Around one million people in the United States are affected by Parkinson’s disease, a disorder that makes everyday activities challenging.
This condition occurs when certain brain cells that produce dopamine, a chemical that controls movement, die off.
As a result, individuals with Parkinson’s experience shaking, stiffness, and difficulties with walking and coordination.
As the disease progresses, it can also affect memory and lead to dementia.
Another related condition, Lewy Body Dementia (LBD), affects about 1.4 million people in the U.S., and it is characterized by early memory problems.
Recently, scientists from Scripps Research made some exciting discoveries that could help us better understand the causes and progression of these diseases.
The Hidden Culprits: Nitrogen Molecules and Clumpy Proteins
Research has shown that Parkinson’s disease and LBD are associated with the production of highly reactive nitrogen molecules, including one called nitric oxide. These nitrogen molecules can wreak havoc in our cells.
The scientists at Scripps Research found that reactions involving these nitrogen molecules can disrupt a cellular cleaning system called “autophagy.”
Autophagy is essential for keeping our cells healthy by getting rid of harmful protein clumps. These clumps involve a protein called alpha-synuclein.
In healthy cells, alpha-synuclein and other proteins are regularly cleared away. But in people with Parkinson’s and LBD, these proteins stick together, forming clumps that the cell can’t get rid of. This can lead to damage in brain cells.
The Guardian of Cellular Health: p62
The protein p62 is like a superhero in this story. Normally, it helps with autophagy by removing potentially harmful protein clumps.
However, the Scripps Research team discovered that in models of Parkinson’s disease, p62 gets modified by those troublesome nitrogen molecules through a process called S-nitrosylation. This modification happens at unusually high levels in the affected neurons.
This modification interferes with p62’s ability to do its job, resulting in a buildup of harmful alpha-synuclein clumps inside the cells.
The Chain Reaction: Spreading the Damage
When alpha-synuclein clumps pile up within a brain cell, it’s just the beginning. These clumps can escape from the cell and enter nearby neurons, causing the disease to spread throughout the brain.
This spreading process mirrors what happens in the brains of people with Parkinson’s and LBD. The alteration of p62 seems to be a crucial step in a chain reaction that puts stress on individual brain cells and spreads that stress to others.
Hope for New Treatments
These discoveries open up new possibilities for treatments. If scientists can find a way to prevent the S-nitrosylation of p62, it might stop the buildup and spread of harmful alpha-synuclein clumps in the brain. This could offer a fresh approach to treating or even preventing Parkinson’s disease and LBD.
Additionally, researchers are exploring the potential benefits of vitamins E and D in preventing and treating Parkinson’s disease, offering more avenues for investigation.
In conclusion, these findings from Stuart Lipton and his colleagues at Scripps Research provide hope for understanding and potentially treating Parkinson’s disease and Lewy Body Dementia.
By targeting the processes involving nitrogen molecules and protein clumps, we may be one step closer to finding effective therapies for these devastating conditions.
If you care about brain health, please read studies about inflammation that may actually slow down cognitive decline in older people, and low vitamin D may speed up cognitive decline.
For more information about brain health, please see recent studies about common exercises that could protect against cognitive decline, and results showing that this MIND diet may protect your cognitive function, prevent dementia.
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