Targeting the GUCY2C protein in the gut could prevent Parkinson’s disease by protecting the brain from damage caused by toxins, a study suggests.
- Researchers have discovered that a specific protein in the gut microbiota, called GUCY2C, is able to prevent the development of Parkinson’s disease by protecting the brain against damage and toxic insults.
- They found that mice in which GUCY2C expression was inhibited or suppressed had more brain cell damage and were more sensitive to toxins.
- And when rodents with normal levels of GUCY2C were exposed to a toxin, GUCY2C levels naturally increased. “It’s almost as if GUCY2C plays a protective role in the cells or neurons in the mouse brain.”
Touching more than 160,000 people in France and nearly ten million worldwide, Parkinson’s disease is a neurodegenerative disease that manifests itself through tremors and muscle rigidity, due to a loss of the chemical dopamine in the brain. “One of the causes of the disease is exposure to toxins”recalls Dr. Scott A. Waldman.
Now, he and his team of researchers from Thomas Jefferson University in the United States have discovered that a specific protein in the intestinal microbiota is capable of preventing the development of the disease by protecting the brain against damage and toxic attacks. Their work, published in the journal npj Parkinson’s Diseasepotentially open the way to new treatments.
GUCY2C protein plays protective role in mouse brain
The protein in question, called GUCY2C, has been studied for years for its notorious role in the secretion of water and salt in the intestine. But it is also produced in the brain. Previous studies have shown that removing it from intestinal cells in mice increases the expression of genes associated with Parkinson’s. “That’s when we established the gateway from the gut to the brain, explains Professor Waldman. If we deleted GUCY2C in the brain, would that impact the risk of developing Parkinson’s disease?”
Conducting further experiments in mice, the researchers found that rodents in which GUCY2C expression was inhibited or suppressed had more brain cell damage and were more susceptible to toxins, compared to mice with normal levels of GUCY2C.
Additionally, when rodents with normal levels of GUCY2C were exposed to a toxin, GUCY2C levels naturally increased. This suggests, the scientists say, that “It’s almost as if GUCY2C plays a protective role in mouse brain cells or neurons, which is surprising given its usual role in the gut.”
A new therapeutic avenue against Parkinson’s disease?
These observations led the team of researchers to examine human brain samples to see if GUCY2C expression showed the same trends. As a result, they found that patients with Parkinson’s had elevated levels of GUCY2C compared to patients without the disease.
“Current Parkinson’s therapies mimic dopamine and only manage the symptoms of the disease, say the authors of the study. Targeting GUCY2C could be a promising way to potentially prevent disease progression by protecting the brain from neuron-induced damage.”
