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Each year in Fort Lauderdale, Florida over 8,000 of the World's top
ophthalmologists and eye researchers gather for the biggest meeting of the year to report new knowledge about the eye and update colleagues on important developments in ophthalmology
practice.
It's the Annual Meeting of the venerable Association for Research in Vision and Ophthalmology
(ARVO).
The Macular Degeneration Foundation was there, listening, learning and engaging the best
and the brightest researchers in discussion about ways to achieve sight saving solutions sooner.
While the bulk of papers presented still focussed on eye diseases other than
macular degeneration, there was an encouraging increase in the amount of work being done in MD.
The MD research reported fell into three categories:
1. Developing a better understanding of what
goes right in the normal macula and what goes wrong in a diseased one.
2. Determining the structure and function of the newly discovered genes linked to Stargardt and some forms of
macular degeneration
3. Looking at ways to stimulate the macula to repair itself using stem cells
New Insights into What Goes Wrong
ARVO Researchers shared new facts about age-related changes to
Bruch's membrane (BM), the fine tissue layer that is sandwiched between the macular blood supply and the retinal pigment epithelium (RPE), the sponge like layer that supplies
nutrients and oxygen to the macular cones (sight sensing cells).
First, scientists at Wilmer Eye Institute announced that they had created a potential mouse model for
degeneration of the RPE, and the BM using a breed of mice that undergo accelerated aging, known as senescence accelerated mice. The mice were induced to show some of the neovascular
(new blood vessel) changes that humans with the wet from of macular degeneration have. The implications of this work for humans with the disease are that we may now have a
better animal model to study the disease and test new therapies in an accelerated fashion.
Is drusen the
battle-scar from a war you wage with your own macula?
The origin of drusen, remains a complex
mystery, but three papers from prominent research groups in Santa Barbara, Iowa and Sydney, Australia suggested that some drusen might well be the fallout from an immune attack
launched by your own body against exposed areas of the RPE or BM .
The theory - something disrupts the normal integrity of these structures. Then the body's immune system
attacks the tissues in the breached area as if it were a foreign invader, creating mounds of dead material and immune complexes that appear as drusen. More research is required to
further define this process. The hope is that it may be possible to develop and use targeted medicines that control excessive immune responses to minimize drusen formation in
carefully selected cases.
Activated Enzymes show Promise as Primers of Pumps that clear Debris from the
Macula
Scientists at St. Thomas Hospital in London presented tantalizing evidence that a class of
human enzymes called matrix metalloproteases (MMP's) could increase flow across the BM. This improved pump function would prevent the build-up of waste products in the BM that are
believed to contribute to drusen.
One specific variant called MMP-9 was more effective that others in the family. MMP's are abundant in younger people but tend to diminish with
age. The researchers suggested that MMP-9 may one day be useful as a medicine to prevent or treat macular degeneration.
The Controversy Continues - are Stargardt and AMD Genes the same?
As more and more geneticists weigh into the fray, conflicting studies were presented, with Australian researchers reporting no association
between the same mutations seen in ABCR gene of Stargardt patients and those of AMD patients.
The ABCR gene is responsible for manufacturing the ABCR transporter protein
previously discovered in rod (black and white) photoreceptors, malfunction of which is implicated in juvenile macular degeneration or Stargardt disease.
However, other studies
in China and Canada continue to demonstrate an association. Several larger studies are now under way hoping to resolve the controversy and provide a more detailed map of areas of the
ABCR gene that may be the most appropriate targets for investigation.
Importantly, the Canadian researchers showed that the ABCR
transporter protein was also found in color
sensing cells or cones (the macula zone of your retina only has cones) as well as the black and white sensing rods found in the peripheral retina.
Your financial support can
assist the MDF Gene Library Project that helps genetic researchers around the Nation recruit suitable family members to share their disease history and provide tissue samples to
accelerate this vital research. (See below)
Regeneration Edges One Step Closer to Reality
For us the most promising work presented at ARVO revolved around the possibility of waking up nests of
sleeping neural stem cells and putting them to work in the macula zone of the retina. Working independently, small groups of US and Chinese scientists reported injecting these cells
into the space beneath rat retinas and stimulating them to grow into macular light sensing cells or photoreceptors. For our full report on this important development, click here.
What are the implications of this research for
patients with macular degeneration?
First, this work explodes the myth that macular degeneration is
irreversible. As the MDF has long held, it clearly is not. These landmark studies demonstrate that, in adult eyes, one can resurrect vision-related cells like photoreceptors and
induce production of critical visual-process-dependent chemicals such as rhodopsin.
Second it emphasizes the critical importance of more funding for omni-potent cell related
research as the best hope yet for a cure for this disease. The MDF is redoubling its efforts to fund additional studies to broaden our understanding of these remarkable cells and
develop the best ways to accelerate application of this new knowledge for humans.
You can help us to help you or someone you love by contributing to the MDF Cells for Sight
Initiative. Together we can help better fund the existing small group of researchers, enabling them to accelerate their work and add new talent and resources to the development of
human therapies based upon this exciting discovery. David Seftel, MD
Director of Research Development |
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