Chapter 10. Vision: From Eye to Brain
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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
Despite virtual reality’s recent renaissance, the technology still has some obvious problems. One, you look like a dumbass using it. Two, the stomach-churning mismatch between what you see and what you feel contributes to “virtual reality sickness.” But there’s another, less obvious flaw that could add to that off-kilter sensation: an eye-focusing problem called vergence-accommodation conflict. It’s only less obvious because, well, you rarely experience it outside of virtual reality. At SIGGRAPH in Los Angeles this week, Stanford professor Gordon Wetzstein and his colleagues are presenting a new head-mounted display that minimizes the vergence-accommodation conflict. This isn’t just some esoteric academic problem. Leading VR companies like Oculus and Microsoft know all too well their headsets are off, and Magic Leap, the super secret augmented reality company in Florida, is betting the house on finding a solution first. “It’s an exciting area of research,” says Martin Banks, a vision scientist at the University of California, Berkeley. “I think it’s going to be the next big thing in displays.” Okay okay, so what’s the big deal with the vergence-accommodation conflict? Two things happen when you simply “look” at an object. First, you point your eyeballs. If an object is close, your eyes naturally converge on it; if it’s far, they diverge. Hence, vergence. If your eyes don’t line up correctly, you end up seeing double. The second thing that happens is the lenses inside your eyes focus on the object, aka accommodation. Normally, vergence and accommodation are coupled. “The visual system has developed a circuit where the two response talk to each other,” says Banks. “That makes perfect sense in the natural environment. They’re both trying to get to the same distance, so why wouldn’t they talk to one another?” In other words, your meat brain has figured out a handy shortcut for the real world.
Link ID: 21287 - Posted: 08.12.2015
Nell Greenfieldboyce Take a close look at a house cat's eyes and you'll see pupils that look like vertical slits. But a tiger has round pupils — like humans do. And the eyes of other animals, like goats and horses, have slits that are horizontal. Scientists have now done the first comprehensive study of these three kinds of pupils. The shape of the animal's pupil, it turns out, is closely related to the animal's size and whether it's a predator or prey. The pupil is the hole that lets light in, and it comes in lots of different shapes. "There are some weird ones out there," says Martin Banks, a vision scientist at the University of California, Berkeley. Cuttlefish have pupils that look like the letter "W," and dolphins have pupils shaped like crescents. Some frogs have heart-shaped pupils, while geckos have pupils that look like pinholes arranged in a vertical line. Needless to say, scientists want to know why all these different shapes evolved. "It's been an active point of debate for quite some time," says Banks, "because it's something you obviously observe. It's the first thing you see about an animal — where their eye is located and what the pupil shape is." For their recent study, Banks and his colleagues decided to keep things simple. They looked at just land animals, and just three kinds of pupils. "We restricted ourselves to just pupils that are elongated or not," Banks explains. "So they're either vertical, horizontal or round." © 2015 NPR
By Rachel Feltman Ever wondered what the world looks like to nonhuman animals? Scientists do, too. It can actually be a really important question. Sometimes humans can't see things -- like skin markings designed to attract mates or flower colors meant to draw pollinators -- that are incredibly important in the life and behavior of an animal. That's why researchers at the University of Exeter have developed a software that converts photos to "animal vision." The software, which is available for free online, is described in a recent paper in the journal Methods in Ecology and Evolution. Its creators have already used it extensively themselves to perform studies on animals who see light outside the spectrum visible to humans. They've also used it to track imperceptible color changes that occur in women's faces during ovulation. The software works by integrating photos taken using ultraviolet filters with those taken using regular color filters, a process that scientists used to have to dial in manually for whatever species they were studying. By meshing the visible light spectrum with information from a full-spectrum image, the software can replicate the visual experience of animals who see more colors than humans, including light in the ultraviolet range.
Link ID: 21272 - Posted: 08.08.2015
By Hanae Armitage Cataracts cloud the eyes of tens of millions of people around the world and nearly 17.2% of Americans over the age of 40. Currently, the only treatment is surgery—lasers or scalpels cut away the molecular grout that builds in the eye as cataracts develop, and surgeons sometimes replace the lens. But now, a team of scientists and ophthalmologists has tested a solution in dogs that may be able to dissolve the cataract right out of the eye’s lens. And the solution is itself a solution: a steroid-based eye drop. Though scientists don’t fully understand how cataracts form, they do know that the “fog” often seen by patients is a glob of broken proteins, stuck together in a malfunctioning clump. When healthy, these proteins, called crystallins, help the eye’s lens keep its structure and transparency. But as humans and animals alike get older, these crystallin proteins start to come unglued and lose their ability to function. Then they clump together and form a sheathlike obstruction in the lens, causing the signature “steamy glass” vision that accompanies cataracts. Coming up with a solution other than surgery has been tough. Scientists have been hunting for years for mutations in crystallin proteins that might offer new insights and pave the way to an alternate therapy. Now, it looks like a team led by University of California (UC), San Diego, molecular biologist Ling Zhao may have done just that. Her team came up with the eye drop idea after finding that children with a genetically inherited form of cataracts shared a mutation that stopped the production of lanosterol, an important steroid in the body. When their parents did not have the same mutation, the adults produced lanosterol and had no cataracts. © 2015 American Association for the Advancement of Science.
Link ID: 21205 - Posted: 07.23.2015
It’s a good combination. Gene therapy to reverse blindness repairs damaged cells in the eye and also rearranges the brain to help process the new information. Visual pathways in the brain are made up of millions of interconnected neurons. When sensory signals are sent along them, the connections between neurons become strong. If underused – for example, as people lose their sight – the connections become weak and disorganised. Over the past few years, a type of gene therapy – injecting healthy genes into the eye to repair mutations – has emerged as a promising way to treat congenital and degenerative blindness. One of the first successful trials began in 2007. It involved 10 blind volunteers with a hereditary disease called Leber’s congenital amaurosis. The condition causes the retina to degenerate and leaves people completely blind early in life. Mutations in at least 19 genes can cause the disease, but all of the people in the trial had mutations in a gene called RPE65. The participants got an injection of a harmless virus in one of their eyes. The virus inserted healthy copies of RPE65 into their retina. Some of the volunteers went from straining to see a hand waving half a metre from their face to being able to read six lines on a sight chart. Others were able to navigate around an obstacle course in dim light – something that would have been impossible before the therapy. © Copyright Reed Business Information Ltd.
By Chris Foxx Technology reporter Twitter has responded to an epilepsy charity that said two of its online adverts were "irresponsible". The social media giant had uploaded two short videos on Vine that featured a looping, rapid succession of flashing colours. "Twitter's ads were dangerous to people living with photo-sensitive epilepsy," said Epilepsy Action's deputy chief executive, Simon Wigglesworth. Twitter told the BBC it had removed the videos on Friday morning. Around one in 3,500 people in the UK has photosensitive epilepsy, according to Epilepsy Action. Seizures can be triggered by flashing lights and bold patterns. An episode of Japanese cartoon Pokemon was famously blamed for triggering convulsions in 1997. "Eighty seven people are diagnosed with epilepsy every day and that first seizure can often come out of nowhere," said Mr Wigglesworth. "For a huge corporation like Twitter to take that risk was irresponsible." The Advertising Standards Authority told the BBC that "marketing communications", even those uploaded on a company's own website, should not include "visual effects or techniques that are likely to adversely affect members of the public with photosensitive epilepsy". It said both online and broadcast adverts in the UK had to adhere to rules made by the Committees of Advertising Practice. "We take very seriously ads in online media that might cause harm to people with photosensitive epilepsy," an ASA spokeswoman told the BBC. Twitter's flashing Vine videos were online for 18 hours before the company removed them. © 2015 BBC
Spider-like cells inside the brain, spinal cord and eye hunt for invaders, capturing and then devouring them. These cells, called microglia, often play a beneficial role by helping to clear trash and protect the central nervous system against infection. But a new study by researchers at the National Eye Institute (NEI) shows that they also accelerate damage wrought by blinding eye disorders, such as retinitis pigmentosa. NEI is part of the National Institutes of Health. “These findings are important because they suggest that microglia may provide a target for entirely new therapeutic strategies aimed at halting blinding eye diseases of the retina,” said NEI Director, Paul A. Sieving, M.D. “New targets create untapped opportunities for preventing disease-related damage to the eye, and preserving vision for as long as possible.” The findings were published in the journal EMBO Molecular Medicine. Retinitis pigmentosa, an inherited disorder that affects roughly 1 in 4,000 people, damages the retina, the light-sensitive tissue at the back of the eye. Research has shown links between retinitis pigmentosa and several mutations in genes for photoreceptors, the cells in the retina that convert light into electrical signals that are sent to the brain via the optic nerve. In the early stages of the disease, rod photoreceptors, which enable us to see in low light, are lost, causing night blindness. As the disease progresses, cone photoreceptors, which are needed for sharp vision and seeing colors, can also die off, eventually leading to complete blindness.