Durham, N.H. University of New Hampshire professor Rick Cote has received $1.4 million from the National Institutes of Health (NIH) to continue research into the central enzyme that controls initial steps of vision and that, when defective, can result in retinitis pigmentosa, a leading inherited cause of blindness.
Retinitis pigmentosa, or RP, affects 1.5 million people worldwide. Typically, symptoms begin in childhood or early adulthood and progress from impairments in night vision to tunnel vision. The degree of vision loss varies, but in some cases RP leads to total blindness.
Cote, a professor of biochemistry and molecular biology who has received NIH funding through the National Eye Institute for 18 years, conducts fundamental research into visual signaling pathways in the photoreceptors of the retina. "Until you know how the retina functions normally, you're not going to be able to understand how genetic or environmental defects in the visual pathway can cause vision loss or total blindness, or how to slow or prevent disease progression," he says.
Normal functioning of the retina begins with light being absorbed by the photoreceptor cells, called rods and cones. Cones are responsible for color perception, daylight vision, and visual discrimination tasks like reading, while rods provide peripheral vision and vision in low light.
Central to rod and cone visual signaling is the phosphodiesterase (PDE) protein. This enzyme is activated by light and is directly responsible for the nerve impulse that signals the perception of light. "It's therefore not surprising that this exquisitely light-sensitive enzyme can also cause retinal disease when its regulation or catalytic activity is impaired by a genetic mutation, as in certain forms of RP," says Cote. Most of Cote's research career has focused on better understanding how PDE functions. With such knowledge, he says, "we might someday be able to intervene therapeutically t
Contact: Beth Potier
University of New Hampshire