For years, scientists have known that mitochondria—the energy factories inside our cells—don’t work properly in people with Parkinson’s disease.
But they weren’t sure whether these energy problems were the cause of the disease or simply a result of the damage the brain experiences during the illness. A new study may finally provide an answer.
Researchers from the Gladstone Institutes have discovered that faulty mitochondria can actually start the chain of events that leads to Parkinson’s disease. This breakthrough could help scientists develop new treatments that stop the disease before it damages the brain.
The study, published in the journal Science Advances, used a special mouse model that mimics a rare inherited form of Parkinson’s disease.
Although this type of Parkinson’s is uncommon, it looks very similar to the more common type, which affects about 90% of patients. This means that what scientists learned from this model could apply to many people with Parkinson’s.
Parkinson’s is the second-most-common brain disease that worsens over time, after Alzheimer’s. It affects more than one million people in the U.S., usually after the age of 60.
The disease causes brain cells that make dopamine—a chemical that helps control movement—to die. As a result, patients may develop shaking, muscle stiffness, and problems with walking or balance.
In the new study, researchers looked at a protein called CHCHD2 that is normally found in mitochondria. When there is a mutation, or change, in the gene that makes this protein, it can lead to Parkinson’s.
In the mouse model, the scientists watched how this faulty protein built up inside the mitochondria, making them swell and lose their proper shape. Eventually, the mitochondria stopped making energy the normal way and began relying on less efficient energy methods.
This change led to a rise in harmful molecules known as reactive oxygen species. These unstable molecules can damage cells if they aren’t cleaned up properly. In this case, the CHCHD2 mutation seemed to interfere with the proteins that usually remove these damaging molecules.
As the stress inside the cells built up, another dangerous process began. The scientists saw that a protein called alpha-synuclein started to clump together. These clumps, known as Lewy bodies, are a key feature in the brains of almost all people with Parkinson’s disease.
One important discovery was that the alpha-synuclein didn’t start building up until after the level of reactive oxygen species had already increased. This supports the idea that the oxidative stress caused by faulty mitochondria may be what triggers the buildup of alpha-synuclein.
To make sure these findings applied to humans, the researchers worked with scientists in Australia to study brain tissue from people who had died with Parkinson’s disease. They found the same pattern: the CHCHD2 protein was found in early clumps of alpha-synuclein in the brains of these patients.
This research shows clearly how a damaged mitochondrial protein can play a direct role in causing Parkinson’s.
But the scientists believe there could be other triggers, like environmental factors or different gene changes, that might also set off the same chain of events: damaged mitochondria, loss of energy, buildup of harmful molecules, and then the accumulation of toxic proteins.
Looking ahead, the researchers plan to study more about how the CHCHD2 protein causes oxidative stress. They also want to find out if new drugs that block these harmful molecules or improve energy production inside cells could prevent or slow down Parkinson’s disease.
This is an exciting step forward in understanding a disease that affects so many people. By identifying how the damage begins, scientists may be closer to finding a way to stop Parkinson’s before it starts.
If you care about Alzheimer’s disease, please read studies about the protective power of dietary antioxidants against Alzheimer’s, and eating habits linked to higher Alzheimer’s risk.
For more health information, please see recent studies that oral cannabis extract may help reduce Alzheimer’s symptoms, and Vitamin E may help prevent Parkinson’s disease.
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