Parkinson’s disease is a brain disorder that affects about one million people in the U.S. It happens when the brain loses cells that produce dopamine, a chemical needed for movement and coordination.
As a result, people with Parkinson’s experience symptoms like shaking, stiffness, and difficulty moving. Over time, the disease can also affect memory and, in some cases, lead to dementia.
A similar condition, Lewy Body Dementia (LBD), affects about 1.4 million Americans. Unlike Parkinson’s, LBD often causes severe memory problems early in the disease. Despite these differences, the two conditions share common features and challenges.
Scientists at Scripps Research have recently discovered new details about how Parkinson’s and LBD might develop and progress. These findings could pave the way for better treatments in the future.
How Harmful Proteins Build Up in the Brain
In both Parkinson’s and LBD, a protein called alpha-synuclein clumps together inside brain cells. These clumps, or aggregates, are toxic and damage the cells.
Normally, the body has a cleaning system called autophagy to get rid of such harmful proteins. However, in these diseases, this system doesn’t work properly, allowing the toxic clumps to build up.
The researchers found that highly reactive nitrogen molecules, including one called nitric oxide, might play a key role in disrupting autophagy. These molecules interfere with the body’s ability to clear out alpha-synuclein aggregates, leading to cell damage.
The Role of a Key Protein, p62
A specific protein called p62 helps with the autophagy process. It acts like a helper, tagging harmful proteins for removal. However, in people with Parkinson’s, p62 often gets modified in a way that stops it from working.
This modification, called S-nitrosylation, happens when reactive nitrogen molecules interact with p62. When p62 is impaired, alpha-synuclein clumps cannot be cleared, allowing them to pile up inside brain cells.
How the Disease Spreads in the Brain
The damage caused by alpha-synuclein aggregates doesn’t stay in one place. After these toxic clumps build up in a brain cell, they can be released and taken in by nearby cells.
This starts a chain reaction, spreading damage from cell to cell and causing the disease to progress throughout the brain.
This spread is a hallmark of Parkinson’s and LBD. The Scripps Research team believes that the faulty modification of p62 might be what triggers this harmful cycle.
New Hope for Treatment
The findings offer a promising new idea for treatment. If scientists can figure out how to prevent the S-nitrosylation of p62, they might be able to stop the buildup of harmful protein clumps and their spread in the brain.
This approach could lead to new ways to slow down or even prevent Parkinson’s disease and LBD. The research also suggests that studying nutrients like vitamins E and D, which have shown some potential in protecting the brain, might offer additional strategies.
Looking Ahead
While these discoveries are exciting, more research is needed to turn them into real-world treatments. Understanding how to protect p62 and support the brain’s natural cleaning system could make a big difference for people living with Parkinson’s and LBD.
This study, led by Stuart Lipton, was published in The Journal of Neuroscience. It provides a glimpse into how these diseases work and offers hope for better treatments in the future.
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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