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Robert E. (Gene) Anderson, MD, PhD

George Lynn Cross Research Professor Emeritus of Ophthalmology

George Lynn Cross Research Professor Emeritus of Cell Biology

University of Oklahoma College of Medicine

Dean McGee Eye Institute

Special Interests

  • Role of unique fatty acids found primarily in photoreceptor cells in preserving structure and function of the retina.  Mutation of the gene encoding the protein that synthesizes these fatty acids leads to dominantly inherited Stargardt-like macular dystrophy, a juvenile form of macular degeneration.
  • Identification and utilization of synthetic and naturally occurring compounds that can prevent retinal degeneration in human diseases such as age-related macular degeneration (AMD) and retinopathy of prematurity (ROP).

 

Training

  • BA: Mathematics, Texas A&M University, College Station, TX
  • PhD: Biochemistry and Biophysics, Texas A&M University, College Station, TX
  • MD: Baylor College of Medicine, Houston, TX
  • Postdoctoral Training: Oak Ridge Associated Universities, Oak Ridge, TN
Robert E.-Gene Anderson MD PhD

Research Summary

Our research focuses on the metabolic pathways that (1) provide molecules essential for the normal function of the retina and (2) protect against stress-induced retinal degenerations. Disruptions in the former, which occurs in dominantly inherited Stargardt-like Macular Dystrophy (STGD3), leads to macular degeneration in children. We recently discovered that a unique group of fatty acids found primarily in photoreceptor membranes is greatly reduced in retinas of an animal model of STGD3. Current studies are focused on finding ways to deliver these essential fatty acids to the retina with the goal of preventing the retinas from degenerating. Environmental and hereditary stresses can lead to retinal degeneration. We discovered that the insulin receptor can be activated by light and initiate a series of “downstream” reactions that can protect the retina from light stress-induced degeneration. Current studies are focused on finding ways to fortify these pathways so that the retinas of persons susceptible to retinal diseases become more resistant to stress-induced degeneration. Finally, we have identified a number of synthetic and naturally occurring compounds that can protect the retina from oxidant stress-induced degeneration. Current research focuses on identifying the specific metabolic pathways these compounds affect and to test their efficacy in animal models of human age-related macular degeneration.

 

Recent Publications