damaged mitochondria, which in turn reduces the neuron’s ability to produce energy.
Over time, this lack of energy causes the neurons to deteriorate and die, leading to the development of Parkinson’s symptoms and, in many cases, progression to dementia.
The researchers discovered that the blockage is tied to a dysregulation of immune genes, which are crucial not only for combating viruses but also for regulating the energy supply within nerve cells.
Interestingly, these pathways are also involved in microbial and virus recognition, which is important for fighting infections such as COVID-19. A mutation in a related gene has even been linked to severe outcomes from COVID-19.
By analyzing four separate data sets, the team examined neurons from the brains of individuals with Parkinson’s disease to determine which genes were being expressed and how these patterns were disturbed, particularly in those who had also developed dementia associated with Parkinson’s.
They found that the damaged mitochondria lead to an increase in other toxic proteins.
A key finding from the study was the high expression of a protein called PIAS2 in the neurons of Parkinson’s patients compared to healthy individuals of the same age.
This suggests that PIAS2 and its associated pathways could be significant not only in typical Parkinson’s disease but also in familial forms of the disease.
The implications of this research are profound, as understanding this pathway blockage opens up potential avenues for developing treatments that could prevent or reverse the progression of Parkinson’s disease and its associated cognitive decline.
The team is optimistic that their findings will spur further research aimed at counteracting these blockages, offering hope for improved therapies in the future.
For individuals interested in further exploring Parkinson’s disease and cognitive health, ongoing research continues to unveil ways to potentially slow or prevent age-related cognitive decline and address neurodegenerative diseases effectively.
If you care about Parkinson’s disease, please read studies about Vitamin E that may help prevent Parkinson’s disease, and Vitamin D could benefit people with Parkinson’s disease.
For more information about brain health, please see recent studies about new way to treat Parkinson’s disease, and results showing COVID-19 may be linked to Parkinson’s disease.
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