Eye diseases identified by how we watch TV

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

One of the leading causes of blindness worldwide could be detected by how our eyes respond to watching TV according to a new study from researchers at City University London.

The researchers, who were funded by the UK charity Fight for Sight, found that they could identify diseases such as glaucoma by looking at maps of people’s eye movements while they watched a film.

With an estimated half a million people in the UK living with undiagnosed glaucoma, the research could help speed up diagnosis, enabling clinicians to identify the disease earlier and allowing treatment to begin before the onset of permanent damage.

Affecting around 65 million people worldwide, glaucoma describes a group of eye conditions that result in progressive damage to the optic nerve which connects the retina to the brain, causing people to gradually lose vision.

What makes glaucoma dangerous, however, is that this sort of vision loss can be subtle at first. People often do not know they have loss of peripheral vision. Unfortunately, as glaucoma worsens, these compensatory perceptive mechanisms unravel leading to noticeable sight loss, visual impairment and in some cases blindness. The condition is irreversible.

The team, which was led by Professor David Crabb along with Dr Nicholas Smith and Dr Haogang Zhu, compared a group of 32 elderly people with healthy vision to 44 patients with a clinical diagnosis of glaucoma. Both groups underwent standard vision examinations and disease severity was also measured for the group with clinical diagnoses.

Participants were then shown three unmodified TV and film clips on a computer while an eye-tracking device recorded all eye movement, and particularly the direction in which people were looking. These data were then used to produce detailed maps which enabled the diagnosis of glaucoma. The paper is published in the journal Frontiers in Aging Neuroscience.

David Crabb, Professor of Statistics and Vision Research, said: “These are early results but we’ve found we can identify patients with glaucoma by monitoring how people watch TV. This could make a huge difference in detecting or monitoring a disease which currently results in one in ten of all blindness registrations in the UK and about a million NHS appointments a year for those with the disease. Once the damage is done it cannot be reversed, so early diagnosis is vital for identifying a disease which will continue to get more prevalent as our population ages.”

Dr Dolores M Conroy, Director of Research at Fight for Sight said: “One of Fight for Sight’s six long-term goals is to enable conditions such as glaucoma to be detected earlier. Early diagnosis and treatment can stop people losing their sight, so we’re very pleased that this proof-of-principle eye movement study opens the door to developing a new clinical test for glaucoma. Furthermore it address one of the priorities for glaucoma research identified by the Sight Loss and Vision Priority Setting Partnership-a consultation with patients, relatives, carers and eye health professionals.”

Major cause of blindness linked to calcium deposits in the eye

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

Microscopic spheres of calcium phosphate have been linked to the development of age-related macular degeneration (AMD), a major cause of blindness, by UCL-led research.

AMD affects 1 in 5 people over 75, causing their vision to slowly deteriorate, but the cause of the most common form of the disease remains a mystery.* The ability to spot the disease early and reliably halt its progression would improve the lives of millions, but this is simply not possible with current knowledge and techniques.

The latest research, published in Proceedings of the National Academy of Sciences, has implicated tiny spheres of mineralised calcium phosphate, ‘hydroxylapatite’, in AMD progression. This not only offers a possible explanation for how AMD develops, but also opens up new ways to diagnose and treat the disease.

AMD is characterised by a build-up of mainly protein and fat containing deposits called ‘drusen’ in the retina, which can prevent essential nutrients from reaching the eye’s light-sensitive cells, ‘photoreceptors’. Photoreceptors are regularly recycled by cellular processes, creating waste products, but drusen can trap this ‘junk’ inside the retina, worsening the build-up. Until now, nobody understood how drusen formed and grew to clinically relevant size.

The new study shows that tiny calcium-based hydroxyapatite, commonly found in bones and teeth, could explain the origin of drusen. The researchers believe that these spheres attract proteins and fats to their surface, which build up over years to form drusen. Through post-mortem examination of 30 eyes from donors between 43 and 96 years old, the researchers used fluorescent dyes to identify the tiny spheres, just a few microns — thousandths of a millimetre — across.

“We found these miniscule hollow spheres inside all of the eyes and all the deposits that we examined, from donors with and without AMD,” explains Dr Imre Lengyel, Senior Research Fellow at the UCL Institute of Ophthalmology and Honorary Research Fellow at Moorfields Eye Hospital, who led the study. “Eyes with more of these spheres contained more drusen. The spheres appear long before drusen become visible on clinical examination.

“The fluorescent labelling technique that we used can identify the early signs of drusen build-up long before they become visible with current methods. The dyes that we used should be compatible with existing diagnostic machines. If we could develop a safe way of getting these dyes into the eye, we could advance AMD diagnoses by a decade or more and could follow early progression more precisely.”

Some of the mineral spheres identified in the eye samples were coated with amyloid beta, which is linked to Alzheimer’s disease. If a technique were developed to identify these spheres for AMD diagnosis, it may also aid early diagnosis of Alzheimer’s. Whether these spheres are a cause or symptom of AMD is still unclear, but their diagnostic value is significant either way. As drusen are hallmarks of AMD, then strategies to prevent build-up could potentially stop AMD from developing altogether.

“The calcium-based spheres are made up of the same compound that gives teeth and bone their strength, so removal may not be an option,” says Dr Lengyel. “However, if we could get to the spheres before the fat and protein build-up, we could prevent further growth. This can already be done in the lab, but much more work is needed before this could be translated into patients.”

“Our discovery opens up an exciting new avenue of scientific research into potential new diagnostics and treatments, but this is only the beginning of a long road.” says Dr Richard Thompson, the main international collaborator from the University of Maryland School of Medicine, USA.

The work was supported by the Bill Brown Charitable Trust, Moorfields Eye Hospital, Mercer Fund from Fight for Sight, and the Bright Focus Foundation. The UCL-led international collaboration involved researchers from the University of Maryland School of Medicine, Imperial College London, the University of Tübingen, George Mason University, Fairfax, and the University of Chicago.

*A minority (10%) of cases are ‘wet’ AMD, which is caused by leaking blood vessels and can sometimes be treated with eye injections. The majority (90%) of cases are ‘dry’ AMD, whose cause remains a mystery and for which there are no reliable treatments.

Gene tied to profound vision loss discovered by scientists

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

An exhaustive hereditary analysis of a large Louisiana family with vision issues has uncovered a new gene tied to an incurable eye disorder called retinitis pigmentosa, according to an examination led by scientists at The University of Texas Health Science Center at Houston (UTHealth). It is a family of eye diseases that affects more than 200,000 in the United States and millions worldwide.

The retina converts images into electrical signals that can be processed by the brain. It acts much like the film in a camera. Retinitis pigmentosa damages this film (the retina) and its early symptoms include decreased night vision and peripheral vision. Once it starts, the loss of vision is relentlessly progressive, often ending in blindness.

In the journal Investigative Ophthalmology & Visual Science, UTHealth’s Stephen P. Daiger, Ph.D., and his colleagues report their discovery of a new gene tied to retinitis pigmentosa, which brings the total of genes associated with this sight-threatening disease to more than 60. The gene is called hexokinase 1 (HK1).

This information is important because it helps affected families cope with the disorder, helps explain the biologic basis of these diseases and suggests targets for drug treatments and gene therapy, said Daiger, the report’s senior author and holder of the Thomas Stull Matney Ph.D. Endowed Professorship in Environmental and Genetic Sciences at UTHealth School of Public Health.

“The challenge now is to block the activity of these mutations and clinical trials are underway to do just that,” he said.

“Dr. Daiger is trying to make a breakthrough in potentially blinding diseases with no known treatments,” said Richard S. Ruiz, M.D., professor of ophthalmology and holder of the John S. Dunn Distinguished University Chair in Ophthalmology at UTHealth. “Right now, we address the symptoms of the disease and help patients make the most of their existing vision.”

For approximately three decades, Daiger, a member of the Human Genetics Center at the UTHealth School of Public Health, has been following the progress of hundreds of families across the country with retinitis pigmentosa. “We’ve found the cause of disease in 80 percent of the families we have studied,” Daiger said. “Our goal is to find the cause in the remaining 20 percent.”

Equipped with the genetic profiles of family members, Daiger’s team has identified differences in the genetic makeup of those with the disease. The researchers also use family histories and DNA tests to glean information about the condition’s hereditary nature.

There are different types of retinitis pigmentosa and Daiger’s laboratory is focused on the autosomal dominant type. This means that only one parent needs the mutation in order to pass the disease to a child. This type accounts for about a third of all cases and many of its disease-causing genes have been discovered, several by Daiger’s research group.

“The story of the HK1 mutation is itself interesting. What we found is a mutation present in families from Louisiana, Canada and Sicily. Our evidence suggests the mutation arose in a common ancestor who lived centuries ago,” Daiger said. “The mutation spread in Europe and North America, and may be common among Acadians in Louisiana. This is called a founder mutation.”

Scientists study effects of sunlight to reduce number of nearsighted kids

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

Despite what many parents may think, kids who spend a lot of time reading or squinting at tiny electronic screens aren’t more likely to become nearsighted than kids who don’t. However, that risk is only reduced if the child spends plenty of quality time outside.

The “outdoor effect” on nearsightedness, or myopia, is a longstanding observation backed by both scientific and anecdotal evidence. It’s so compelling that some nations in Asia, which have among the highest myopia rates in the world, have increased the amount of daily outdoor time for children in the hopes of reducing the need for glasses.

But so far, no one has defined exactly what it is about being outside that seems to offer a protective effect against the condition, which causes distant objects to appear blurry.

“Data suggest that a child who is genetically predisposed to myopia are three times less likely to need glasses if they spend more than 14 hours a week outdoors,” says optometrist Donald Mutti, OD, PhD, of The Ohio State University College of Optometry. “But we don’t really know what makes outdoor time so special. If we knew, we could change how we approach myopia.”

Supported by a pilot grant from Ohio State’s Center for Clinical and Translational Science (CCTS), Mutti is now focusing his research on the variables he feels have the most potential: invisible ultraviolet B rays (UVB) and vitamin D, and visible bright light and dopamine.

“Between the ages of five and nine, a child’s eye is still growing. Sometimes this growth causes the distance between the lens and retina to lengthen, leading to nearsightedness,” explained Mutti. “We think these different types of outdoor light may help preserve the proper shape and length of the eye during that growth period.”

UVB and Vitamin D

UVB light is invisible to the human eye, but triggers several cellular functions in the body, including the production of vitamin D. Vitamin D is thought to support the function of the smooth muscle tissue found around the lens in the eye. This muscle not only helps focus light on the retina, but may also maintain the proper eye shape and length between the lens and the retina, something that can become distorted during the rapid growth of a child’s eye.

Some studies, including one by Mutti, show that people with myopia have lower blood levels of vitamin D — indicating that they have spent less time outdoors, with possible negative effects on the eye.

However, the data are difficult to interpret because vitamin D levels are hard to measure and change dramatically from season to season. While people usually get most of their UVB exposure during the summer, vitamin D levels don’t spike until the fall — something that could make study results less accurate if not taken into consideration.

In order to develop a protocol for measuring vitamin D levels, Mutti is conducting a study in which participants are wearing monitors that detect exposure to UV and visible light. Levels of vitamin D are also being measured via blood and saliva samples.

“We don’t know if vitamin D is simply a proxy for measuring outdoor time, or if it is actually exerting a biological effect on how the eye works and develops,” said Mutti. “The current study will validate the way we measure vitamin D, so that we can more accurately figure out what role it really plays in large-scale studies.”

Visible bright light and dopamine

There’s another part of sunlight that could help prevent myopia: exposure to visible bright light. Even on a cloudy day, visible light outdoors is at least 10 times brighter than the light indoors.

When exposed to outdoor light, specialized cells in the retina help control how big or little the pupil dilates to let more or less light in. The cells connect to others that release dopamine — an important neurotransmitter in the eye and brain. Previous research suggests that dopamine also slows down the growth of the eye, but there isn’t technology currently available that can measure dopamine release in the eye directly.

However, thanks to another CCTS-funded researcher, Andrew Hartwick, OD, PhD, there is a way to measure the activity of these specialized cells by looking at how the pupil reacts to light. Mutti thinks he can use Hartwick’s procedure — developed as an early detection test for glaucoma — as a stand in for measuring dopamine release.

“Dr. Hartwick developed a protocol that measures how much these specialized retinal cells contribute to pupil responses to blue and red light,” said Mutti. “Our initial research suggests that the pupil responds more if these cells have been exposed to a lot of sunlight in the previous few days. That could serve as a proxy for how much dopamine the eye has been producing.”

Looking ahead

Last week, Mutti and his research team presented their results at the American Academy of Optometry annual meeting, including some of their early findings from studies looking at what happens to the pupil after visible light exposure.

These data and other ongoing studies will help Mutti develop rock-solid methodologies that he hopes can ultimately be used in large scale clinical trials — and help get the answers that so many scientists and parents would like to know.

“I think the research we are doing now will help us finally solve the mystery of the outdoor effect, and maybe help some people avoid a lifetime of wearing glasses,” said Mutti. “In the meantime, I tell parents don’t worry about reading, get their kids outside, but don’t forget sunglasses and sunscreen.”

Laser treatment reverses effects of early age-related macular degeneration

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

A new technique reported in the February 2015 issue of The FASEB Journal suggests that during early stages, it might be possible to reverse age-related macular degeneration, a leading cause of blindness that is currently irreversible. The treatment involving a nanosecond laser may also have further implications for other eye diseases such as diabetic macular oedema, diabetic retinopathy and retinopathy of prematurity.

“It is hoped that this study will provide a basis for the clinical use of the low energy nanosecond laser in those with early stage age-related macular degeneration and that such a treatment will limit the progression of the disease to the advanced, sight-threatening forms,” said Erica L. Fletcher, O.D., Ph.D., FAAO, a researcher involved in the work from the Department of Anatomy and Neuroscience at the University of Melbourne in Victoria, Australia.

To make their discovery, Fletcher and colleagues treated a group of individuals with intermediate AMD in one eye with a single session of nanosecond laser treatment. These individuals underwent eye examinations every six months, out to two years post-treatment and the results were compared to an untreated group with early AMD. Anatomical examination of human and mouse eyes was used to determine the effect of the laser on the sensitive light-detecting retina. In order to determine how this laser may help in limiting AMD, a mouse with a genetic mutation that predisposes it to developing one of the hallmark signs of AMD, was treated with the nanosecond laser and structural and gene analysis was performed. Results showed that treating those with early AMD with this new low energy nanosecond laser may limit disease progression. Importantly, unlike other lasers currently used to treat eye disease, the nanosecond laser does not result in damage to the sensitive retina. This study also showed evidence that nanosecond laser treatment in one eye can also produce positive effects in the other untreated eye. This raises the possibility that monocular treatment may be sufficient to treat disease in both eyes.

“This truly remarkable research is worth watching,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal, “because it may help usher in an era in which age-related macular degeneration is either eliminated or no longer considered a serious disease.”

Human eye can see ‘invisible’ infrared light

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

Any science textbook will tell you we can’t see infrared light. Like X-rays and radio waves, infrared light waves are outside the visual spectrum.

But an international team of researchers co-led by scientists at Washington University School of Medicine in St. Louis has found that under certain conditions, the retina can sense infrared light after all.

Using cells from the retinas of mice and people, and powerful lasers that emit pulses of infrared light, the researchers found that when laser light pulses rapidly, light-sensing cells in the retina sometimes get a double hit of infrared energy. When that happens, the eye is able to detect light that falls outside the visible spectrum.

“We’re using what we learned in these experiments to try to develop a new tool that would allow physicians to not only examine the eye but also to stimulate specific parts of the retina to determine whether it’s functioning properly,” said senior investigator Vladimir J. Kefalov, PhD, associate professor of ophthalmology and visual sciences at Washington University. “We hope that ultimately this discovery will have some very practical applications.”

The findings are published Dec. 1 in the Proceedings of the National Academy of Sciences (PNAS) Online Early Edition. Collaborators include scientists in Cleveland, Poland, Switzerland and Norway,

The research was initiated after scientists on the research team reported seeing occasional flashes of green light while working with an infrared laser. Unlike the laser pointers used in lecture halls or as toys, the powerful infrared laser the scientists worked with emits light waves thought to be invisible to the human eye.

“They were able to see the laser light, which was outside of the normal visible range, and we really wanted to figure out how they were able to sense light that was supposed to be invisible,” said Frans Vinberg, PhD, one of the study’s lead authors and a postdoctoral research associate in the Department of Ophthalmology and Visual Sciences at Washington University.

Vinberg, Kefalov and their colleagues examined the scientific literature and revisited reports of people seeing infrared light. They repeated previous experiments in which infrared light had been seen, and they analyzed such light from several lasers to see what they could learn about how and why it sometimes is visible.

“We experimented with laser pulses of different durations that delivered the same total number of photons, and we found that the shorter the pulse, the more likely it was a person could see it,” Vinberg explained. “Although the length of time between pulses was so short that it couldn’t be noticed by the naked eye, the existence of those pulses was very important in allowing people to see this invisible light.”

Normally, a particle of light, called a photon, is absorbed by the retina, which then creates a molecule called a photopigment, which begins the process of converting light into vision. In standard vision, each of a large number of photopigments absorbs a single photon.

But packing a lot of photons in a short pulse of the rapidly pulsing laser light makes it possible for two photons to be absorbed at one time by a single photopigment, and the combined energy of the two light particles is enough to activate the pigment and allow the eye to see what normally is invisible.

“The visible spectrum includes waves of light that are 400-720 nanometers long,” explained Kefalov, an associate professor of ophthalmology and visual sciences. “But if a pigment molecule in the retina is hit in rapid succession by a pair of photons that are 1,000 nanometers long, those light particles will deliver the same amount of energy as a single hit from a 500-nanometer photon, which is well within the visible spectrum. That’s how we are able to see it.”

Although the researchers are the first to report that the eye can sense light through this mechanism, the idea of using less powerful laser light to make things visible isn’t new. The two-photon microscope, for example, uses lasers to detect fluorescent molecules deep in tissues. And the researchers said they already are working on ways to use the two-photon approach in a new type of ophthalmoscope, which is a tool that allows physicians to examine the inside of the eye.

The idea is that by shining a pulsing, infrared laser into the eye, doctors might be able to stimulate parts of the retina to learn more about its structure and function in healthy eyes and in people with retinal diseases such as macular degeneration.

The research was made possible, in part, by the Kefalov team’s development of a tool that allowed the scientists to obtain light responses from retinal cells and photopigment molecules. That device already is commercially available and being used at several vision research centers around the world.

Funded by the National Eye Institute (NEI) and the National Institute on Aging (NIA) of the National Institutes of Health (NIH), Research to Prevent Blindness, the Norwegian Research Council, the TEAM project financed by the European Union and the Foundation for Polish Science.

Key discovery to preventing blindness, stroke devastation

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

Research led by Nicolas Bazan, MD, PhD, Boyd Professor, Ernest C. and Yvette C. Villere Chair of Retinal Degeneration Research, and Director of the Neuroscience Center of Excellence at LSU Health New Orleans, has discovered gene interactions that determine whether cells live or die in such conditions as age-related macular degeneration and ischemic stroke. These common molecular mechanisms in vision and brain integrity can prevent blindness and also promote recovery from a stroke. The paper is published online in Cell Death & Differentiation, a Nature journal.

“Studying the eye and the brain might hold the key to creating therapeutic solutions for blindness, stroke and other seemingly unrelated conditions associated with the central nervous system,” notes Dr. Bazan. “The eye is a window to the brain.”

Dr. Bazan and his research team discovered Neuroprotectin D1 (NPD1), which is made from the essential fatty acid, docosahexaenoic acid (DHA). Previous work showed that while it protected cells, the molecular principles underlying this protection were not known.

“During the last few years, my laboratory has been immersed in studying gene regulation,” Dr. Bazan says. “We have uncovered a novel control that makes definitive decisions about whether a retina or brain cell will survive or die when threatened with disease onset. The gene mechanism that we discovered is the interplay of two genes turned on by the messenger Neuroprotectin D1.”

Age-related macular degeneration (AMD) is a devastating disease that targets the retina of the elderly and destroys cells in charge of receiving photons and transferring light signals to the brain for decoding. The causal mechanisms of this disease remain elusive. The retinal pigment epithelium (RPE) is a single layer of cells that accomplishes multiple functions, such as providing survival molecules that prevent photoreceptors from dying.

The research team worked with human RPE cells and an experimental model of ischemic stroke. They discovered novel mechanisms in cells with the ability to activate pathways that crosstalk one to another and then assemble consolidated responses that decide cell fate. The researchers found that the powerful messenger, NPD1, is produced on-demand in the brain and retina and that it elicits a network of positive signals essential for the well-being of vision and cognition. They showed that NDP1 bioactivity governs key gene interactions decisive in cell survival when threatened by disease or injury. They demonstrated that not only does NPD1 protect photoreceptors, but it also promotes remarkable neurological recovery from the most frequent form of stroke in humans.

New laser therapy helps slow macular degeneration

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

A new, low impact low energy laser treatment for patients with early age-related macular degeneration (AMD) has produced positive results by reducing indicators of the disease.

Researchers from the University of Melbourne found unlike other laser treatments, this new faster laser did not result in damage to the retina, the sensitive light detecting tissue at the back of the eye.

Associate Professor Erica Fletcher from the Department of Anatomy and Neuroscience said this was the first report detailing how this new laser treatment may improve eye health in those with AMD. In the early stages, the disease is characterised by the presence of small fatty deposits called drusen and thickening in a membrane at the back of the eye.

Published in Journal of the Federation of American Societies for Experimental Biology (FASEB), the study explores how this laser may help in limiting retinal disease, showing that it improved the health of important supporting cells at the back of the eye.

“These findings suggest treating people with AMD with this new nanosecond laser reduces signs of the disease. Importantly, unlike other lasers currently used to treat eye disease, the nanosecond laser does not result in damage to the sensitive retina,” she said.

The study also showed evidence that nanosecond laser treatment in one eye can also produce positive effects in the other untreated eye. This raises the possibility that monocular treatment may be sufficient to treat disease in both eyes.

AMD affects one in seven people over the age of 50 with the incidence increasing in age. It is responsible for 48 per cent of severe vision loss in Australia with an estimated 17,700 new cases each year.

Nanotubes may restore sight to blind retinas

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

The aging process affects everything from cardiovascular function to memory to sexuality. Most worrisome for many, however, is the potential loss of eyesight due to retinal degeneration.

New progress towards a prosthetic retina could help alleviate conditions that result from problems with this vital part of the eye. An encouraging new study published in Nano Letters describes a revolutionary novel device, tested on animal-derived retinal models, that has the potential to treat a number of eye diseases. The proof-of-concept artificial retina was developed by an international team led by Prof. Yael Hanein of Tel Aviv University’s School of Electrical Engineering and head of TAU’s Center for Nanoscience and Nanotechnology and including researchers from TAU, the Hebrew University of Jerusalem, and Newcastle University.

“Compared to the technologies tested in the past, this new device is more efficient, more flexible, and can stimulate neurons more effectively,” said Prof. Hanein. “The new prosthetic is compact, unlike previous designs that used wires or metals while attempting to sense light. Additionally, the new material is capable of higher spatial resolution, whereas older designs struggled in this area.”

A natural shape

The researchers combined semiconductor nanorods and carbon nanotubes to create a wireless, light-sensitive, flexible film that could potentially replace a damaged retina. The researchers tested the new device with chick retinas which were not yet light sensitive to prove that the artificial retina is able to induce neuronal activity in response to light.

Patients with age-related macular degeneration (AMD), which usually affects people age 60 or older who have damage to a specific part of the retina, will stand to benefit from the nanotube device if it is proved compatible in animals over the long term.

According to TAU doctoral student and research team member Dr. Lilach Bareket, there are already medical devices that attempt to treat visual impairment by sending sensory signals to the brain. While scientists are trying different approaches to develop an implant that can “see” light and send visual signals to a person’s brain, to counter the effects of AMD and related vision disorders, many of these approaches require the use of metallic parts and cumbersome wiring or result in low resolution images. The researchers set out to make a more compact device.

Progress in the right direction

“In comparison with other technologies, our new material is more durable, flexible, and efficient, as well as better able to stimulate neurons,” said Prof. Hanein. “We hope our carbon nanotube and semiconductor nanorod film will serve as a compact replacement for damaged retinas.”

“We are still far away from actually replacing the damaged retina,” said Dr. Bareket. “But we have now demonstrated that this new material stimulates neurons efficiently and wirelessly with light. If you compare this to other devices based on silicon technology, which require wiring to outside energy or light sources, this is a groundbreaking new direction.”

The research team received funding for their study from the Israel Ministry of Science and Technology, the European Research Council, and the Biotechnology and Biological Sciences Research Council.

Artificial retina could someday help restore vision

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Posted on 9th February 2015 by Pacific ClearVision Institute in General |Retina

The loss of eyesight, often caused by retinal degeneration, is a life-altering health issue for many people, especially as they age. But a new development toward a prosthetic retina could help counter conditions that result from problems with this crucial part of the eye. Scientists published their research on a new device, which they tested on tissue from laboratory animals, in the ACS journal Nano Letters.

Yael Hanein and colleagues point out that a growing range of medical devices has become available to treat conditions, including visual impairment, that involve sending sensory signals to the brain. Patients with one type of eye disorder called age-related macular degeneration (AMD), for example, could potentially benefit from such a device, they say. AMD usually affects people age 60 or older who have damage to a specific part of the retina, limiting their vision. Scientists are trying different approaches to develop an implant that can “see” light and send visual signals to a person’s brain, countering the effects of AMD and related vision disorders. But many attempts so far use metallic parts, cumbersome wiring or have low resolution. The researchers, an interdisciplinary team from Tel Aviv University, the Hebrew University of Jerusalem Centers for Nanoscience and Nanotechnology and Newcastle University, wanted to make a more compact device.

The researchers combined semiconductor nanorods and carbon nanotubes to create a wireless, light-sensitive, flexible film that could potentially act in the place of a damaged retina. When they tested it with a chick retina that normally doesn’t respond to light, they found that the film absorbed light and, in response, sparked neuronal activity. In comparison with other technologies, the researchers conclude theirs is more durable, flexible and efficient, as well as better able to stimulate neurons.

The authors acknowledge funding from the Israel Ministry of Science and Technology, the European Research Council and the Biotechnology and Biological Sciences Research Council.