As the U.S. population
ages, the number of Americans with eye disease and vision problems will continue to spiral upward. A new report released by Prevent Blindness, “
The Future of Vision: Forecasting the Prevalence and Costs of Vision Problems
,” predicts more than $384 billion in 2032 and $717 billion in 2050 in nominal costs related to eye disease and vision problems.
Statistics from the report, commissioned from researchers at the University of Chicago, point to some alarming projections, including:
• Costs related to eye disease, including government, insurance and patient costs, are projected to increase 376 percent by 2050.
• Hispanics are projected to exhibit extremely high growth in diabetic retinopathy, glaucoma and cataract cases.
• As the baby-boomer generation ages into the Medicare program, costs will further shift from patients and private insurance to government. By 2050, government will pay more than 41 percent of costs, while patients will pay 44 percent, and private insurers, 16 percent.
• Women will continue to outnumber men in prevalence of all eye disease and vision loss categories except for diabetic retinopathy.
• Those aged 90 and older project to be by far the fastest growing population segment. This will have a significant effect on those living with eye disease, as many of these conditions are age-related.
The estimated average age of AMD patients is 80 years old, the oldest of any of the included eye diseases. Diabetic retinopathy patients have an average age of 66 years, the youngest of any of the included eye diseases.
“We cannot stand by and passively accept vision loss as an inevitable condition of growing old,” said Hugh R. Parry, president and CEO of Prevent Blindness. “The sheer numbers of those who are and will be personally and financially impacted by vision impairment and blindness is far too great to ignore. The time to plan and develop a national strategy for saving sight is now.”
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Study Uncovers The Brain’s Role in Glaucoma
published in Translational Vision Science & Technology
show the brain, not the eye, controls the cellular process that leads to glaucoma. The results may help develop treatments for glaucoma and contribute to the development of future therapies for preserving brain function in other age-related disorders like Alzheimer’s.
The researchers performed a data and symmetry analysis of 47 patients with moderate to severe glaucoma in both eyes. In glaucoma, the loss of vision in each eye appears to be haphazard. Conversely, neural damage within the brain caused by strokes or tumors produces visual field loss that is almost identical for each eye, supporting the idea that the entire degenerative process in glaucoma must occur at random in the individual eye—without brain involvement.
However, the team’s analysis revealed that as previously disabled optic nerve axons—that can lead to vision loss—recover, the remaining areas of permanent visual loss in one eye coincide with the areas that can still see in the other eye. The team found that the visual field of the two eyes fit together like a jigsaw puzzle, resulting in much better vision with both eyes open than could possibly arise by chance.
“As age and other insults to ocular health take their toll on each eye, discrete bundles of the small axons within the larger optic nerve are sacrificed so the rest of the axons can continue to carry sight information to the brain,” said author William Eric Sponsel, MD, of the University of Texas at San Antonio, Department of Biomedical Engineering. “This quite intentional sacrifice of some wires to save the rest, when there are decreasing resources to support them all (called apoptosis), is analogous to pruning some of the limbs on a stressed fruit tree so the other branches can continue to bear healthy fruit.”
Sensor in Eye Could Track Intraocular Pressure |
University of Washington engineers have designed a low-power sensor that could be placed permanently in a person’s eye to track changes in eye pressure. The sensor would be embedded with an artificial lens during cataract surgery and would detect pressure changes instantaneously, then transmit the data wirelessly using radio frequency waves.
“No one has ever put electronics inside the lens of the eye, so this is a little more radical,” said Karl Böhringer, PhD, a UW professor of electrical engineering and of bioengineering. “We have shown this is possible in principle. If you can fit this sensor device into an intraocular lens implant during cataract surgery, it won’t require any further surgery for patients.”
The research team wanted to find an easy way to measure eye pressure for management of glaucoma. “The implementation of the monitoring device has to be well-suited clinically and must be designed to be simple and reliable,” said Tueng Shen, MD, PhD, a collaborator and UW professor of ophthalmology. “We want every surgeon who does cataract surgeries to be able to use this.” The UW engineering team built a prototype that uses radio frequency for wireless power and data transfer. A thin, circular antenna spans the perimeter of the device—roughly tracing a person’s iris—and harnesses enough energy from the surrounding field to power a small pressure sensor chip. The chip communicates with a close-by receiver about any shifts in frequency, which signify a change in pressure. Actual pressure is then calculated and those changes are tracked and recorded in real-time.
The team is working on downscaling the prototype to be tested in an actual artificial lens. Designing a final product that’s affordable for patients is the ultimate goal, researchers said. “I think if the cost is reasonable and if the new device offers information that’s not measureable by current technology, patients and surgeons would be really eager to adopt it,” Dr. Shen said.
The researchers published their results in the
Journal of Micromechanics and Microengineering.
The researchers say the cellular process used for pruning small optic nerve axons in glaucoma is “remarkably similar to the apoptotic mechanism that operates in the brains of people afflicted with Alzheimer’s disease.”
“The extent and statistical strength of the jigsaw effect in conserving the binocular visual field among the clinical population turned out to be remarkably strong,” said Dr. Sponsel. “The entire phenomenon appears to be under the meticulous control of the brain.”
The TVST paper is the first evidence in humans that the brain plays a part in pruning optic nerve axon cells. In a previous study, a mouse model suggested the possibility that following injury to the optic nerve cells in the eye, the brain controlled a pruning of those cells at its end of the nerve. This ultimately caused the injured cells to die.
“Our basic science work has demonstrated that axons undergo functional deficits in transport at central brain sites well before any structural loss of axons,” said David J. Calkins, PhD, of the Vanderbilt Eye Institute and author of the previous study. “Indeed, we found no evidence of actual pruning of axon synapses until much, much later. Similarly, projection neurons in the brain persisted much longer, as well.
“This is consistent with the partial recovery of more diffuse overlapping visual field defects observed by Dr. Sponsel that helped unmask the more permanent interlocking jigsaw patterns once the eyes of his severely affected patients had been surgically stabilized,” said Dr. Calkins.
Dr. Sponsel has already seen how these findings have positively affected surgically stabilized patients who were previously worried about going blind. “When shown the complementarity of their isolated right and left eye visual fields, they become far less perplexed and more reassured,” he said. “It would be relatively straightforward to modify existing equipment to allow for the performance of simultaneous binocular visual fields in addition to standard right eye and left eye testing.”
The authors suggest their findings can assist in future research with cellular processes similar to the one used for pruning small optic nerve axons in glaucoma, such as occurs in the brains of individuals affected by Alzheimer’s.
From Stem Cells, Light-Sensitive Photoreceptors
Using a type of
human stem cell, Johns Hopkins researchers say they have created a three-dimensional complement of human retinal tissue in the laboratory, which notably includes functioning photoreceptor cells capable of responding to light.
“We have basically created a miniature human retina in a dish that not only has the architectural organization of the retina but also has the ability to sense light,” said study leader M. Valeria Canto-Soler, PhD, an assistant professor of ophthalmology at the Johns Hopkins University School of Medicine. She said the work,
reported online June 10 in Nature Communications
, “advances opportunities for vision-saving research and may ultimately lead to technologies that restore vision in people with retinal diseases.”
Dr. Canto-Soler cautions that photoreceptors are only part of the story in the complex eye-brain process of vision, and her lab hasn’t yet recreated all of the functions of the human eye and its links to the visual cortex of the brain. “Is our lab retina capable of producing a visual signal that the brain can interpret into an image? Probably not, but this is a good start,” she said.
The achievement emerged from experiments with human induced pluripotent stem cells and could eventually enable genetically engineered retinal cell transplants that halt or even reverse a patient’s march toward blindness, the researchers say. They turned iPS cells into retinal progenitor cells destined to form light-sensitive retinal tissue. Using a simple, straightforward technique they developed to foster the growth of the retinal progenitors, Dr. Canto-Soler and her team saw retinal cells and then tissue grow in their petri dishes. The growth corresponded in timing and duration to retinal development in a human fetus in the womb. Moreover, the photoreceptors were mature enough to develop outer segments, a structure essential for photoreceptors to function.
The lab-grown retinas recreate the three-dimensional architecture of the human retina. “We knew that a 3-D cellular structure was necessary if we wanted to reproduce functional characteristics of the retina,” said Dr. Canto-Soler, “but when we began this work, we didn’t think stem cells would be able to build up a retina almost on their own. In our system, somehow the cells knew what to do.”
When the retinal tissue was at a stage equivalent to 28 weeks of development in the womb, with fairly mature photoreceptors, the researchers tested these mini-retinas to see if the photoreceptors could in fact sense and transform light into visual signals.
They did so by placing an electrode into a single photoreceptor cell and then giving a pulse of light to the cell, which reacted in a biochemical pattern similar to the behavior of photoreceptors in people exposed to light.
Dr. Canto-Soler said the new system gives them the ability to generate hundreds of mini-retinas at a time directly from a person affected by a particular retinal disease such as retinitis pigmentosa. This provides a unique biological system to study the cause of retinal diseases directly in human tissue, instead of relying on animal models.
The system opens an array of possibilities for personalized medicine such as testing drugs to treat these diseases in a patient-specific way. In the long term, the potential is also there to replace diseased or dead retinal tissue with lab-grown material to restore vision.