A research team is a step closer to uncovering the mysterious origins of Parkinson’s disease, finding that the incurable disorder appears to take root in the human gut.
The team found that waste produced by E. coli causes protein chunks—called alpha-synucleinaggregates—to form.
“So, if you can stop the aggregates from forming in the gut, there’s a chance that the proteins won’t reach the brain and cause Parkinson’s.
Now that the intestinal origins of the protein chunks are becoming clear, Bess and her team are planning to reveal the protein chunks’ journey in greater detail.
“The idea that Parkinson’s disease can start in the gut is a bit weird in terms of the typical dogma for thinking about Parkinson’s disease,” says Bess.
According to a research team, Parkinson’s disease seems to have its roots in the human gut, bringing them one step closer to understanding the disease’s enigmatic causes.
Elizabeth Bess, the lead researcher on the study and a professor in the University of California, Irvine’s chemistry department, explains that Parkinson’s disease occurs when proteins accumulate in parts of the brain that regulate bodily functions.
When those proteins accumulate in that area of the brain, the neurons die, which prevents people from moving their bodies as freely as they would like. “”.
Patients with Parkinson’s disease are unable to voluntarily control their body movements. In the US, it affects roughly one million people.
Bess’s lab focuses on the human microbiome, which is the community of trillions of unrelated microbes that live in your gut. The multidisciplinary team led by Bess discovered that the well-known E appeared to cause the formation of protein fragments in the intestine that aggregate in the brain and cause Parkinson’s disease. coli bacteria that lives in our digestive tract.
The group discovered that E. produced waste. Coli leads to the formation of alpha-synuclein aggregates, which are protein chunks.
“The vagus nerve that connects these organs may carry these disease-causing protein clumps from the gut to the brain,” Bess says.
“There is a chance that Parkinson’s disease will result from the proteins not getting to the brain if the aggregates are prevented from forming in the gut. We can also find strategies to stop these protein aggregates from forming now that we understand how they do so. “.”.
Bess’ team recently discovered that a component of coffee can stop the formation of protein aggregates in intestinal cells, in collaboration with Aida Ebrahimi, a professor of electrical engineering at Penn State.
The results of Bess’s team are paving the way for novel treatments that target the proteins before they ever reach the brain. “Other studies have shown that drinking coffee decreases the risk of developing Parkinson’s disease, and our findings shed light on how this could work,” Bess says.
Bess and her team are preparing to delve deeper into the protein chunks’ journey now that their intestinal origins are becoming more known. Bess’ team is working with chemistry professor Jennifer Prescher to tag the proteins with light-emitting, traceable bioluminescent molecules that travel throughout the body.
As for the suggested route of passage from the gut to the brain, Bess says, “We can track the protein from intestinal cells and see if it goes into neurons.”.
Since the gut contains clusters of alpha-synuclein years before symptoms of the disease appear, there is a window of opportunity to prevent the formation of these pathogen proteins before they become more problematic. “.”.
It is novel to consider that a treatment for a brain-related illness, such as Parkinson’s, may start in the gut.
“According to the conventional paradigm for thinking about Parkinson’s disease, the notion that it can begin in the gut is a little strange,” Bess says.
However, our research is mapping out how this is feasible. We hope that our efforts will pave the way for improved therapies to benefit those who suffer from this illness. “.”.
Both ACS Chemical Biology and ACS Chemical Neuroscience publish the study.
The National Institute of Neurological Disease and Stroke at the NIH provided funding for the study, and Scialog Grants made possible by the Paul G. Pauli Foundation, the Frederick Gardner Cottrell Foundation, and the Research Corporation for Science Advancement together provided funding. The Allen Frontiers Group.
