■ To combat the incidence of glaucoma, researchers at Augusta University in Georgia want to help the neurons in our eyes better protect themselves and get better help from their friends. The researchers are working to see whether agents that activate the innate neuron protector sigma 1 receptor, or S1R, can do both. Kathryn Bollinger, MD, ophthalmologist, glaucoma specialist, and retinal cell biologist, has evidence that a good additional strategy would be directly enhancing protection of neurons in our eyes, called retinal ganglion cells, hopefully by directly activating S1R.
“We may be able to protect the retinal ganglion cells more long term,” says Dr. Bollinger, a faculty member in the Department of Ophthalmology at the Medical College of Georgia and recent recipient of a $1.5 million grant from the National Eye Institute.
S1R stimulation has been shown to protect retinal ganglion cells in other disease models, but this appears to be the first work in glaucoma, Dr. Bollinger says of the protein that is expressed in both neurons and their astrocytes throughout our visual system. Her work over the past year has focused on the impact of activating S1R in the astrocytes.
The new grant is enabling her also to look at whether activating S1R, with existing drugs already used in patients for other reasons, enables neurons to better protect themselves. The high IOP that glaucoma produces inside the eye seems to transform astrocytes, a type of brain cell that provides nutrition and other support to the neurons, into a nemesis that instead releases toxically high levels of substances like nitric oxide and reactive oxygen species.
Dr. Bollinger’s team is further exploring the impact of activating S1R with known agonists like the pain reliever pentazocine and the antidepressant selective serotonin reuptake inhibitors. They are looking at their impact on neuron survival and function and the level of support from protective proteins like brain-derived neurotrophic factor, which aids neuron survival as well as new neuron growth.