Robert E. (Gene) Anderson, MD, PhD

  • Dean A. McGee Professor
  • Professor of Ophthalmology and Cell Biology
  • Interim Chair of the Department of Cell Biology
  • Adjunct Professor of Biochemistry & Molecular Biology and Geriatric Medicine
  • George Lynn Cross Research Professor

Special Interests

  • Relationship between the insulin receptor and the phosphoinositide signaling pathway in providing neuroprotection of the retina from stress-induced degeneration. We have shown that disruption of this pathway leads to light-induced oxidant stress that kills photoreceptor cells.
  • Mechanism of retinal degeneration in a mouse model of human autosomal dominant Stargardt Macular Dystrophy. We recently discovered that the protein that is mutated in this disease is an enzyme critical to the synthesis of a unique class of fatty acids found primarily in retinal membranes.
  • We are searching for synthetic and naturally occurring compounds that can prevent stress-induced retinal degeneration in animal models of age-related macular degeneration.


  • PhD, Biochemistry and Biophysics, Texas A&M University, College Station, Texas
  • MD, Baylor College of Medicine, Houston, Texas
  • Postdoctoral Training, Oak Ridge Associated Universities, Oak Ridge, Tennessee

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 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

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Funding Sources

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