A new study in mice hints at the promise of an eventual alternative treatment option for the 'wet' version of age-related macular degeneration . Researchers determined in mice that an enzyme related to cell growth and division is a culprit in the blood vessel invasion in the back of the eye that causes blurred central vision in wet AMD. Targeting the enzyme, called telomerase, with an experimental drug suppressed abnormal vascular growth in the animals' retina.
The only current treatment for wet AMD is injection into the eye of a medication that blocks the activity of a growth factor protein, called VEGF, which is also known to prompt formation of abnormal blood vessel growth in this condition. Wet AMD, also known as neovascular AMD, is caused by the growth of new blood vessels that invade the retina, a space normally free of vascular activity.
A series of experiments first confirmed telomerase has a role in abnormal blood vessel formation in a mouse model of wet AMD. Researchers found that, compared to control mice, expression and activity of one of two genes carrying instructions for making telomerase were higher in the eyes of mice in which rapid growth of new blood vessels was induced with a laser.
Telomerase's job is to rebuild telomeres, which function as protective caps at the end of chromosomes. Telomeres are known to shorten in many types of cells as a consequence of aging, but Kerur said the study suggested localized blocking of telomerase in the eye had no bearing on the enzyme's telomere-building function.
This work was supported by National Institutes of Health grants, the Ohio Lions Eye Research Foundation and a Research to Prevent Blindness grant.
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