Shedding Light on AMD: Investigating Fat Metabolism in Eye Cells
Age-related macular degeneration (AMD) is an eye disease that causes irreversible damage to the macula, a region of the retina that controls central vision, and can lead to blurred vision, blind spots, and difficulty with activities like reading, driving, and recognizing faces. In 2025, an estimated 20 million Americans will be living with AMD. Jason Miller, M.D., Ph.D., the James Grosfeld Endowed Professor and Assistant Professor of Ophthalmology and Visual Sciences, devotes his clinical and research focus to AMD. Dr. Miller’s work explores the underlying molecular mechanisms contributing to AMD progression, with the goal of developing innovative strategies to diagnose and treat the disease. By combining his expertise in both clinical ophthalmology and scientific research, he aims to improve outcomes for patients affected by AMD, advance the understanding of retinal diseases, and contribute to the development of more effective treatments. This year, Dr. Miller received a grant from the Foundation Fighting Blindness to study how the eye cells that die in macular degeneration, called the retinal pigment epithelium (RPE), use fat for energy, and how this process might affect AMD. In AMD, fat builds up just outside the RPE cells and triggers RPE cell death. “We are looking at how the RPE deals with extra fat,” he says. “There is a process in RPE, called beta-oxidation, that turns fat into energy. Our goal is to help the RPE burn up the fat for energy, instead of letting the fat build up and form the harmful fat deposits that characterize AMD and trigger RPE degeneration.” Dr. Miller emphasizes the need to learn why RPE cells are slow to break down fats. “If we can discover the underlying reasons, we might be able to help these cells process fats more efficiently,” he says. “We suspect these cells may prefer to use energy sources other than fat, and we want to determine why. We also aim to learn whether impaired fat breakdown directly leads to the harmful fat deposits seen in AMD. Currently, the treatments for dry AMD are minimally effective, so we’re seeking new approaches to treating the disease. Targeting fat in the RPE represents one such alternative approach.”
Unlocking the Eye’s Defense: Investigates How Cells Combat Fat Buildup in AMD
Jason Miller, M.D., Ph.D., the James Grosfeld Endowed Professor and Assistant Professor of Ophthalmology and Visual Sciences, has received a grant from Research to Prevent Blindness to study how two important parts of eye cells work together to break down fat. “Too much fat in the eye is linked to diseases like age-related macular degeneration (AMD), a major cause of vision loss,” says Dr. Miller. Normally, the mitochondria in cells act like tiny power plants, turning fats into energy that the cell can use. Another small part of the cell called the peroxisome also helps process fats, but usually only certain kinds. In AMD, mitochondria do not work well. Dr. Miller and his team want to see if peroxisomes can step in and help burn fats normally destined for the mitochondria in situations like AMD where mitochondria are damaged. First, they’re starting with lab-grown cells, and later they’ll move on to tests in animals. “By finding ways to boost the power of peroxisomes, we hope to help the eye process fat better and possibly slow down or stop diseases like AMD,” he says. “If successful, this research could lead to entirely new treatments for preventing vision loss in AMD, something that drug companies haven’t really explored yet.”