Catalyst for a Cure: An Innovative Research Model

CFC Researchers (neuroprotection)
CFC Researchers (neuroprotection)

Catalyst for a Cure (CFC) is a major collaborative scientific effort in the field of glaucoma that represents an entirely unique approach to research, both by its design and its intent.

In order to expedite outcomes in support of our goal to discover a cure for glaucoma, we chose a different type of research model when forming the Catalyst for Cure.

How is CFC Different?

In traditional research laboratories, individual scientists work on separate projects and typically only publicly reveal their findings at conferences or in publications. Often, scientists in the same field are in competition for grant money to fund their work so there is an inherent need for discretion and confidentiality until results are made public. In the CFC research model, we guarantee a level of funding that allows the scientists to focus on their collaborative effort to find a cure for glaucoma.

At the outset, we set up a volunteer Advisory Board comprised of top neuroscientists who contacted university and institutional department chairs and asked them to suggest promising young post-docs who might be interested in glaucoma and had a willingness to collaborate. From this unconventional recruitment process, we identified four promising young researchers eager to collaborate on glaucoma research.

Our funding for CFC is on par with that of a government grant. To date, we have invested more than $7 million dollars in this collaborative research focused on clear goals and useful results.

Research Progress

In the first year of the Catalyst for a Cure consortium, the four principal researchers established research objectives to be tackled collaboratively. One key objective was to study the disease’s early progression.

  • In 2004, their research results indicated glaucoma is not a disease of the eye, but a disease of the central nervous system.
  • In 2005, their major results addressed identifying consistent changes in immune response genes at an early stage of the disease. That year also marked their development of three new hypotheses for how glaucoma is initiated and where new therapeutic targets may be found.
  • In 2006, in Investigative Ophthalmology & Visual Science, the scientists demonstrated that microglia may actually protect retinal ganglion cells (RGCs) from death. In glaucoma, the response of astrocytes and microglia is generally associated with negative effects on RGCs. The CFC researchers identified that a cytokine is an important factor released by microglia that can significantly reduce RGC death caused by elevated pressure. In a second published paper, they also demonstrated that the release of this cytokine occurs via cellular mechanisms similar to cytokine production in other neurological insults and diseases.
  • 2008 marked a turning point for the Catalyst for a Cure. Completed work found its way into key publications. Of note were two papers in the Journal of Neuroscience. These described early changes in glaucoma associated with the neurochemistry of the retina and optic nerve and the persistence of retinal neurons long after those changes occur. Papers in Investigative Ophthalmology and Visual Science described how silencing the immune system in glaucoma can increase survival of the optic nerve.
  • In 2010, the CFC’s work has elucidated an aggregation of a protein called gamma synuclein, which is very similar to what is observed in other neurodegenerative diseases such as Parkinson’s and Alzheimer’s. This study , published in the Proceedings of the National Academy of Sciences in 2011, also found an unusual degenerative pathway caused by a subpopulation of retinal cells called astrocytes happening exactly where the blinding insult that occurs in glaucoma is likely to be since it would account for the typical pattern of vision loss found in glaucoma. Therapies directed at this degradative process might be borrowed from other metabolic disorders that have similar defects in degradative processes.
  • In 2011, the investigators of the Catalyst for a Cure consortium continued to probe how and why retinal ganglion cells degenerate in glaucoma. Notably they investigated how diverse cellular players and molecular pathways contribute to disease onset and progression. Their work will ultimately help define new diagnostic strategies or treatments for glaucoma.
  • In 2012, GRF launched a second team of four investigators to work collaboratively to identify a new, specific and sensitive biomarker for glaucoma, which could potentially help predict glaucoma in patients who do not yet show symptoms of vision loss.

Accelerated Success

With backing from the Glaucoma Research Foundation, and their commitment to collaboration, the CFC is poised to make significant inroads in the knowledge and understanding of the disease. Multi-disciplinary approaches, fresh thinking and cross-pollination of ideas set the stage for accelerated success and serve as a model for other researchers in all other disease areas.

Collaborative research thus far has yielded important findings in an accelerated time frame that would have taken a good deal longer had the scientists not regularly shared their early results with each other.

Biomarker Discovery

Launched in 2002, the original team of four “Catalyst for a Cure” investigators 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.

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CFC biomarkers team launched in 2012

In 2012, the Glaucoma Research Foundation assembled a second team of four investigators to work collaboratively and further expand our knowledge of glaucoma. This new team, focused on biomarkers, will add critical skills and fresh perspectives to the Catalyst for a Cure.

The expanded Catalyst for a Cure research consortium includes David Calkins, PhD, Vanderbilt University; Alfredo Dubra, PhD, Medical College of Wisconsin; Jeffrey Goldberg, MD, PhD, Shiley Eye Center, University of California San Diego; Philip Horner, PhD, University of Washington; Andrew Huberman, PhD, University of California San Diego; Nicholas Marsh-Armstrong, PhD, Johns Hopkins University; Vivek Srinivasan, PhD, University of California Davis; and Monica Vetter, PhD, University of Utah.

Last reviewed on February 14, 2014

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