Physicians find clues to vision deterioration.
The disease damages an area, called the macula lutea, at the center of the retina. The retina comprises the tissue at the back of the eye that converts optical images to electrical impulses, which then travel to the brain via the optic nerve.
A new theory suggests that some age-related macular degeneration results from overeager repair of mild injuries to retinal cells. Moreover, high fat concentrations in the bloodstream may exacerbate this immune overreaction. Another line of research suggests that the disease may result from constricted blood flow and gradual starving of retinal cells.
Scientists know that age-related macular degeneration can attack the retina in two ways. The so-called dry form results when plaquelike deposits appear under the retina's outer layer. The plaque damages vital light-sensing cells, and as these die off, vision--especially in the center of a person's field--fades.
The so-called wet form of the disease is less common but more likely to cause blindness. It arises when extra blood vessels form in an outer layer of the eye called the choroid. These vessels invade the retina and leak fluid into it. The assault kills light-sensing cells and forms scar tissue.
Scientists at the University of Miami School of Medicine have new evidence that cellular repair runs amok in the dry form of the disease. After mild damage, such as that caused by a bright light, retinal cells in a test tube didn't appear to heal properly. They shed some of their cellular material into blebs, or small sacs of fluid, between the outer layers of the retina, reports ophthalmologist Scott W. Cousins. He and his colleagues spotted the new blebs after the team engineered retinal cells to glow fluorescently in a laboratory dish.
The blebs appear to trigger an immune overreaction. In a separate experiment, scavenging cells called macrophages from about one-third of study participants with the dry form of age-related macular degeneration showed an overresponse when they came into contact with blebs, spurring an inflammatory reaction, Cousins says.
In some patients, macrophages may rush to the scene of a mild injury and release toxins "that make the damage worse," Cousins suspects.
In studies on mice, Cousins' team also found that high-fat diets made old mice prone to bleb formation, whereas feeding them vitamin E helped prevent it. Destructive chemical groups called free radicals that are fueled by fats may induce blebbing, Cousins says. "Essentially, we're suggesting that these kinds of toxins can be looked at as potential trigger mechanisms for the deposit formation of macular degeneration," Cousins concludes. He presented the findings this week at a meeting in Universal City, Calif., sponsored by Research to Prevent Blindness.
Also at the meeting, researchers from the University of Pennsylvania in Philadelphia reported that some patients with the dry form of the disease have lower-than-normal blood flow to the retina. Poor circulation fails to deliver nutrients and does a poor job of clearing away existing cellular waste products from the area between the retina and choroid, says ophthalmologist Juan E. Grunwald.
By shining laser light into the eyes of healthy people, Grunwald's team noted that the older participants had only about two-thirds the blood flow from the choroid as the younger volunteers did. Examination of patients with dry age-related macular degeneration showed an even greater decrease in blood flow with age.
Patients with the dry form of the disease are more likely to develop the wet form than healthy people are, and this difference may be due to the poor circulation, Grunwald says. His team is now investigating that possibility.
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|Title Annotation:||research on age-related macular degeneration|
|Article Type:||Brief Article|
|Date:||Oct 2, 1999|
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