Research unravels mysterious cause of Parkinson’s disease

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A Brief Introduction to Parkinson’s Disease

Parkinson’s disease is a neurodegenerative condition that affects the brain, making it difficult for those affected to carry out everyday activities.

It is estimated that approximately one million people in the United States alone are living with this disease.

Parkinson’s disease leads to the death of brain cells in a specific pattern.

When brain cells that produce dopamine, a chemical that sends signals to the part of the brain that controls movement, start to die, it leads to symptoms like shaking, stiffness, and difficulty with walking and coordination.

These are the symptoms we usually associate with Parkinson’s disease.

But as the disease progresses, it can also affect other areas of the brain, leading to a wide range of symptoms, including memory problems and even dementia in later stages.

There is another related condition called Lewy Body Dementia (LBD), where dementia or severe memory problems appear early in the disease.

Approximately 1.4 million people in the U.S. are believed to be living with LBD.

The Unseen Culprits: Nitrogen Molecules and Protein Aggregates

Scientists have long been trying to understand what triggers the onset and progression of Parkinson’s disease.

Previous research has shown that the disease process in Parkinson’s and LBD generates highly reactive molecules containing nitrogen, including one called nitric oxide.

In a groundbreaking new study, scientists from Scripps Research have discovered that a reaction involving these nitrogen molecules can disrupt a crucial system within our cells that helps keep them clean and healthy.

This cellular system, known as autophagy, acts like a waste disposal unit, helping to get rid of harmful protein aggregates that can build up inside cells.

These protein aggregates involve a protein called alpha-synuclein. In healthy cells, these proteins are usually cleared away, but in the cells of people with Parkinson’s disease, they form sticky clumps that the cell cannot remove.

These clumps are thought to cause damage to brain cells.

The Role of p62: The Guardian of Cellular Health

The Scripps Research team found that a protein called p62 plays a crucial role in this process. Under normal conditions, p62 assists in autophagy, helping to clear away potentially harmful protein aggregates.

However, in cell and animal models of Parkinson’s, the researchers found that p62 is modified by a reaction involving nitrogen molecules.

This reaction, called S-nitrosylation, happens at unusually high levels in the affected neurons, or brain cells.

This modification changes how p62 works, and it is no longer able to help with the clearance of alpha-synuclein aggregates. As a result, these harmful protein clumps build up within the cell.

The Domino Effect: Spread of Harmful Aggregates

The buildup of alpha-synuclein aggregates within a brain cell is only the beginning of the problem.

Once the aggregates accumulate, they can be released from the cell and taken up by other nearby neurons. This is how the disease spreads in the brain.

In their study, the Scripps Research team observed that this process is similar to what happens in the brains of people with Parkinson’s and LBD.

The modification of p62 could be a key factor in a chain reaction that not only puts too much stress on individual brain cells but also helps to spread the stress to other cells.

Potential New Treatment Strategies

The findings of this research present a new target for potential treatments. If scientists can find a way to prevent the S-nitrosylation of p62, it could help to stop the buildup and spread of harmful alpha-synuclein aggregates in the brain.

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 ways to treat Parkinson’s disease, and results showing COVID-19 may be linked to Parkinson’s disease.

The study was conducted by Stuart Lipton et al and published in The Journal of Neuroscience.

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