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.
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