University of Alabama student Aidan Meyers spent his summer with the worms. C. elegans, to be exact.
Meyers, a student in the department of biology and a Blount Scholar, received a Summer Student Fellowship from the Parkinson’s Foundation earlier this year to support research on a gene that appears to be related to Parkinson’s Disease. Meyers was one of only twelve students worldwide, including medical students, to receive the grant.
Now a senior, Meyers began working in UA’s Caldwell Lab in his freshman year. He knew he wanted to pursue biomedical research, and when he heard about the lab’s work studying Parkinson’s using worms, he was intrigued.
Dr. Guy Caldwell, a university distinguished research professor in biological sciences, and Dr. Kim Caldwell, a professor in the same department, jointly run the lab that carries their name. Aidan is one of the youngest — and brightest — students to work in the Caldwells’ lab, said the former. Meyers also had the most charismatic way of asking to join the lab.
“He took a picture of himself in the Blount dormitory next to a whiteboard filled with chemical structures he had been working on, based on a paper of ours he read,” Guy Caldwell said.
He initially dismissed Aidan’s gesture, but the closer he looked, the more he realized the student had read the paper and thought deeply about it. And the work was solid. It was enough to secure Meyers a meeting with the Caldwells, and he has been a fixture in their lab ever since.
Modeling Parkinson’s in C. elegans Worms
Meyers’ project grew out of experimental research by a former graduate student in the Caldwell Lab, Karolina Willicott. C. elegans shares several biological pathways with humans, which makes it useful for biomedical research. Willicott had identified several worm genes that are related to cell stress, an aggravating factor in Parkinson’s disease and other neurodegenerative disorders.
Aidan decided to work with the gene ABTS-4, which is similar to a human gene named SLC4A2. Both gene versions are related to controlling acidity in cells, especially in the digestive system. Not much is known about these genes and how they function.
In C. elegans, researchers can induce neurodegeneration by introducing the human protein alpha synuclein, a well-known factor in Parkinson’s disease. Meyers found that his worms’ dopamine-producing neurons were more likely to deteriorate if the ABTS-4 gene was switched off.
“This means that ABTS-4 helps protect these cells from damage,” Meyers said. His experiments also found that this protective effect happens directly in the nerve cells. The fact that the human SLC4A2 gene is found in the intestines could support the growing evidence for a mind-gut connection in Parkinson’s disease and suggest new approaches to treatment.
C. elegans worms are about a millimeter in length and have a total of six dopamine neurons. Meyers would set up experiments, breed new animals by genetic crosses when needed, and then count the number of damaged vs. undamaged neurons in the worms without a working ABTS-4 gene. It isn’t glamorous work, but Meyers enjoyed knowing he was contributing something new to Parkinson’s research.
“This is something that will lead to future steps and we hope to continue the research,” Caldwell said. “It’s one thing to have a hypothesis and another to show it in the animal model, as we have done.”
A Personal Connection to the Research
Advancing scientific knowledge may be its own reward, but the project is even more meaningful to Meyers. A few weeks after he joined the Caldwell lab as a freshman, his grandfather learned he had Parkinson’s disease.
“When you’re working with a model organism, it can become abstract that it helps human Parkinson’s research. The Parkinson’s Foundation award was a tangible way to remind myself that what we do in our lab is doing real good,” Meyers said.
“And obviously I took a lot of joy in getting to tell my grandfather about it.”