Diabetes is the leading cause of blindness in adults age 20-74, according to the National Institutes of Health.
Loss of vision due to retinopathy is one of the long-term and potentially disabling complications of diabetes. A degenerative disorder, it sneaks up gradually.
Diabetic retinopathy happens when blood vessels in the retina are damaged, and it is commonly found among people who have had diabetes, particularly those who are insulin-dependent, for at least 10 years.
But what triggers diabetic retinopathy? University of Minnesota neuroscientist Eric Newman, Ph.D., thinks he knows. And in a new project that’s received initial funding from the National Institutes of Health (NIH), he’s investigating whether a simple change in lighting could help to combat it.
Newman, a Distinguished McKnight University Professor, has studied the retina for more than 35 years. He’s particularly interested in the signaling that occurs among the nerve cells, glial cells, and blood vessels in the retina.
The glia are housekeeping cells; they provide nutrients and structural support for the neurons. But Newman thinks they also play a direct role in information processing, and for the past 10 years he’s been investigating the cellular and molecular mechanisms that neurons and glial cells use to control blood vessel dilation—a process called neurovascular coupling.
“Classically, diabetes is considered a disease of the microvasculature, but there are also changes in neurons, and particularly the glial cells, that happen very early,” he says. “We’re interested in all those changes and what causes them.”
Supply and demand
Part of the central nervous system, the retina is composed of a variety of nerve cells, including, at the very back of the eye, the photoreceptors. Commonly known as rods and cones, the photoreceptors are hard workers. They have a higher metabolic rate and consume more oxygen and glucose than any other cell in the body. This requires such a huge amount of blood they actually have their own blood supply. The demand is even greater in the dark, when the photoreceptors are working at full tilt.
If the retina is hypoxic or starved for oxygen, as is thought to be the case in the early stages of diabetes, this is a problem. The demand for blood exceeds the supply and thus may accelerate the onset of diabetic retinopathy.
Newman is now testing a theory that suggests the progression to retinopathy could be slowed by simply preventing the retina from ever being completely in the dark. “All you need is a very low level of light to reduce the metabolism of the photoreceptors,” he says.
“We know the first step to diabetic retinopathy is an increase in glucose; sugar levels go up. From there to the loss of neurons and changes in the glia and eventually to changes in the blood vessels we don’t understand. We really want to know how this all fits together.”
With a grant of $275,000 from the NIH, Newman and postdoctoral research associate Joanna Kur, Ph.D., will be testing three groups of diabetic rats: one kept in 12 hours of light and 12 hours of darkness; a second group in 12 hours of light and 12 hours of dim light, which Newman believes should block the increase in metabolism; and a third in complete darkness, which should make the hypoxia worse.
The investigators will use a special instrument to precisely measure the level of oxygen in the animals’ retinas. Eventually, they will determine whether the progression to retinopathy is slowed or accelerated under different conditions.
If their results support the hypothesis, their next step would be a trial with human patients.
Newman’s NIH grant will support this research for two years. An additional $200,000 will be required to complete the project.
“The beauty of this theory is that if it turns out to be helpful, the therapy will be very inexpensive,” Newman says. It could be as simple as leaving the lights on while sleeping or wearing a mask with a built-in light, he adds.
To learn more or make a gift to this research, contact Jean Gorell at 612-625-0497 or firstname.lastname@example.org.