For those of us lucky enough to have sight in an image-driven world, vision is the sense that best anchors us. But it’s a fragile tether. Our eyes can sprout leaky new blood vessels that hemorrhage. The gel at the back of the eye can liquefy, causing the retina to collapse upon itself and detach from the eye wall, taking our sight with it. Time, trauma, or disease can damage the cones and rods that make vision possible. Even lasers can leave scar tissue that compromises vision.
Brion McKee had been treated for years for severe damage caused by diabetes. When he consulted Dr. Rajendra Apte, who holds a distinguished professorship in ophthalmology and visual science at the Washington University School of Medicine, McKee was blind in one eye and losing sight in the other.
“This might not get better,” Apte warned him, “but if you’re willing to go through more interventions, we can try surgery.” The difference was one of delicacy: Using the latest instrumentation, Apte could remove scar tissue, drain away blood, and reattach the retina, all through openings so small, they needn’t even be sutured.
McKee regained his vision.
Vision is the sense that best anchors us. But it’s a fragile tether.
Such surgeries—which can also repair the damage done by traumatic brain injury—are deeply gratifying. But they’re just one item on a long list of breakthroughs.
The discovery Apte’s most excited about holds the potential to prevent cell death. We know that a molecule called NAD revs a cell’s power supply, restoring the metabolism and energy that begin to flag as we age. Now Apte and his colleagues have found that a precursor molecule, NMN, boosts the level of NAD. “It’s been shown to work in mice,” he says, “and human trials began this past spring.” A drug that increases NAD could make a dramatic difference. First, it could ward off the blindness caused by many eye diseases, including some for which there’s currently no treatment. Second, it could be useful in countless other chronic and progressive diseases, because aging drains the energy from cells all over the body. “Every cell needs NAD to function,” Apte says. Find a way to boost its production, and you improve the function of the body’s cells.
Another breakthrough promises to inhibit a molecule called FGF, which causes new blood vessels to grow after an injury. In the eye, diabetes or macular degeneration triggers this sudden bloom of blood vessels—but they’re abnormal and not helpful. They leak, further obscuring vision. Stopping their formation would make a huge difference and could complement current therapies, increasing their effectiveness.
A third discovery would help with glaucoma, the second leading cause of blindness in the world. Apte and other Wash. U. researchers have identified a biomarker that indicates how severely the cells are damaged. “Hopefully, we will now be able to predict the progression of the disease,” he says. The biomarker can warn doctors when a patient is in danger of losing sight, and it can help them formulate treatment and see precisely how effective it is.
Meanwhile, existing procedures continue to improve.
Joseph Lombardo, who supervises the computed tomography division of the radiology department at Barnes-Jewish Hospital, was 52 and fit, working out regularly. He woke up on February 11, 2016, and dressed for a 7 a.m. meeting. He noticed a little cloudiness in his left eye and concluded that his contact lens must be dirty.
Several times that day, he tried to clean the lens, but the cloudiness just got worse. “If you’re a guy and it doesn’t hurt, then it’s gonna get better,” he remarks, explaining why he waited until Sunday—when he woke up and couldn’t see—to text colleagues in radiology for advice. Both physicians texted back instantly: Go to the ER.
The retina had almost fully detached. “You have a vitreous gel at the back of the eye that, as you get older, becomes more liquid,” Apte explains. Usually that’s in the sixth or seventh decade; Lombardo’s was early. “Sometimes as the gel liquefies and separates from the eye wall, it can cause a tear in the retina, allowing the fluid to seep underneath and causing the retina to come off.”
Lombardo needed surgery—as soon as possible. The longer his retina was separated from its sources of nutrition, the more damage could occur. Apte had two alternatives: to tack the retina back into place using just a laser or to also inject a gas bubble into the eye that would hold the retina in place until it healed. “Mine was so bad, he had to do both,” Lombardo says, “but I got my vision back.”
Another patient, Sister Pauline (baptized Dorothy Frances) Komrska, was in her eighties, working as a library assistant, when she saw a shadow in her right eye. “I was going to read all these books the rest of my life!” she says. “God had other plans.
“I knew it was wet macular,” she says. “I’m 91 years old. I know a lot about life.” She consulted Apte and agreed to participate in one of his studies. “They sucked me up—I felt like an octopus got hold of me,” she says. “One hour!”
Meanwhile, Apte began giving her injections to fend off the degeneration. “It’s like a little drip of water inside your eye,” she says, “and if you get enough, you need a shot to dry it up, or you’ll go blind.” She waits a beat. “I’m 91, and I haven’t yet.”
Now there’s a new drug, and because it’s longer lasting, she can wait up to three times as long between the dread injections. (She adores Apte, says he’s gentle and “sympathetic but not gushy, straight to the point,” but she still can’t believe she lets him stick a needle in her eyeball. She bakes chocolate chip cookies for the techs who deaden the pain, and she brings Apte his favorite dark chocolate. “It’s not a bribe,” she told him when he protested. “The years you have studied, the work you have put into what you are doing to keep me from going blind…”
It’s a gift she doesn’t take lightly.
