A new study in mice hints at the promise of an eventual alternative treatment option for the “wet” version of age-related macular degeneration (AMD).
Researchers at The Ohio State University and colleagues 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.
Previous cancer research has linked high activity of telomerase to rapid production and migration of cells lining blood vessels that enables tumor growth, and has also shown the enzyme can stimulate production of VEGF. Based on those findings, the researchers sought in this study to see if telomerase could have a similar damaging effect in the eye.
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.
The team then tested the effects of an experimental compound that inhibits telomerase activity. They confirmed that the drug lowered telomerase activity in healthy mice, and found that injecting it into the eyes of mice with symptoms mimicking wet AMD significantly reduced the abnormal blood vessel invasion.