Last summer, biology major Sunny Greene ’19 was part of a research team in the Undiagnosed Diseases Program (UDP) at the National Institutes of Health (NIH). One of only 1,300 students chosen to work in the program from over 10,000 national and international applicants, Greene spent 12 weeks investigating a rare genetic disorder called Chediak-Higashi Disease (CHD), of which there are only 300 cases known worldwide.
The NIH experience offered Greene valuable credentials and crucial preparation for achieving her goal of gaining acceptance to one of the nation’s highly selective M.D./Ph.D. programs, so she was delighted when the UDP invited her back this summer to continue her research into CHD.
“I was back in the same lab working with the same people, but this summer’s research focused on a different facet of the disease,” she explains. “Last year, I primarily conducted tissue culture experiments on fibroblast skin cells, but this year I was studying CHD’s neuropathology.”
While the classic CHD case affects children and is characterized by partial albinism, easy bruising, prolonged bleeding and clotting issues, and immunodeficiency, adult sufferers of CHD are prone to experiencing neurological symptoms similar to Parkinson’s: balance issues, motor skill loss, and/or some developmental delay. “We have no idea what causes these neurological symptoms, so I did a lot of experiments on the neuropathology of the mouse models of CHD.”
Greene zeroed in two factors that cause Parkinson’s, the first being Purkinje cell loss in the cerebellum. “This part of the brain is located at the base of the skull and Purkinje cells are responsible for the cerebellum’s role in managing motor function. One theory is that Purkinje cell loss or death might cause Parkinson’s, because if you lose them, they never grow back, and you’re going to lose motor function over time.”
She also explored a particular pathway in the brain that, if not functioning correctly, could create symptoms of Parkinson’s. “An enzyme called tyrosine hydroxylase, or TH for short, is part of this pathway and it converts the amino acid L-DOPA into dopamine, a neurotransmitter that helps in part to regulate movement. If TH isn’t functioning properly, you’re stuck with just L-DOPA and you’re not going to have enough dopamine.”
While this research shows promise, Greene says much of her work proved frustrating. But, she found that her experience with failure as a researcher last summer with NIH was invaluable in building her persistence and resilience.
“What I learned from my epigenetic reading is that the essence of research is that you’re not trying to prove anything, you’re trying to disprove something. In order to be successful, you have to fail. Goodness knows, I failed so many times this summer, but I was more prepared for it having gone through it the previous summer.”
Greene was also ready to handle lab politics for the first time. “The research world can be dog-eat-dog and very competitive. Sometimes egos get into the way of each other. But I drew upon my experience from the Batten Leadership Institute (BLI) at Hollins to deal with that, and as a result I feel that someday I can be a successful leader in the lab.”
Greene says she is tentatively planning to work at NIH again next summer as a springboard to gaining one to two more years of solid research experience, a prerequisite for many M.D./Ph.D. programs. In the meantime, she’s enjoying her senior year experience at Hollins. “It’s a time to reflect and enjoy where you are and who you are, and so honestly my goal this year is to have fun with that. I’m taking Latin 101 and learning about Roman culture, and I’m also taking a theatre appreciation class because I’ve always loved theatre, and I’m mentoring students through BLI.
“I want to do things to make myself a well-rounded person. M.D./Ph.D. programs want to see that. Of course, they want to know that you are dedicated to your science, but they also want to know what you’re doing outside of that to enrich your research.”
