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Catalyst for a Cure: Neuroprotection (CFC1)

The CFC1 Researchers in 2012
The CFC1 Researchers in 2012

“Having our work cited so often by other scientists, many of whom we respect to a high degree, is just evidence to us that we’re having a big impact in driving the future of glaucoma research.”

- Nicholas Marsh-Armstrong, PhD

Catalyst for a Cure (CFC) is a major collaborative research effort redefining how glaucoma research is conducted.

Launched in 2002, the original team of four Catalyst for a Cure investigators (CFC1) has made a significant impact on the field of glaucoma research. Their findings have redefined our understanding of how glaucoma steals sight and created possibilities for new therapeutic approaches to the disease.

The CFC was formed by convening four investigative groups chosen by the Glaucoma Research Foundation’s CFC Scientific Advisory Board for their particular expertise in neurobiology, ophthalmology and developmental genetics.

Glaucoma Research Foundation has developed and driven this cutting-edge, collaborative research model in order to better understand how glaucoma steals sight, find ways to improve treatment, and ultimately cure the disease. The Foundation pioneered collaborative glaucoma research with the introduction of Catalyst for a Cure, which paved the way for many such research programs across other fields of study.

Even more unique, the CFC consortium recruited specialists in their fields who were not previously researching glaucoma to ensure a fresh perspective and bring new ideas to accelerate a cure.

Research Focused on Results

A key result from the first Catalyst for a Cure team (CFC1) was to change the conventional understanding of glaucoma as an eye disease to a new understanding of glaucoma as a neurodegenerative disease.

CFC research has yielded promising results on two fronts: preventing vision loss from late stage glaucoma, and therapeutic treatment to stop glaucoma before it starts. For example, two papers from the CFC published in the Journal of Neuroscience uncovered important findings:

  • In the early stages of glaucoma, there is a failure of transport of important scaffolding material, nutrients and individual fibers in the optic nerve. This shows up first not in the eye, but in the visual centers of the brain — and coincides with a build-up of oxidative stress and a slowing down of tiny energy batteries in the nerves known as mitochondria.
  • While this is occurring, the connections in the retina that begin the transfer of visual information are targeted for removal, which is affected by specialized sentinels in the retina called microglia. In the early stages of glaucoma, microglia scan the retina for signs of damaged connections and mark those connections for removal by the immune system, leading to vision loss.

The original CFC researchers and their laboratories have continued to chase down the mechanisms underlying transport loss, oxidative stress, and loss of connections, seeking potential new therapeutic interventions.

Citations as Evidence of Research Impact

Research results published by the first team of Catalyst for a Cure investigators has resulted in nearly 8,000 citations by other scientists. A citation is when someone in another lab writes and publishes a scientific report and they reference your research papers in that scientific report.

“Having our work cited so often by other scientists, many of whom we respect to a high degree, is just evidence to us that we’re having a big impact in driving the future of glaucoma research.”

- Nicholas Marsh-Armstrong, PhD, Catalyst for a Cure investigator (CFC1)

A Window of Opportunity to Prevent Vision Loss

Catalyst for a Cure researchers identified a window of opportunity for preventing vision loss in the very early stages of glaucoma progression. Research conducted by the original team of investigators demonstrated a "window of structural persistence" in which connectivity between the optic nerve and brain remains even when glaucoma affects visual function.

During this "window," optic nerve fibers attempt to boost their electrical activity through natural self-repair mechanisms. Subsequent research by CFC investigators shows that enhanced neural activity can also help optic nerve fibers regenerate.

“Perhaps the best approach to a new type of nerve-based glaucoma treatment would combine optic nerve regenerative techniques with those that promote intrinsic repair in the brain.”

- David J. Calkins, PhD, Catalyst for a Cure investigator (CFC1), and Chair of the GRF Research Committee


Catalyst for a Cure Principal Investigators (Neuroprotection)

The original team of Catalyst for a Cure investigators, funded by Glaucoma Research Foundation from 2002 to 2012, made significant breakthroughs that helped redefine glaucoma as a neurodegenerative disease.

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David J. Calkins, PhD
Vice-Chairman and Director of Research;
Denis M. O’Day Professor of Ophthalmology and Visual Sciences, Neuroscience and Psychology
Director, Vanderbilt Vision Research Center
Vanderbilt Eye Institute, Nashville, Tennessee

The Calkins lab focuses on the mechanisms of neurodegeneration in glaucoma. Using systems, cellular and molecular approaches, they investigate how risk factors contribute to neurodegeneration and test new treatments. Dr. Calkins specializes in molecular mechanisms of the retina and optic nerve.


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Philip J. Horner, PhD
Professor of Neuroregeneration, Institute for Academic Medicine
Scientific Director, Center for Neuroregeneration
Houston Methodist, Weill Cornell Medical College
Houston, Texas

The Horner lab is focused on neurodegeneration and neural regeneration in models of glaucoma and spinal cord injury. The lab established a reliable glaucoma model that helped the team to study and test hypotheses. Dr. Horner's experience in spinal cord injury and glial cells, applied to glaucoma, led to new findings on the role of gliosis and oxidative stress in glaucoma.


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Nicholas Marsh-Armstrong, PhD
Associate Professor, Department of Ophthalmology and Vision Science
University of California, Davis
Davis, California

The Marsh-Armstrong laboratory studies molecular mechanisms involved in gene regulation, development and disease of the central nervous system, focusing principally on the retina. Marsh-Armstrong has identified gamma-synuclein aggregates in glaucoma in the CFC model of glaucoma — an important finding relating glaucoma to other neurodegenerative diseases.


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Monica L. Vetter, PhD
Professor and Chair, Department of Neurobiology and Anatomy
University of Utah
Salt Lake City, Utah

The Vetter lab is studying glaucoma at the molecular level to understand how genetics influence and determine the fate of neurons in the retina and central nervous system. Their goal is to reveal principles governing cell biology that will lead to new disease treatments. Dr. Vetter is committed to better understanding the role of microglia in retinal ganglion cell pathology in glaucoma.

Last reviewed on May 21, 2019

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