"MitoQ selectively accumulates in the mitochondria," said McManus, who is now studying mitochondrial genetics and dysfunction as a postdoctoral researcher at Children's Hospital of Philadelphia.
"It is more effective for the treatment to go straight to the mitochondria, rather than being present in the cell in general," she said.
Although he had not previously conducted research on Alzheimer's disease, Franklin was moved to approve McManus' research proposal to take his laboratory research in a more clinical direction in part because of her family's history with the disease.
"Two of my grandparents had Alzheimer's disease, but they presented with it very differently. While my granddad often couldn't remember who we were, he was still the same soulful funnyman I'd always loved. But the disease changed my grandmother's mind in a different way, and turned her into someone we'd never known," said McManus.
"So the complexity of the disease was most intriguing to me. I wanted to know how and why it was happening, and more importantly, how to stop it from happening to other people," she said.
In their study, mice engineered to carry three genes associated with familial Alzheimer's were tested for cognitive impairment using the Morris Water Maze, a common test for memory retention. The mice that had received MitoQ in their drinking water performed significantly better than those that didn't. Additionally, the treated mice tested negative for the oxidative stress, amyloid burden, neural death and synaptic loss associated with Alzheimer's.
|Contact: James Franklin|
University of Georgia