The gut may play a role in protecting us from Parkinson’s disease, researchers at the University of Iowa (UI) have found. Immune cells of the intestinal tract can initiate an immune response that can protect neurons from damage that is caused by Parkinson’s disease. These cells act as a kind of detective, uncovering damaged cellular machinery in the cells and removing the dysfunctional parts. This process acts to save the neurons that cause Parkinson’s disease when they are impaired or dead.
"We think somehow the gut is protecting neurons," explained Veena Prahlad, an Assistant Professor in Biology at UI and the corresponding author of a
report describing the research published in the journal Cell Reports.
Parkinson's disease affects around 500,000 people in the United States, according to the National Institutes of Health. It’s a disorder of the brain characterized by degenerative motor control and balance, because of dying neurons in the brain. Those neurons normally produce dopamine, and after they are impaired or they die off, a shortage of dopamine results in the physical problems that are associated with the disease. If you’d like to know more, check out the video below.
Scientists are trying to understand how Parkinson’s is linked to mitochondria, as research as shown. Damages mitochondria are connected to other disorders of the nervous system like ALS and Alzheimer’s as well.
In this work, the researchers used a poison called rotenone on a worm model organism, C. elegans. Rotenone is known to kill the neurons that can cause Parkinson’s when damaged. Indeed, the mitochondria in the worms’ neurons began to suffer damage. However, the impaired mitochondria didn’t kill off all of the dopamine-producing neurons in the worms. Instead, only an average of about seven percent of the worms lost those neurons after poison exposure.
"That seemed intriguing, and we wondered whether there was some innate mechanism to protect the animal from the rotenone," explained Prahlad.
That hypothesis turned out to be correct. The immune defenses of the worms became active when the rotenone was introduced, and it functioned to discard most of the defective mitochondria. That stopped a sequence of events that could have resulted in the loss of dopamine-producing neurons. Critically, it was observed that the immune response began in the intestine and not the nervous system.
"If we can understand how this is done in the roundworm, we can understand how this may happen in mammals," said Prahlad. "How it's happening is suggestive of the possibility that the innate immune response is constantly checking its mitochondria, perhaps because of the bacterial origin of the mitochondria," Prahlad concluded.
There is a popular theory that the mitochondria organelle was first a bacterium before it was eventually incorporated into the cell. Cellular watchdogs of the intestine might be keeping an eye on these mitochondria, "because they don't trust them," Prahlad suggests. The immune response in the intestine may be very sensitive to any change in the function of mitochondria, not only because dysfunctional mitochondria can be dangerous, but also because of the ancient past of the organelle.
Sources:
Eurekalert!/AAAS via
UI,
Cell Reports
