Susan A. Keirstead, Ph.D.
University of Minnesota
Minneapolis, MN
Project: Responses of Retinal Ganglion Cells to Optic Nerve Injury

Abnormalities in the processes of retinal ganglion cells (RGCs) can lead to cell death and vision loss. One of the signals that may lead to cell death in RGCs is an influx of calcium. Dr. Keirstead has developed a surgical procedure to examine retinal ganglion cells in vivo in an anesthetized mouse. In a previous study funded by NGR, she made progress in developing a method of labeling ganglion cells with a dye that allows her to measure changes in the cells' calcium concentration. Her current goal is to optimize this method of examining changes in calcium in response to nerve cell damage. The further refinement of this method will allow Dr. Keirstead to directly assess the role of calcium in optic nerve damage, and to test the effects of various drugs on this process.

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E. Timothy O'Brien, Ph.D.
University of North Carolina at Chapel Hill
Chapel Hill, NC
Project: Telomere Lengths in POAG Trabecular Meshwork Cells

The ends of chromosomes, called telomeres, shorten each time that most cells in the body divide. When telomeres become too short, cells can no longer divide and eventually die. Dr. O'Brien has uncovered evidence that trabecular meshwork cells from eyes with primary open angle glaucoma (POAG) undergo fewer cell divisions in culture than normal TM cells. He is exploring the possibility that these cells have shorter telomeres and therefore a decreased proliferative capacity. If telomere length is found to be decreased in POAG TM cultures, Dr. O'Brien will attempt to introduce the gene required for telomere maintenance (telomerase) to determine if he can restore proliferative capacity. If the TM cells can be preserved in this way, this research could lead to new treatments for glaucoma patients.

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