Parkinson’s disease is a neurodegenerative disorder affecting about one million people in the United States. It disrupts daily activities due to the loss of dopamine-producing brain cells, leading to symptoms such as shaking, stiffness, and coordination problems.
As the disease progresses, it can also affect memory and potentially lead to dementia. A related condition, Lewy Body Dementia (LBD), which causes severe memory issues early on, impacts an estimated 1.4 million people in the U.S.
Recent discoveries by scientists from Scripps Research may provide new insights into the origins and progression of these conditions.
The Role of Nitrogen Molecules and Protein Aggregates
Parkinson’s disease and LBD are linked to highly reactive nitrogen molecules, including nitric oxide. The Scripps Research team found that these nitrogen molecules interfere with autophagy, a cellular system responsible for removing harmful protein aggregates.
These protein clumps are composed of a protein called alpha-synuclein. Normally, cells clear out alpha-synuclein, but in people with Parkinson’s and LBD, these proteins form sticky aggregates that the cell cannot eliminate, leading to brain cell damage.
p62: The Guardian Protein
A protein called p62 is crucial in this process. It supports autophagy by helping eliminate potentially harmful protein aggregates.
However, in Parkinson’s disease, p62 undergoes a modification known as S-nitrosylation, which occurs at high levels in affected neurons. This modification impairs p62’s function, resulting in the accumulation of harmful alpha-synuclein aggregates in cells.
The Domino Effect: Spread of Harmful Aggregates
The buildup of alpha-synuclein aggregates within a brain cell is just the beginning. These aggregates can be released from the cell and absorbed by nearby neurons, causing the disease to spread throughout the brain.
This process mirrors what happens in the brains of individuals with Parkinson’s and LBD. The modification of p62 may trigger a chain reaction that stresses individual brain cells and spreads this stress to other cells.
New Treatment Strategies
These findings suggest a new potential target for treatments. If scientists can prevent the S-nitrosylation of p62, it might stop the buildup and spread of harmful alpha-synuclein aggregates in the brain. This could provide a new approach to treating or preventing Parkinson’s disease and LBD.
Future Research and Implications
Further research is necessary to explore the benefits of preventing p62 modification. Studies on vitamins E and D have also shown potential in Parkinson’s prevention and treatment, offering additional avenues of investigation.
For more information on brain health, you can explore recent research on new treatment methods for Parkinson’s disease and the links between COVID-19 and Parkinson’s. The study, conducted by Stuart Lipton and his team, 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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