Parkinson’s disease is a brain disorder that affects movement, making everyday tasks difficult for nearly one million people in the U.S. It happens when brain cells that produce dopamine—an important chemical that helps control movement—start to die. This leads to symptoms like shaking, stiffness, and difficulty walking.
As the disease gets worse, it can also affect memory and thinking, sometimes leading to dementia. A related condition, Lewy Body Dementia (LBD), also involves memory problems, but in this case, they appear much earlier. About 1.4 million people in the U.S. live with LBD.
Scientists at Scripps Research have made an important discovery that could explain how these diseases start and spread. Their research suggests that certain molecules inside brain cells may play a key role in triggering damage and allowing the disease to progress.
The Hidden Problem: Toxic Nitrogen Molecules
Researchers found that both Parkinson’s and LBD produce highly reactive nitrogen molecules, such as nitric oxide. These molecules interfere with a natural process in the body called autophagy, which is responsible for cleaning out harmful waste inside cells.
One type of waste that needs to be cleared out is a protein called alpha-synuclein. In healthy people, this protein is broken down and removed before it causes any harm. But in people with Parkinson’s and LBD, alpha-synuclein starts to clump together inside brain cells, forming sticky clusters that the body can’t get rid of.
Over time, these protein clumps damage brain cells and may be a major reason why the diseases develop.
The Role of p62: A Key Defender Gone Wrong
Normally, a protein called p62 helps clear out these dangerous protein clusters by supporting the autophagy process. But the study found that in Parkinson’s patients, p62 is damaged by a reaction involving nitrogen molecules—something called S-nitrosylation.
When p62 undergoes this reaction, it stops working properly. As a result, harmful protein clusters start to build up inside brain cells. This could explain why the brain cells of people with Parkinson’s and LBD struggle to get rid of toxic proteins, leading to cell death and worsening symptoms over time.
How the Disease Spreads
The trouble doesn’t stop with just one damaged cell. When enough toxic protein clumps accumulate inside a cell, they can be released into the surrounding brain tissue. Neighboring brain cells then absorb these harmful proteins, spreading the damage further. This pattern matches what scientists already know about how Parkinson’s and LBD progress in the brain.
The new study suggests that the damage to p62 could be a key factor in setting off this harmful chain reaction. If p62 can no longer do its job, more and more brain cells become stressed, leading to widespread damage.
Hope for New Treatments
This discovery offers a promising new target for potential treatments. If scientists can find a way to prevent S-nitrosylation from damaging p62, they may be able to stop the buildup of harmful proteins. This could slow or even prevent the spread of Parkinson’s and LBD in the brain.
Researchers are now looking at possible ways to block this reaction and protect p62. Other studies have also suggested that vitamins E and D may help protect the brain from Parkinson’s disease, providing more areas for future research.
If you are interested in brain health, scientists are also exploring new treatment methods for Parkinson’s and studying links between COVID-19 and neurological diseases.
The study was led by Dr. Stuart Lipton and his team and was published in The Journal of Neuroscience.
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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