Parkinson’s disease is a brain disorder that affects nearly one million people in the United States. It makes everyday activities harder by causing symptoms like shaking, muscle stiffness, and trouble walking or keeping balance.
As the disease gets worse, it can also affect memory and may lead to dementia. A closely related condition called Lewy Body Dementia (LBD), which causes serious memory problems early on, affects about 1.4 million Americans.
Now, scientists from Scripps Research may have uncovered important details that could help us better understand what causes these diseases—and how they spread in the brain.
Their research focused on two main problems: the buildup of harmful clumps of proteins inside brain cells and the role of certain damaging molecules in this process.
In both Parkinson’s and LBD, a protein called alpha-synuclein starts to build up in brain cells. These proteins are normally cleared away by a cleaning system inside our cells, called autophagy. This system acts like the cell’s recycling center, helping to remove waste and unwanted materials.
However, in people with Parkinson’s or LBD, this cleaning system doesn’t work properly. The Scripps Research team found that one reason for this could be the presence of highly reactive nitrogen-based molecules—especially nitric oxide—which are produced in high amounts in affected brain cells.
These nitrogen molecules can react with and change other proteins in the cell. One key protein they found being affected is called p62. This protein normally plays a major role in helping autophagy work properly, guiding harmful waste like alpha-synuclein to be removed from the cell.
But in the brains of people with Parkinson’s and LBD, the researchers discovered that p62 is being changed by a process called S-nitrosylation. This chemical reaction, caused by nitric oxide, interferes with p62’s job. As a result, the cleaning system breaks down, and toxic alpha-synuclein clumps start to build up.
Worse still, these clumps don’t just stay inside one cell. Once they form, they can leak out and be taken in by nearby brain cells. This starts a chain reaction, spreading the damage throughout the brain—just like scientists see in real cases of Parkinson’s and LBD.
This discovery points to a new possible way to treat or even prevent these diseases. If researchers can find a way to stop p62 from being damaged by S-nitrosylation, the cleaning system in the cell might work better, helping to remove alpha-synuclein before it becomes harmful and spreads.
The study also adds to growing research that links oxidative stress—when harmful molecules like nitric oxide build up in the body—to brain diseases. Scientists are also looking into how vitamins like E and D might help prevent or slow down Parkinson’s disease by protecting brain cells from damage.
This research was led by Dr. Stuart Lipton and his team and published in The Journal of Neuroscience. While more studies are needed, this work opens new doors to understanding how Parkinson’s and LBD develop—and how we might one day stop them.
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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