Researchers have found that the gut may be key to preventing Parkinson’s disease. Cells located in the intestine spark an immune response that protects neurons against damage connected with Parkinson’s disease. Acting like detectives, the immune intestinal cells identify damaged machinery within neurons and discard the defective parts. That action ultimately preserves neurons whose impairment or death is known to cause Parkinson’s. The research was published in the journal Cell Reports.
Scientists have previously linked Parkinson’s to defects in mitochondria, but why and how mitochondrial defects effect neurons remain a mystery. Whatever the answer, damaged mitochondria have been linked to other nervous disorders as well, including ALS and Alzheimer’s.
The research team exposed roundworms to a poison called rotenone, which scientists know kills neurons whose death is linked to Parkinson’s. As expected, the rotenone began damaging the mitochondria in the worms’ neurons. To the researchers’ surprise, though, the damaged mitochondria did not kill all of the worms’ dopamine-producing neurons; in fact, over a series of trials, an average of only seven percent of the worms, roughly 210 out of 3,000, lost dopamine-producing neurons when given the poison.
It turns out that the roundworms’ immune defenses, activated when the rotenone was introduced, discarded many of the defected mitochondria, halting a sequence that would’ve led to the loss of dopamine-producing neurons. Importantly, the immune response originated in the intestine, not the nervous system.
Prevailing theory holds that mitochondria originated independently as a type of bacterium and were only later incorporated into the cells of animal, plants, and fungi as an energy producer. If that theory is correct, the intestinal immune responders may be especially sensitive to changes in mitochondrial function not only for its potential damaging effects, the researchers say, but because of the mitochondria’s ancient and foreign past as well.
Reprinted from materials provided by the University of Iowa.