See a Better Tomorrow:
BrightFocus' National Glaucoma Research Highlights

Dr. Joel Schuman

The most important factor to consider in glaucoma is the pressure of the eye, which is controlled by the slow outflow of fluid within a drainage system in the front of the eye. Dr. Joel Schuman and his colleagues, including lead co-investigator Larry Kagemann, M.S., have developed a way to visualize and measure how fast this drainage occurs without touching the eye and without any bright lights. Their work has led to an entirely new branch of research in non-invasive 3D imaging.

For the first time, when this study is complete, eye doctors will be able to measure how an eye responds to a glaucoma medication, and surgeons will be able to know before the operation where the best place to implant a drainage device would be. The field of glaucoma medicine will know how much of the drainage system is actually used under normal conditions. Read more about Dr. Schuman's research

Dr. Jeffrey Goldberg

In glaucoma, the optic nerve becomes damaged and fails to regenerate. Because the optic nerve is the only connection between the eye and the brain, this failure of regeneration causes permanent vision loss. Dr. Goldberg's team recently discovered a group of genes called Kruppel-Like Factors (KLFs) that appear to control optic nerve regeneration. In these experiments, Dr. Goldberg is testing whether they can enhance optic nerve regeneration further with gene therapy. If successful, this will represent a new approach to treating glaucoma and to restoring lost vision.

• Read more about Dr. Goldberg's research and his work that led to receiving the 2012 Cogan Award, which recognizes a researcher who is 40 years of age or younger and who has made important contributions to research in ophthalmology or visual science
• View a video of Tommy Apara, a doctoral candidate working in the lab of Dr. Jeffrey Goldberg, who discusses research into why cells in the eye fail to regenerate and how this could lead to new therapies for brain and vision disorders.

Dr. Adriana Di Polo

Current therapeutic strategies for glaucoma are insufficient, and new approaches to delay disease progression are urgently needed. This study is investigating the clinical potential of galantamine, which has nerve protection properties, for the treatment of glaucoma. Galantamine as nerve cell protection therapy in glaucoma has several positive features including:

• efficacy to delay degeneration of retinal ganglion cells in experimental glaucoma,
• previous FDA approval for Alzheimer's disease treatment that could lead to rapid availability for patients with glaucoma, and
• a good safety profile

The researchers will determine whether galantamine can protect vision after sustained periods of eye pressure damage. They will also elucidate the mechanisms by which galantamine protects nerve cells from glaucoma damage. The study may lead to more effective drug-based therapies for treatment and provide insight for the design of small compounds that can protect the optic nerve with few side effects. Read more about Dr. Di Polo's research.

Dr. Brian Samuels

An increase in eye pressure can damage the optic nerve and lead to glaucoma. However, new studies have shown that an eye pressure change may not be the only situation that can cause an increased risk of developing glaucoma. Dr. Brian Samuels and colleagues are studying how certain cells within the brain control the pressure inside both the eye and the brain. They believe that changes to the pressure in the brain may be just as important as eye pressure in understanding the development of glaucoma. Using rat models, they are identifying the exact location of the brain cells that control some of the daily changes in the eye and brain pressure. Once they locate these brain cells, they plan to target these cells for new glaucoma therapies. In addition, discovering how the brain cells control both eye and brain pressure could lead to new treatments of other diseases that affect the brain and nerves. Read more about Dr. Samuels' research.