Parkinson’s disease is a brain condition that makes it difficult for people to move and do daily activities. It affects about one million people in the U.S. Symptoms include shaking, stiffness, and trouble walking or balancing.
Over time, the disease can also affect memory and lead to dementia. A similar condition called Lewy Body Dementia (LBD), which causes severe memory problems early on, affects about 1.4 million Americans.
Researchers at Scripps Research have uncovered important clues about what might cause Parkinson’s and LBD. Their findings may help explain how these diseases develop and open doors for new treatments.
What’s Going Wrong in the Brain?
In both Parkinson’s and LBD, certain molecules called reactive nitrogen species, including nitric oxide, are produced in large amounts. These molecules can interfere with a vital process in cells called autophagy. Autophagy acts like the cell’s cleaning system, removing harmful waste, such as clumps of proteins.
One protein involved is alpha-synuclein. In healthy brains, alpha-synuclein is cleared out through autophagy. But in people with Parkinson’s or LBD, the protein forms sticky clumps that the cells cannot clean up. These clumps damage brain cells and contribute to the symptoms of the diseases.
The Role of p62: A Key Player in Cell Cleanup
A protein called p62 is essential for autophagy. It helps clean out harmful protein clumps like alpha-synuclein. However, the Scripps Research team found that in Parkinson’s and LBD, p62 gets altered by a chemical process called S-nitrosylation. This process happens more often in affected brain cells due to the excess reactive nitrogen molecules.
When p62 is modified this way, it stops working properly. Without functioning p62, the cells can’t remove the harmful protein clumps, which then build up and cause further damage.
How the Problem Spreads
The buildup of alpha-synuclein clumps doesn’t just harm one cell. These clumps can leave the cell and spread to nearby brain cells, triggering a chain reaction. This may explain why Parkinson’s and LBD worsen over time, as the damage spreads through the brain.
The researchers believe that the modification of p62 could be a key reason this process happens, acting like a domino that sets off the spread of disease.
Hope for New Treatments
This discovery could lead to better treatments for Parkinson’s and LBD. If scientists can prevent S-nitrosylation from affecting p62, they might stop the harmful clumps of alpha-synuclein from building up and spreading. This approach could slow or even prevent the progression of these diseases.
Other studies have also suggested that vitamins E and D might help protect against Parkinson’s. These findings provide additional options to explore in the search for effective treatments.
Looking Ahead
The work by Stuart Lipton and his team at Scripps Research, published in The Journal of Neuroscience, gives new insight into Parkinson’s and LBD. It highlights how a breakdown in the cell’s cleaning system contributes to these diseases and offers a new target for treatment.
While more research is needed, this discovery is a step forward in understanding and potentially treating these challenging conditions.
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 health information, please see recent studies about how wheat gluten might be influencing our brain health, and Olive oil: a daily dose for better brain health..
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