The BBSRC reported on January 4, 2010, that scientists at University College London (UCL) have discovered that the relationship between two blood proteins has a central role in preventing the onset of Age-related macular degeneration (AMD). In a paper to be published in the American Journal of Biological Chemistry, January 8, 2010, the UK research team will present their new findings on how the interaction of blood proteins work to promote or hinder the development of AMD.
Chronic Degenerative Condition
AMD is the single most common cause of eye disease in the world's elderly population, accounting for some 15 million cases in the US alone, and many millions more throughout the world. The disease attacks the macula, the centre of the eye where the sharpest vision takes place, and leaves the victim with blurred or pitted vision - dark holes in sight.
This is caused by the breakdown of retinal cells that can lead to 'dry' AMD, or the more serious 'wet' form. The latter affects only about 10% of all AMD sufferers, but is the most common cause of the majority of cases of blindness.
In the wet from of AMD the membrane underneath the retina thickens, then dislodges. This results in a disruption of the oxygen supply to the macula, which in turn leads the body to compensate by growing new, abnormal blood vessels. These begin to grow, pushing up from beneath the membrane through the cracks behind the retina, heading towards the macula. The retina will often appear raised. Damage to the macula results in central vision loss, which can happen very quickly. Once lost it is irreparable.
New Insight Helps Fight Disease
The UCL research team have studied the way in which a common blood protein, present in the degenerative process, pulls in another related blood protein. It is this other blood protein that provides the key to serious eye damage. In the presence of inflammation, its production increases at a vast rate, causing macular deterioration.
"By starting to understand these interactions in greater detail, we can begin to devise methods that will ultimately prevent the development of blindness in the elderly," says Zuby Okemefuna, the lead author of the paper.
"It is believed that both forms start on a common molecular route and then deviate into wet or dry AMD," explained research leader Steve Perkins. An early indicator of the condition, he goes on to explain, are the yellowish deposits (drusen) usually discovered by an ophthalmologist.. By studying this material the team were able to isolate two blood proteins involved in its formation - blood protein factor H, and a second known as C-reactive protein.
During the normal aging process the eye will naturally lose cells, and this is offset by the blood supply bringing C-reactive protein at a low level of activity to assist in the routine clearing away of dead cells through mild inflammation.
"In conditions of high inflammation," explains Okemefuna, "the levels of C-reactive protein will increase dramatically." This sets up a vicious circle in which uncontrolled C-reactive protein causes damage to the retina, followed by more inflammation, then more retinal damage, and so on. "It is the debris resulting from this process," says Okemefuna, "that is known as drusen."
The team also discovered that a genetically different form of Factor H does not bind to the C-reactive protein as well as the conventional one, which suggests that those individuals carrying this different type are more susceptible to inflammation and the build up of drusen.
In most cases Factor H acts as a braking mechanism, inhibiting high C-reactive protein levels, and protecting the eye from damage to the retina. C-reactive protein also prevents Factor H from banding together in clumps and hastening the formation of drusen.
In the typical group of individuals suffering from AMD, those without the genetically modified blood protein, Factor H presents as being helpful in restraining C-reactive protein from getting out of control, and being responsive to C-reactive protein as an inhibitor of drusen build up.
Hope for the Future
"It is interesting how the interaction of these two blood proteins protects the eye during crisis," Perkins said. "We now are better positioned to begin to work out preventative strategies for these diseases."
While there is no cure for AMD, this new insight into the natural defense mechanisms of the eye, will help to design therapies that are aimed at more effective treatment of symptoms, and delay the progression of disease.
Source:
"New research findings may help stop age related macular degeneration at the molecular level" -BBSRC press release, January 04, 2010.
Alister Gillies - Alister's background is in project development. He is trained in counselling and personal development, although his academic background is ...
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