A new, $1.9 million National Eye Institute (NEI) grant will allow John A. Moran Eye Center scientists to answer a fundamental question about the eye’s response to age-related macular degeneration (AMD), a leading cause of blindness among Americans 55 and older.
Ophthalmologists have long thought of the abnormal eye blood vessel growth associated with AMD, known as choroidal neovascularization (CNV), as the villain in its story. These blood vessels may leak and rupture, and physicians usually treat their patients to curb their growth.
But what if a silent form of this growth—without any leak or ruptures—actually preserves vision?
Moran physician scientist Monika Fleckenstein, MD, is ready to find out.
“This theory goes back many decades as pathologists identified a new vascular layer established in the eyes of AMD patients,” explains Fleckenstein, primary investigator on the grant. “The idea is that the eye develops a layer of new blood vessels as a rescue mechanism to get nutrition to light-sensing photoreceptor cells, saving them from death.”
Clinical Study will Track AMD Progression
Thanks to modern technologies and an , the time is ripe for solving the mystery. The first-of-its-kind study will enroll 88 AMD patients and follow them over three years.
Moran scientist Steffen Schmitz-Valckenberg, MD, director of the , will use high-resolution retinal imaging to monitor disease progression. The study will additionally test photoreceptor function on top of the new vascular layers and surrounding areas.
“The hypothesis is that areas on top of this layer are protected, and their function will stay stable or show only relatively minor changes over the years,” says Schmitz-Valckenberg.
If the hypothesis is correct, it could lead to potential new treatment approaches for AMD.
The new study builds upon foundational work conducted by Fleckenstein and Schmitz-Valckenberg at the 㽶Ƶ of Bonn. A 2020 study conducted there using retinal imaging only determined silent CNV may protect retinal cells in the immediate area from progressive atrophy.