Chapter 10. Vision: From Eye to Brain
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Nancy Shute In September, we reported on a charming little study that found people who feel blue after watching sad videos have a harder time perceiving colors on the blue-yellow axis. Now the researchers may be feeling blue themselves. On Thursday they retracted their study, saying that errors in how they structured the experiment skewed the results. Shortly after the study was published online, commenters started looking skeptically at the results. And because the researchers had posted their data online, those commenters were able to run the numbers themselves. They didn't like what they found. As one blogger wrote: "A major problem is that the authors are claiming that they've found an interaction between video condition and color axis, but they haven't actually tested this interaction, they've just done a pair of independent t-tests and found different results." As the indefatigable crew at the Retraction Watch blog points out, it's not the first time scientists have messed this up. "This exact experimental oversight occurs all too often, according to a 2011 paper in Nature Neuroscience, which found that the same number of papers performed the procedure incorrectly as did it correctly." And there were other problems, too, such as not testing participants' color perception before the study. © 2015 npr
By Christof Koch Artificial intelligence has been much in the news lately, driven by ever cheaper computer processing power that has become effectively a near universal commodity. The excitement swirls around mathematical abstractions called deep convolutional neural networks, or ConvNets. Applied to photographs and other images, the algorithms that implement ConvNets identify individuals from their faces, classify objects into one of 1,000 distinct categories (cheetah, husky, strawberry, catamaran, and so on)—and can describe whether they see “two pizzas sitting on top of a stove top oven” or “a red motorcycle parked on the side of the road.” All of this happens without human intervention. Researchers looking under the hood of these powerful algorithms are surprised, puzzled and entranced by the beauty of what they find. How do ConvNets work? Conceptually they are but one or two generations removed from the artificial neural networks developed by engineers and learning theorists in the 1980s and early 1990s. These, in turn, are abstracted from the circuits neuroscientists discovered in the visual system of laboratory animals. Already in the 1950s a few pioneers had found cells in the retinas of frogs that responded vigorously to small, dark spots moving on a stationary background, the famed “bug detectors.” Recording from the part of the brain's outer surface that receives visual information, the primary visual cortex, Torsten Wiesel and the late David H. Hubel, both then at Harvard University, found in the early 1960s a set of neurons they called “simple” cells. These neurons responded to a dark or a light bar of a particular orientation in a specific region of the visual field of the animal. © 2015 Scientific American
By Jessica Schmerler Young brains are plastic, meaning their circuitry can be easily rewired to promote learning. By adulthood, however, the brain has lost much of its plasticity and can no longer readily recover lost function after, say, a stroke. Now scientists have successfully restored full youthful plasticity in adult mice by transplanting young neurons into their brain—curing their severe visual impairments in the process. In a groundbreaking study published in May in Neuron, a team of neuroscientists led by Sunil Gandhi of the University of California, Irvine, transplanted embryonic mouse stem cells into the brains of other mice. The cells were primed to become inhibitory neurons, which tamp down brain activity. Prior to this study, “it was widely doubted that the adult brain would allow these cells to disperse, integrate and reactivate plasticity,” says Melissa Davis, first author of the study. Scientists have been attempting such a feat for years, refining their methods along the way, and the Irvine team finally saw success: the cells were integrated in the brain and caused large-scale rewiring, restoring the high-level plasticity of early development. In visually impaired mice, the transplant allowed for the restoration of normal vision, as demonstrated by tests of visual nerve signals and a swimming maze test. The scientists have not yet tested the transplanting technique for other neurological disorders, but they believe the technique has potential for many conditions and injuries depending on how, exactly, the new neurons restore plasticity. It is not yet known whether the proliferation of the transplanted cells accounts for the restored plasticity or if the new cells trigger plasticity in existing neurons. If the latter, the treatment could spur the rewiring and healing of the brain following traumatic brain injury or stroke. © 2015 Scientific American
By Karen Weintraub The short answer is: not yet, but treatments are getting better. Getting older is the leading risk factor for age-related macular degeneration, the leading cause of vision loss in the United States. Macular degeneration comes in two forms: dry and wet. The dry form is milder and usually has no symptoms, but it can degenerate into the wet form, which is characterized by the growth of abnormal blood vessels in the back of the eye, potentially causing blurriness or vision loss in the center of the field of vision. The best treatment for wet macular degeneration is prevention, said Dr. Rahul N. Khurana, a clinical spokesman for the American Academy of Ophthalmology and a retina specialist practicing in Mountain View, Calif. Not smoking, along with eating dark green vegetables and at least two servings of fish a week, may help reduce the risk of macular degeneration, he said. An annual eye exam can catch macular degeneration while it is still in the dry form, Dr. Khurana said, and vitamins can help prevent it from progressing into the wet form, the main cause of vision loss. Dr. Joan W. Miller, chief of ophthalmology at Massachusetts Eye and Ear, said anyone with a family history of the disease should get a retina check at age 50. People should also get an eye exam if they notice problems like trouble adjusting to the dark or needing more light to read. The federally funded Age-Related Eye Disease Study, published in 2001 and updated in 2013, found that people at high risk for advanced age-related macular degeneration could cut that risk by about 25 percent by taking a supplement that included 500 milligrams of vitamin C, 400 I.U.s of vitamin E, 10 milligrams of lutein, 2 milligrams of zeaxanthin, 80 milligrams of zinc, and 2 milligrams of copper. © 2015 The New York Times Company
Link ID: 21551 - Posted: 10.23.2015
By Hanae Armitage CHICAGO, ILLINOIS—Aside from a few animals—like pythons and vampire bats—that can sense infrared light, the world of this particular electromagnetic radiation has been off-limits to most creatures. But now, researchers have engineered rodents to see infrared light by implanting sensors in their visual cortex—a first-ever feat announced here yesterday at the annual meeting of the Society for Neuroscience. Before they wired rats to see infrared light, Duke University neuroscientist Miguel Nicolelis and his postdoc Eric Thomson engineered them to feel it. In 2013, they surgically implanted a single infrared-detecting electrode into an area of the rat’s brain that processes touch called the somatosensory cortex. The other end of the sensor, outside the rat’s head, surveyed the environment for infrared light. When it picked up infrared, the sensor sent electrical messages to the rats’ brains that seemed to give them a physical sensation. At first, the rats would groom and rub their whiskers repeatedly whenever the light went on. But after a short while, they stopped fidgeting. They even learned to associate infrared with a reward-based task in which they followed the light to a bowl of water. In the new experiment, the team inserted three additional electrodes, spaced out equally so that the rats could have 360 degrees of infrared perception. When they were primed to perform the same water-reward task, they learned it in just 4 days, compared to 40 days with the single implant. “Frankly, this was a surprise,” Thomson says. “I thought it would be really confusing for [the rats] to have so much stimulation all over their brain, rather than [at] one location.” © 2015 American Association for the Advancement of Science.
By Kerry Grens Eric Altschuler has been staring at mirrors. Specifically, those of van Eyck, Caravaggio, Parmigianino, Escher, and other painters. The Temple University professor and his colleague V.S. Ramachandran of the University of California, San Diego, are on the hunt for novel ways that artists have presented reflections, as a means of seeking out potentially new modes of therapy. Ramachandran and Altschuler have pioneered methods of using a mirror to alleviate phantom limb pain and other conditions. A patient sits at the side of the mirror with, say, his right arm reflected in front of the glass. The patient peeks around the corner to view the reflection as if he were looking at his left arm—a setup Ramachandran and Altschuler call the parasagittal reflection. In their cataloging of mirrors in art, presented as a poster at the Society for Neuroscience (SfN) meeting held in Chicago this week, Altschuler and Ramachandran found that for 500 or more years, painters presented frontal plane reflections (a straight-on view in the mirror). It wasn’t until 1946 that something different—the parasagittal view, in particular—appeared in fine art: in M.C. Escher’s lithograph, “Magic Mirror,” Altschuler and Ramachandran reported at SfN. The viewer has an angled view at a ball reflected in a mirror, with an identical ball positioned symmetrically behind the mirror—very similar to the concept of mirror therapy. “Magic Mirror” was produced 50 years before Ramachandran first published on mirror therapy, and even then Ramachandran was unaware of the artwork. “Escher was very clever,” Altschuler told The Scientist, noting that perhaps there are other novel approaches just waiting to be discovered in paintings. © 1986-2015 The Scientist
Link ID: 21543 - Posted: 10.22.2015
Gene therapy preserved vision in a study involving dogs with naturally occurring, late-stage retinitis pigmentosa, according to research funded by the National Eye Institute (NEI), part of the National Institutes of Health. The findings contribute to the groundwork needed to move gene therapy forward into clinical trials for people with the blinding eye disorder, for which there is currently no cure. Scientists from the University of Pennsylvania and the University of Florida, Gainesville also determined for the first time that gene therapy may be of potential benefit even after there has been significant loss of cells in the eye. Up to this point, animal studies had shown benefits from gene therapy only when it was used in the earliest stages of the disease. “The study shows that a corrective gene can stop the loss of photoreceptors in the retina, and provides good proof of concept for gene therapy at the intermediate stage of the disease, thus widening the therapeutic window,” said Neeraj Agarwal, Ph.D., a program director at NEI. Retinitis pigmentosa is the most common inherited disease that causes degeneration of the retina, the light-sensitive tissue lining the back of the eye. Roughly 1 in 4,000 people are affected and about 10 to 20 percent have a particularly severe form called X-linked retinitis pigmentosa, which predominately affects males, causing night blindness by age 10 and progressive loss of the visual field by age 45. About 70 percent of people with the X-linked form carry mutations that cause loss of function of the retinitis pigmentosa GTPase Regulator (RPGR) gene, which encodes a protein important for maintaining the health of photoreceptors.
Link ID: 21510 - Posted: 10.14.2015
By Ariana Eunjung Cha When it comes to studies on birth order, first-borns tend to make out pretty well. Research says they tend to be smarter, more outgoing, and exhibit more leadership qualities. Unfortunately, it's not all good news. A new paper published in JAMA Ophthalmology shows that first-borns also tend to be 10 percent more likely to be near-sighted and 20 percent more likely to have severe myopia than their siblings. In fact, the risk for myopia appeared to be progressively lower the later you were born in terms of your birth order. The researchers from Cardiff University suggested that the cause was “parental investment in education” because parents may have a tendency to put more pressure on first-borns. They theorized that parents may be more demanding that first-borns do more "near" activities, such as reading, which may impact their eyesight. Previous studies have shown a strong link between time spent outdoors and a diminished risk of myopia, and it may stand to reason that children who spend more time on studies may be spending less time outdoors. Jeremy Guggenheim, a doctoral student, and colleagues wrote that while there's no way to make a definitive causal link, their study found that when they adjusted for a proxy for educational exposure — the highest educational degree or age at completion of full-time education — they saw a less dramatic association between near-sightedness and birth order.
Link ID: 21497 - Posted: 10.10.2015
By Virginia Morell How homing pigeons find their way home has long mystified scientists. Experiments have shown they rely on smells to create a mental map of their route and on the sun or Earth’s magnetic fields to navigate. But they also use vision, memorizing roads, railway lines, and rivers. To understand just how important pigeons’ visual memories are for homing, scientists trained 12 birds to fly to their home lofts while wearing patches covering one eye (as in the photo above). Each bird wore a GPS logging device and made 18 flights with the left or right eye blocked, followed by another 18 trips with the opposite eye covered. Unlike mammals, birds lack a key neural structure—the corpus callosum—that allows both hemispheres of the brain to access what an animal sees. The experiments revealed that this missing neural structure affects the pigeons’ homing abilities, the scientists report in today’s the Proceedings of the Royal Society B. Pigeons that learned their way home with a blocked left eye couldn’t repeat the same journey when they wore a patch over their right eye, and vice versa. Instead, they flew slightly off course, following more of a curve than a straight line. The new work proves that vision, too, plays a key role in how pigeons find their way home. © 2015 American Association for the Advancement of Science.
By ANDREW POLLACK What could become the first gene therapy to win approval in the United States moved closer to market on Monday, when its developer announced that the medicine had succeeded in a late-stage clinical trial in treating an inherited eye disease that can cause blindness. The developer, Spark Therapeutics, said the treatment had allowed people with certain so-called inherited retinal dystrophies to more easily maneuver in dimmer light than they could before. The company said it planned to apply to the Food and Drug Administration next year for approval to sell the product. “We saw substantial restoration of vision in patients who were progressing toward complete blindness,” Dr. Albert M. Maguire, a professor of ophthalmology at the University of Pennsylvania and a lead researcher in the study, said in a news release being issued by Spark. Dr. Katherine High, Spark’s president and chief scientific officer, said this was the first successful randomized, controlled trial for any gene therapy aimed at an inherited disease. “I’ve been working in gene therapy for most of my career,” she said. “It’s been a long time coming, and I’m delighted.” Besides encouraging the once beleaguered field of gene therapy, the results — if interpreted positively by investors — could help lift biotechnology stocks, which have been battered recently by concerns over a backlash against high drug prices. Still, much remains unknown. Spark did not provide the actual trial data, saying only that the treatment achieved the main goal of the study as well as two out of three of its secondary goals. It is also unclear what the F.D.A. will deem sufficient for approval of the product. Spark’s stock had slumped in the last two months as it changed how it would measure the results of the trial. © 2015 The New York Times Company
Link ID: 21475 - Posted: 10.05.2015
Ellen Brait in New York Mind reading might not be as far-fetched as many people believe, says a study published by researchers at the University of Washington. Their research, published in PLOS One on Wednesday, demonstrated “that a non-invasive brain-to-brain interface (BBI) can be used to allow one human to guess what is on the mind of another human”. With only the use of brainwaves and a specifically designed computer, they examined the potential for exchanging basic information without saying a word. “We are actually still at the beginning of the field of interface technology and we are just mapping out the landscape so every single step is a step that opens up some new possibilities,” said lead author Andrea Stocco, an assistant professor of psychology and a researcher at UW’s Institute for Learning and Brain Sciences. The experiment had five pairs of men and women between the ages of 19 and 39 play a game similar to 20 questions. Each group had a “respondent”, who picked an object from lists provided, and an “inquirer”, who tried to guess the object by asking yes or no questions. They were placed in different rooms, approximately one mile apart. After a question was picked, it appeared on the respondent’s computer screen. They had two seconds to look at the question and one second to choose an answer. To do so, they looked at one of two flashing lights that were labeled yes or no. Each answer generated slightly different types of neural activity. © 2015 Guardian News and Media Limited
For primary school children in China, spending an extra 45 minutes per day outside in a school activity class may reduce the risk of nearsightedness, or "myopia," according to a new study. In some parts of China, 90 per cent of high school graduates have nearsightedness, and rates are lower but increasing in Europe and the Middle East, the authors write. "There were some studies suggesting the protective effect of outdoor time in the development of myopia, but most of this evidence is from cross-sectional studies [survey] data that suggest 'association' instead of causality," said lead author Dr. Mingguang He of Sun Yat-sen University in Guangzhou. "Our study, as a randomized trial, is able to prove causality and also provide the high level of evidence to inform public policy." Intense levels of schooling and little time spent outdoors may have contributed to the epidemic rise of nearsightedness in China, he told Reuters Health by email. The researchers divided 12 primary schools in China into two groups: six schools continued their existing class schedule, while six were assigned to include an additional 40 minutes of outdoor activity at the end of each school day. Parents of children in the second group were also encouraged to engage their children in outdoor activities on the weekends. In total, almost 2,000 first-graders, with an average age of almost seven years old, were included. After three years, 30 per cent of the outdoor activity group had developed nearsightedness, compared to almost 40 per cent of kids in the control group, according to the results in JAMA. ©2015 CBC/Radio-Canada.
Link ID: 21413 - Posted: 09.16.2015
Mo Costandi At some point back in deep time, a group of fish were washed into a limestone cave somewhere in northeastern Mexico. With no way out and little more than bat droppings to eat, the fish began to adapt to their new troglodytic lifestyle. Unable to see other members of their group in the dark, they lost their colourful pigmentation. Then they lost their eyesight, their eyes gradually got smaller, and then disappeared altogether. This was accompanied by a dramatic reduction in the size of the brain’s visual system. Yet, the question of why the blind cave fish lost its eyes and a large part of its brain remains unresolved. Now, biologists in Sweden believe they have found the answer. In new research published today, they report that loss of the visual system saves the fish a substantial amount of energy, and was probably key to their stranded ancestors’ survival. The blind cave fish Astyanax mexicanus is adapted to its subterranean environment in other ways. As its vision regressed, it became more reliant on smell and taste, and its taste buds grew larger and more numerous. They also developed an enhanced ability to detect changes in mechanical pressure, which made them more sensitive to water movements. Last year, Damian Moran of Lund University and his colleagues reported that blind cave fish eliminated the circadian rhythm in their metabolism during their course of evolution, and that this leads to a massive 27% reduction in their energy expenditure. This new study was designed test whether or not they lost their visual system for the same reason. © 2015 Guardian News and Media Limited
When we move our head, the whole visual world moves across our eyes. Yet we can still make out a bee buzzing by or a hawk flying overhead, thanks to unique cells in the eye called object motion sensors. A new study on mice helps explain how these cells do their job, and may bring scientists closer to understanding how complex circuits are formed throughout the nervous system. The study was funded by the National Institutes of Health, and was published online in Nature. “Understanding how neurons are wired together to form circuits in the eye is fundamental for advancing potential new therapies for blinding eye diseases,” said Paul A. Sieving, M.D., Ph.D., director of NIH’s National Eye Institute (NEI). “Research aimed at regenerating photoreceptors, for example, is enriched by efforts to understand the circuitry in the eye.” Object motion sensors are one of about 30 different types of retinal ganglion cells (RGCs) in the retina, the light-sensitive tissue at the back of the eye. These cells are unique because they fire only when the timing of a small object’s movement differs from that of the background; they are silent when the object and the background move in sync. Researchers believe this is critical to our ability to see small objects moving against a backdrop of complex motion. The cells in the retina are wired up like an electrical circuit. Vision begins with photoreceptors, cells that detect light entering the eye and convert it into electrical signals. Middleman neurons, called interneurons, shuttle signals from photoreceptors to the RGCs. And each RGC sends the output visual information deeper into the brain for processing. This all takes place within fractions of a second, so the scientists were surprised to discover that before it reaches object motion sensors, visual information about object motion takes a detour through a unique type of interneuron. Their results represent an ongoing effort by scientists to map out complex circuits of the nervous system.
Link ID: 21368 - Posted: 09.01.2015
By SINDYA N. BHANOO The human eye has a blind spot, though few of us realize it. Now, a new study suggests that it is possible to reduce the spot with training. The optic nerve, which carries visual signals to the brain, passes through the retina, a light-sensitive layer of tissue. There are no so-called photoreceptors at the point where the optic nerve intersects the retina. The right eye generally compensates for the left eye’s blind spot and vice versa, so the spot is hardly noticed. Researchers trained 10 people using a computer monitor and an eye patch. The participants were shown a waveform in the visual field of their blind spot day after day. After 20 days of this repeated stimulation, the blind spot shrunk by about 10 percent. The researchers believe that neurons at the periphery of the blind spot became more responsive, effectively reducing the extent of functional blindness. The findings add to a growing body of research suggesting that the human eye can be trained, said Paul Miller, a psychologist at the University of Queensland in Australia and an author of the study, which appeared in the journal Current Biology. This kind of training may help researchers develop better treatments for visual impairments like macular degeneration. “This is the leading cause of blindness in the western world,” Mr. Miller said. © 2015 The New York Times Company
By James Gallagher Health editor, BBC News website Close your eyes and imagine walking along a sandy beach and then gazing over the horizon as the Sun rises. How clear is the image that springs to mind? Most people can readily conjure images inside their head - known as their mind's eye. But this year scientists have described a condition, aphantasia, in which some people are unable to visualise mental images. Niel Kenmuir, from Lancaster, has always had a blind mind's eye. He knew he was different even in childhood. "My stepfather, when I couldn't sleep, told me to count sheep, and he explained what he meant, I tried to do it and I couldn't," he says. "I couldn't see any sheep jumping over fences, there was nothing to count." Our memories are often tied up in images, think back to a wedding or first day at school. As a result, Niel admits, some aspects of his memory are "terrible", but he is very good at remembering facts. And, like others with aphantasia, he struggles to recognise faces. Yet he does not see aphantasia as a disability, but simply a different way of experiencing life. Take the aphantasia test It is impossible to see what someone else is picturing inside their head. Psychologists use the Vividness of Visual Imagery Questionnaire, which asks you to rate different mental images, to test the strength of the mind's eye. The University of Exeter has developed an abridged version that lets you see how your mind compares. © 2015 BBC.
By Jessica Schmerler In the modern age of technology it is not uncommon to come home after a long day at work or school and blow off steam by reading an e-book or watching television. Lately, however, scientists have been cautioning against using light-emitting devices before bed. Why? The light from our devices is “short-wavelength-enriched,” meaning it has a higher concentration of blue light than natural light—and blue light affects levels of the sleep-inducing hormone melatonin more than any other wavelength. Changes in sleep patterns can in turn shift the body’s natural clock, known as its circadian rhythm. Recent studies have shown that shifts in this clock can have devastating health effects because it controls not only our wakefulness but also individual clocks that dictate function in the body’s organs. In other words, stressors that affect our circadian clocks, such as blue-light exposure, can have much more serious consequences than originally thought. How did you become interested in the effects of light on sleep? Brainard: I was interested in the effects of light on animals as a teenager. I never planned to be a scientist—I wanted to be a writer! So I learned more about the topic out of pure curiosity. When I began my career as a journalist, I interviewed researchers on the topic who encouraged me to pursue a career in science. So I returned to school to get my doctorate and studied the effects of different wavelengths and intensities of light on rodents. I have exclusively studied the effects of light on humans for the past 30 years. © 2015 Scientific American
By Mitch Leslie Some microbes that naturally dwell in our intestines might be bad for our eyes, triggering autoimmune uveitis, one of the leading causes of blindness. A new study suggests that certain gut residents produce proteins that enable destructive immune cells to enter the eyes. The idea that gut microbes might promote autoimmune uveitis “has been there in the back of our minds,” says ocular immunologist Andrew Taylor of the Boston University School of Medicine, who wasn’t connected to the research. “This is the first time that it’s been shown that the gut flora seems to be part of the process.” As many as 400,000 people in the United States have autoimmune uveitis, in which T cells—the commanders of the immune system—invade the eye and damage its middle layer. All T cells are triggered by specific molecules called antigens, and for T cells that cause autoimmune uveitis, certain eye proteins are the antigens. Even healthy people carry these T cells, yet they don't usually swarm the eyes and unleash the disease. That's because they first have to be triggered by their matching antigen. However, those proteins don't normally leave the eye. So what could stimulate the T cells? One possible explanation is microbes in the gut. In the new study, immunologist Rachel Caspi of the National Eye Institute in Bethesda, Maryland, and colleagues genetically engineered mice so their T cells recognized one of the same eye proteins targeted in autoimmune uveitis. The rodents developed the disease around the time they were weaned. But dosing the animals with four antibiotics that killed off most of their gut microbes delayed the onset and reduced the severity of the disease. © 2015 American Association for the Advancement of Science.
By CLAIRE MARTIN The eyeglass lenses that Don McPherson invented were meant for surgeons. But through serendipity he found an entirely different use for them: as a possible treatment for colorblindness. Mr. McPherson is a glass scientist and an avid Ultimate Frisbee player. He discovered that the lenses he had invented, which protect surgeons’ eyes from lasers and help them differentiate human tissue, caused the world at large to look candy-colored — including the Frisbee field. At a tournament in Santa Cruz, Calif., in 2002, while standing on a grassy field dotted with orange goal-line cones, he lent a pair of glasses with the lenses to a friend who happened to be colorblind. “He said something to the effect of, ‘Dude, these are amazing,’ ” Mr. McPherson says. “He’s like, ‘I see orange cones. I’ve never seen them before.’ ” Mr. McPherson was intrigued. He said he did not know the first thing about colorblindness, but felt compelled to figure out why the lenses were having this effect. Mr. McPherson had been inserting the lenses into glasses that he bought at stores, then selling them through Bay Glass Research, his company at the time. Mr. McPherson went on to study colorblindness, fine-tune the lens technology and start a company called EnChroma that now sells glasses for people who are colorblind. His is among a range of companies that have brought inadvertent or accidental inventions to market. Such inventions have included products as varied as Play-Doh, which started as a wallpaper cleaner, and the pacemaker, discovered through a study of hypothermia. To learn more about color vision and the feasibility of creating filters to correct colorblindness, Mr. McPherson applied for a grant from the National Institutes of Health in 2005. He worked with vision scientists and a mathematician and computer scientist named Andrew Schmeder. They weren’t the first to venture into this industry; the history of glassmakers claiming to improve colorblindness is long and riddled with controversy. © 2015 The New York Times Company
Link ID: 21303 - Posted: 08.17.2015
When the owl swooped, the “blind” mice ran away. This was thanks to a new type of gene therapy to reprogramme cells deep in the eye to sense light. After treatment, the mice ran for cover when played a video of an approaching owl, just like mice with normal vision. “You could say they were trying to escape, but we don’t know for sure,” says Rob Lucas of the University of Manchester, UK, co-leader of the team that developed and tested the treatment. “What we can say is that they react to the owl in the same way as sighted mice, whereas the untreated mice didn’t do anything.” This is the team’s best evidence yet that injecting the gene for a pigment that detects light into the eyes of blind mice can help them see real objects again. This approach aims to treat all types of blindness caused by damaged or missing rods and cones, the eye’s light receptor cells. Most gene therapies for blindness so far have concentrated on replacing faulty genes in rarer, specific forms of inherited blindness, such as Leber congenital amaurosis. Deep down The new treatment works by enabling other cells that lie deeper within the retina to capture light. While rod and cone cells normally detect light and convert this into an electrical signal, the ganglion and bipolar cells behind them are responsible for processing these signals and sending them to the brain. By giving these cells the ability to produce their own light-detecting pigment, they can to some extent compensate for the lost receptors, or so it seems.
Link ID: 21298 - Posted: 08.15.2015