Colin J. Barnstable, D.Phil. Back to Speakers

Extracted from: Macula Vision Research Foundation, where Dr. Barnstable is on the Board of Scientific Advisors.

Dr. Barnstable has published over 130 papers, most of them on retinal structure and development. He has served on the editorial boards of major scientific journals including the Journal of Neuroscience and the Journal of Neurochemistry, as well as on the review committees of several institutes of the National Institutes of Health.

Dr. Barnstable and his colleagues primarily study the molecular mechanisms of cell differentiation and cell function in the normal mammalian visual system because knowing how the visual system works is critical to understanding how it goes wrong. This work has led to the discovery of many new retinal molecules and pioneered the use of tissue culture to study the role of specific factors in retinal development.

Dr. Barnstable's group was the first to show that cells of the retinal pigment epithelium, the pigmented layer of cells behind the retina, could be converted into retinal tissue. With the potential of using stem cells as a source of replacement tissue in macular degeneration, it has become important to know how to direct their development into the specific cell types needed. Using the tools of modern genetics and biochemistry they have mapped out the molecular pathways by which retinal stem cells can be turned into photoreceptors, an important step if we are ever to use this approach to restore vision.

Using modern methods of bioinformatics and large scale analysis of expressed genes, Dr. Barnstable's group has identified a number of new genes selectively expressed in photoreceptors. Some of these genes may be responsible for forms of human photoreceptor degeneration and others change expression in response to the disease. Understanding how all of these genes work in the normal retina will tell us much about normal vision as well as about the mechanisms of photoreceptor degeneration. Macular degeneration, retinitis pigmentosa and glaucoma are all blinding diseases but have very different causes and lead to loss of different retinal cell types.

Some aspects of the way the cells die are common to all the diseases and Dr. Barnstable's group has recently identified a set of proteins whose activation can lessen the cell death induced in a variety of ways. Current work is aimed at finding drugs to increase the activity of these proteins in the retina so that the loss of cells in a number of retinal diseases can be slowed or abolished.