Growing up in Ghana, Visiting Assistant Professor of Neuroscience Gunnar Kwakye kept hearing stories about his great-grandfather. A man who worked on a farm most of his life, he gradually lost his memory as he got older, exhibiting symptoms of dementia. Though he had never met his great-grandfather in person, Kwakye found himself wanting to know more. As he progressed farther into his studies of neurodegenerative diseases, he decided to ask his mother more about it. Was his great-grandfather ever exposed to pesticides or heavy metal ions on his farm?
Oh, yes, she responded. DDT was pretty common back then.
This was a eureka moment for Kwakye, who now believes that his great-grandfather had a case of undiagnosed Alzheimer’s disease. Delving deeper into his own family’s history led him to discover his passion for studying neurodegenerative diseases like Alzheimer’s, Parkinson’s and Huntington’s.
In spite of the different regions of the brain affected by these diseases, they all cause dysfunction and eventual death of brain cells, manifesting themselves in a wide spectrum of movement, cognitive, and psychiatric abnormalities. While there are therapies to help patients with Alzheimer’s, Parkinson’s, and Huntington’s, there are no cures.
Having left Ghana in 1999, Kwakye went on to earn a bachelor’s degree in biology at the University of Maryland Eastern Shore in 2006 and a PhD in neuroscience at Vanderbilt University in 2011. Since there were no labs actively studying Alzheimer’s at Vanderbilt when he began his graduate studies, Kwakye chose to study Huntington’s in particular and neurodegenerative diseases in general. It was in these subjects that he specialized during his graduate and postdoctoral training at the Vanderbilt University Medical Center until early 2012.
During this time, “I just fell in love with Huntington’s disease,” says Kwakye. “Not the disease itself, obviously, but how unique the gene [that causes it] is, and how scarce the knowledge is.”
Kwakye is particularly interested in the possibility that the age of onset, symptoms, and susceptibility of Huntington’s is highly influenced by environmental factors — that the prolonged exposure to pesticides such as DDT and heavy metal ions like manganese and copper could be contributing to the rising number of patients with the disease worldwide.
Huntington’s mainly affects those of European descent, which is why the disease is prevalent among Americans as well as Europeans. But when rates of patients with Huntington’s start to rise in countries in Africa and South America, where pesticides and metal ions are not as regulated for agricultural and industrial use by the likes of the World Health Organization, then the environmental factor cannot be ignored.
“Huntington’s is a genetic disease. If you don’t have the mutation, you don’t get it,” explains Kwakye. If a parent has the disease, then there is a 50/50 chance that their child will inherit the gene. But now, people who have no records of diagnosed family history of Huntington’s are starting to show similar symptoms of the disease. Take Kwakye’s great-grandfather, for instance — there had been no documented family history of dementia or Alzheimer’s diagnosis, and non of the successive generations have exhibited any signs of the disease.
“It’s not just the gene anymore,” says Kwakye. “Something else is going on. There’s an outside factor.”
To delve deeper into this issue, Kwakye has recruited the help of two students for the summer. Seniors Marion Park and Talia Glass, along with Kwakye, are testing an overall hypothesis that environmental factors do play significant roles in modifying the age of onset, progression, severity, and susceptibility of Huntington’s disease. By exposing mutated and healthy cells to various pesticides and heavy metal ions, the team is able to observe the physiological effects and understand what kind of role these substances play in the cellular processes of Huntington’s disease. Hopefully, then, they might someday be able to pinpoint exactly what triggers the onset and susceptibility differences observed in patients with the disease.
“If you look at what these triggers are,” says Kwakye, “then you can come up with drugs to block that trigger, or educate people on how to avoid certain organophosphates/pesticides or heavy metal ions so that there is no trigger.” There might not be a cure, but there could be simple methods of prevention or mitigating the severity of the disease.
Kwakye’s research will continue into the fall semester and he plans to continue to work with students. In his lab, Kwakye focuses on fostering an atmosphere of collaboration and hard work. “I don’t believe [in] and will not encourage competition amongst students in my lab,” he says. “I only want [the students to have] the drive to get good, publishable data. I will always credit them with their work where it is due.”