Parkinson’s disease affects around one million people in the United States, disrupting their ability to perform everyday activities due to its neurodegenerative impacts.
The disease manifests through symptoms like shaking, stiffness, and coordination problems, stemming from the death of dopamine-producing cells in the brain. As it progresses, Parkinson’s can also impair memory and lead to dementia.
Another related disorder, Lewy Body Dementia (LBD), which is characterized by early severe memory problems, affects an estimated 1.4 million people in the U.S.
Researchers at Scripps Research have been exploring the biological mechanisms behind these debilitating conditions, uncovering potential leads on their origins and progression.
Their latest findings highlight the role of reactive nitrogen molecules, such as nitric oxide, in these diseases.
These nitrogen molecules are part of a reaction that disrupts autophagy—a cellular mechanism essential for clearing out harmful protein aggregates and maintaining cell health. The proteins involved in these aggregates are known as alpha-synuclein.
In healthy cells, alpha-synuclein is routinely cleared away, but in Parkinson’s disease and LBD, these proteins clump together forming aggregates that the cells fail to remove, damaging the brain cells.
A significant player in this process is the protein called p62, which normally helps with the autophagy process. The research team discovered that in Parkinson’s and LBD, p62 undergoes a modification due to a reaction with nitrogen molecules—a process called S-nitrosylation.
This modification is abnormally high in neurons affected by these diseases and impairs the function of p62, leading to an accumulation of harmful alpha-synuclein aggregates.
This buildup of alpha-synuclein does not just stay within one cell. Once the aggregates reach a certain level, they can be released and taken up by other nearby neurons, spreading the disease throughout the brain.
This spreading aligns with the observed patterns in Parkinson’s and LBD progression.
The modification of p62 and the subsequent cellular stress it causes could be crucial in understanding how these diseases develop and spread.
This new insight opens up potential treatment strategies, particularly in finding ways to prevent the S-nitrosylation of p62, which could help stop the buildup and spread of damaging aggregates.
The implications of these findings are significant, suggesting new avenues for treatment and prevention of Parkinson’s disease and LBD. Further research is encouraged, particularly in areas like the potential benefits of vitamins E and D in combating these conditions.
For those interested in learning more about innovative approaches to managing brain health and related disorders, ongoing studies continue to explore new treatment methods for Parkinson’s disease and investigate links between conditions such as COVID-19 and Parkinson’s.
The research, led by Stuart Lipton and his team, provides a valuable contribution to our understanding of these complex diseases and was recently 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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