UA Researchers Explore Root of Diabetic Retinal Damage

The UA’s Erika Eggers has received an Innovative Award from the Juvenile Diabetes Research Foundation to identify the early mechanisms of diabetic retinal damage.

 University of Arizona researchers are working to understand, and eventually counteract, the leading cause of new cases of blindness in working-age adults by examining retinal damage due to diabetes.
Erika Eggers, assistant professor of physiology and biomedical engineering, has received an Innovative Award from the Juvenile Diabetes Research Foundation to identify the early mechanisms of diabetic retinal damage. She is working in collaboration with Heddwen Brooks, UA associate professor of physiology.Eggers and Brooks, both members of the UA’s BIO5 Institute, will use a novel approach that examines retinal neurons down to the cellular level in seeking to understand the exact changes that damage vision. Potentially, the research will identify changes that occur in retinal neurons prior to the onset of blindness.

Eggers’ laboratory has extensive experience with retinal electrical recordings, while Brooks’ laboratory has expertise making diabetic mouse models, so the project harnesses the strengths of both labs.

“If we know specifically what is happening in the eye, then we could target treatments,” Eggers said. “People have been studying the retina for many decades. We know the essential composition of everything, but we don’t know all the details. That’s important for trying to understand how the retina works, but also for repairing disease.”

Clinically, diabetic retinopathy has been described as a disease of the blood vessels in the back of the eye that happens over a long time period. However, recent studies in diabetic humans and animal models have shown that neurons in the retina are damaged and their function decreases long before blood vessel growth is measured.

Since these experiments were measuring general activity changes in the retina and there are many cell types in the retina, it is not yet understood which cells are affected or how diabetes damages retinal neurons.

Eggers and Brooks will be the first researchers to make physiological measurements of individual retinal cell types in the intact retina from a Type 1 diabetes mouse model, where it is possible to determine what neuronal mechanisms have changed due to diabetes. This will enable the researchers to correlate the survival, structure and function of individual cells in the retina.

“The mouse models are useful for research because we can identify specific changes, which is not possible in human patients. Once we have some targets of mechanisms we think are changing, the next step is to treat those in the mouse to try and prevent those changes from happening,” Eggers said.

A central question of the retinal damage is how closely it relates to vascular problems in diabetes and whether there is a correlation between diabetic retinopathy and the blood-vessel damage related to diabetic neuropathy.

Eggers is applying for additional grants from the American Diabetes Association and National Institutes of Health to secure long-term funding for the project.

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