Chapter 13. Memory, Learning, and Development
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|By Brian Bienkowski and Environmental Health News Babies born to mothers with high levels of perchlorate during their first trimester are more likely to have lower IQs later in life, according to a new study. The research is the first to link pregnant women's perchlorate levels to their babies’ brain development. It adds to evidence that the drinking water contaminant may disrupt thyroid hormones that are crucial for proper brain development. Perchlorate, which is both naturally occurring and manmade, is used in rocket fuel, fireworks and fertilizers. It has been found in 4 percent of U.S. public water systems serving an estimated 5 to 17 million people, largely near military bases and defense contractors in the U.S. West, particularly around Las Vegas and in Southern California. “We would not recommend action on perchlorate levels from this study alone, although our report highlights a pressing need for larger studies of perchlorate levels from the general pregnant population and those with undetected hypothyroidism,” the authors from the United Kingdom, Italy and Boston wrote in the study published in The Journal of Clinical Endocrinology & Metabolism. The Environmental Protection Agency for decades has debated setting a national drinking water standard for perchlorate. The agency in 2011 announced it would start developing a standard, reversing an earlier decision. In the meantime, two states, California and Massachusetts, have set their own standards. © 2014 Scientific American
Wild marmosets in the Brazilian forest can learn quite successfully from video demonstrations featuring other marmosets, Austrian scientists have reported, showing not only that marmosets are even better learners than previously known, but that video can be used successfully in experiments in the wild. Tina Gunhold, a cognitive biologist at the University of Vienna, had worked with a population of marmoset monkeys in a bit of Brazilian forest before this particular experiment. The forest is not wilderness. It lies near some apartment complexes, and the marmosets are somewhat used to human beings. But the monkeys are wild, and each extended family group has its own foraging territory. Dr. Gunhold and her colleagues reported in the journal Biology Letters this month that they had tested 12 family groups, setting up a series of video monitors, each with a kind of complicated box that they called an “artificial fruit.” All the boxes contained food. Six of the monitors showed just an unchanging image of a marmoset near a similar box. Three of them showed a marmoset opening the box by pulling a drawer, and three others a marmoset lifting a lid to get at the food. Marmosets are very territorial and would not tolerate a strange individual on their turf, but the image of a strange marmoset on video didn’t seem to bother them. Individual marmosets “differed in their reactions to the video,” Dr. Gunhold said. “Some were more shy, some more bold. The younger ones were more attracted to the video, perhaps because of greater curiosity.” © 2014 The New York Times Company
By David Z. Hambrick, Fernanda Ferreira, and John M. Henderson A decade ago, Magnus Carlsen, who at the time was only 13 years old, created a sensation in the chess world when he defeated former world champion Anatoly Karpov at a chess tournament in Reykjavik, Iceland, and the next day played then-top-rated Garry Kasparov—who is widely regarded as the best chess player of all time—to a draw. Carlsen’s subsequent rise to chess stardom was meteoric: grandmaster status later in 2004; a share of first place in the Norwegian Chess Championship in 2006; youngest player ever to reach World No. 1 in 2010; and highest-rated player in history in 2012. What explains this sort of spectacular success? What makes someone rise to the top in music, games, sports, business, or science? This question is the subject of one of psychology’s oldest debates. In the late 1800s, Francis Galton—founder of the scientific study of intelligence and a cousin of Charles Darwin—analyzed the genealogical records of hundreds of scholars, artists, musicians, and other professionals and found that greatness tends to run in families. For example, he counted more than 20 eminent musicians in the Bach family. (Johann Sebastian was just the most famous.) Galton concluded that experts are “born.” Nearly half a century later, the behaviorist John Watson countered that experts are “made” when he famously guaranteed that he could take any infant at random and “train him to become any type of specialist [he] might select—doctor, lawyer, artist, merchant-chief and, yes, even beggar-man and thief, regardless of his talents.” One player needed 22 times more deliberate practice than another player to become a master. © 2014 The Slate Group LLC.
Keyword: Learning & Memory
Link ID: 20136 - Posted: 09.30.2014
By Gary Stix If it’s good for the heart, it could also be good for the neurons, astrocytes and oligodendrocytes, cells that make up the main items on the brain’s parts list. The heart-brain adage comes from epidemiological studies that show that people with cardiovascular risk factors such as high-blood pressure and elevated cholesterol levels, may be more at risk for Alzheimer’s and other dementias. This connection between heart and brain has also led to some disappointments: clinical trials of lipid-lowering statins have not helped patients diagnosed with Alzheimer’s, although epidemiological studies suggest that long-term use of the drugs may help prevent Alzheimer’s and other dementias. The link between head and heart is still being pursued because new Alzheimer’s drugs have failed time and again. One approach that is now drawing some interest looks at the set of proteins that carry around fats in the brain. These lipoproteins could potentially act as molecular sponges that mop up the amyloid-beta peptide that clogs up connections among brain cells in Alzheimer’s. One of these proteins—Apolipoprotein J, also known as clusterin—intrigues researchers because of the way it interacts with amyloid-beta and the status of its gene as a risk factor for Alzheimer’s. A researcher from the University of Minnesota, Ling Li, recently presented preliminary work at the Alzheimer’s Disease Drug Discovery Foundation annual meeting that showed that, at least in a lab dish, a molecule made up of a group of amino acids from APOJ is capable of protecting against the toxicity of the amyloid-beta peptide. It also quelled inflammation and promoted the health of synapses—the junctions where one brain cell encounters another. Earlier work by another group showed that the peptide prevented the development of lesions in the blood vessels of animals.
Link ID: 20135 - Posted: 09.30.2014
by Elijah Wolfson @elijahwolfson The class was the most difficult of the fall 2013 semester, and J.D. Leadam had missed all but one lecture. His grandfather’s health had worsened, and he left San Jose State, where he was studying for a degree in business, to return home to Los Angeles to help out. Before he knew it, midterm exams had almost arrived. At this point, Leadam had, for a while, been playing around with transcranial direct-current stimulation, or tDCS, an experimental treatment for all sorts of health issues that, at its most basic, involves running a very weak electric current through the brain. When he first came across tDCS, Leadam was immediately intrigued but thought, “There’s no way I’m gonna put electrodes on my head. It’s just not going to happen.” After extensive research, though, he changed his mind. He looked into buying a device online, but there wasn’t much available — just one extremely expensive machine and then a bare-bones $40 device that didn’t even have a switch. So he dug around online and figured he could build one himself. He bought all the pieces he needed and put it together. He tried it a few times, but didn’t notice much, so he put it aside. But now, with the test looming, he picked it back up. The professor had written a book, and Leadam knew all the information he’d be tested on was written in its pages. “But I’m an auditory learner,” he said, “so I knew it wouldn’t work to just read it.” He strapped on the device, turned it on and read the chapters. “Nothing,” he thought. But when he got to the classroom and put pen to paper, he had a revelation. “I could remember concepts down to the exact paragraphs in the textbook,” Leadam said. “I actually ended up getting an A on the test. I couldn’t believe it.”
Keyword: Learning & Memory
Link ID: 20130 - Posted: 09.29.2014
By Smitha Mundasad Health reporter, BBC News A spice commonly found in curries may boost the brain's ability to heal itself, according to a report in the journal Stem Cell Research and Therapy. The German study suggests a compound found in turmeric could encourage the growth of nerve cells thought to be part of the brain's repair kit. Scientists say this work, based in rats, may pave the way for future drugs for strokes and Alzheimer's disease. But they say more trials are needed to see whether this applies to humans. Researchers from the Institute of Neuroscience and Medicine in Julich, Germany, studied the effects of aromatic-turmerone - a compound found naturally in turmeric. Rats were injected with the compound and their brains were then scanned. Particular parts of the brain, known to be involved in nerve cell growth, were seen to be more active after the aromatic-turmerone infusion. Scientists say the compound may encourage a proliferation of brain cells. In a separate part of the trial, researchers bathed rodent neural stem cells (NSCs) in different concentrations of aromatic-tumerone extract. NSCs have the ability to transform into any type of brain cell and scientists suggest they could have a role in repair after damage or disease. Dr Maria Adele Rueger, who was part of the research team, said: "In humans and higher developed animals their abilities do not seem to be sufficient to repair the brain but in fish and smaller animals they seem to work well." Picture of the spice turmeric Turmeric belongs to the same plant family as ginger BBC © 2014
By Dick Miller, CBC News Dan Campbell felt the bullets whiz past his head. The tracer rounds zipped between his legs. It was his first firefight as a Canadian soldier in Afghanistan. "I was completely frightened and scared like I’d never been before in my life,” he says. As the attack continued, the sights, sounds and smells started to form memories inside his brain. The fear he felt released the hormone norepinephrine, and in the complex chemistry of the brain, the memories of the battle became associated with the fear. 'I think one day, hopefully in the not-too-distant future, we will be able to delete a memory.'- Dr. Sheena Josselyn, senior scientist, Hospital For Sick Children Research Institute Six years later, a sight or sound such as a firecracker or car backfiring can remind him of that night in 2008. The fear comes back and he relives rather than remembers the moments. "It can be hard. Physically, you know, there’s the tapping foot, my heart beating,” he says. Like so many soldiers and victims of assault or people who have experienced horrific accidents, Campbell was diagnosed with post traumatic stress disorder. Now a newspaper reporter in Yellowknife, Campbell thinks one day he may get therapy. But for now he is working on his own to control the fear and anger the memories bring. © CBC 2014
by Sarah Zielinski Chimps may be cute and have mannerisms similar to humans, but they are wild animals. A new study finds that chimps raised as pets or entertainers have behavioral problems as adults. There are plenty of good reasons why chimpanzees should not be pets or performers, no matter how cute or humanlike they appear: They are wild animals. They can be violent with each other. And they can be violent toward humans — even humans that have a long history with the chimp. Plus, there’s evidence that seeing an adorable chimp dressed up like a miniature human actually makes us care less about the plight of their species. Now comes evidence that the way that chimps are raised to become pets or entertainers — taking them away from other chimps at a young age and putting them in the care of humans, who may or may not feed and care for them properly — has long-term, negative effects on their behavior. “We now add empirical evidence of the potentially negative welfare effects on the chimpanzees themselves as important considerations in the discussion of privately owned chimpanzees,” Hani Freeman and Stephen Ross of the Lincoln Park Zoo in Chicago write September 23 in PeerJ. Freeman and Ross compiled life history and behavioral data on 60 captive chimps living in zoos. Some of the animals had always lived in zoos and grew up in groups of chimpanzees. Six were raised solely by humans and were later placed in zoos after they became too big or too old for their owners to care for them. Others had a more mixed background. © Society for Science & the Public 2000 - 2014
Jia You In the future, a nurse could determine whether a baby is likely to develop a reading disorder simply by attaching a few electrodes to its scalp and watching its brain waves respond to human speech. Such is the scenario suggested by a new study, which finds a potential biological indicator of how well preschool children perceive rhythm, an ability linked to language development. “It’s really impressive to work with children this young, who are not often looked at,” says Aniruddh Patel, a cognitive neuroscientist at Tufts University in Medford, Massachusetts, who was not involved with the research. Spoken language consists of sound waves occurring over multiple timescales. A syllable, for example, takes place over a quarter of a second, while a sentence unfolds over a few seconds. To make sense of this complex auditory information, humans use rhythmic cues such as stress and pause to discern words and syllables. Adults and school-aged children with reading disorders, however, struggle to pick up on these rhythmic patterns. Scientists estimate that dyslexia and other reading disabilities plague about 5% to 10% of the population. Detecting such impairments early could lead to more effective intervention, but observing telltale signs in younger children who have not learned to read has proven a challenge. So biologist Nina Kraus of Northwestern University in Evanston, Illinois, and her colleagues looked for automatic brain responses that can track language development in preschoolers, who have not learned to read. © 2014 American Association for the Advancement of Science
|By Melinda Wenner Moyer Autism is primarily a disorder of the brain, but research suggests that as many as nine out of 10 individuals with the condition also suffer from gastrointestinal problems such as inflammatory bowel disease and “leaky gut.” The latter condition occurs when the intestines become excessively permeable and leak their contents into the bloodstream. Scientists have long wondered whether the composition of bacteria in the intestines, known as the gut microbiome, might be abnormal in people with autism and drive some of these symptoms. Now a spate of new studies supports this notion and suggests that restoring proper microbial balance could alleviate some of the disorder's behavioral symptoms. At the annual meeting of the American Society for Microbiology held in May in Boston, researchers at Arizona State University reported the results of an experiment in which they measured the levels of various microbial by-products in the feces of children with autism and compared them with those found in healthy children. The levels of 50 of these substances, they found, significantly differed between the two groups. And in a 2013 study published in PLOS ONE, Italian researchers reported that, compared with healthy kids, those with autism had altered levels of several intestinal bacterial species, including fewer Bifidobacterium, a group known to promote good intestinal health. One open question is whether these microbial differences drive the development of the condition or are instead a consequence of it. A study published in December 2013 in Cell supports the former idea. When researchers at the California Institute of Technology incited autismlike symptoms in mice using an established paradigm that involved infecting their mothers with a viruslike molecule during pregnancy, they found that after birth, the mice had altered gut bacteria compared with healthy mice. © 2014 Scientific American,
Link ID: 20104 - Posted: 09.23.2014
By Melissa Dahl Recently, I was visiting my family in Seattle, and we were doing that thing families do: retelling old stories. As we talked, a common theme emerged. My brother hardly remembered anything from our childhood, even the stories in which he was the star player. (That time he fell down the basement steps and needed stitches in the ER? Nope. That panicky afternoon when we all thought he’d disappeared, only to discover he’d been hiding in his room, and then fell asleep? Nothing.) “Boys never remember anything,” my mom huffed. She’s right. Researchers are finding some preliminary evidence that women are indeed better at recalling memories, especially autobiographical ones. Girls and women tend to recall these memories faster and with more specific details, and some studies have demonstrated that these memories tend to be more accurate, too, when compared to those of boys and men. And there’s an explanation for this: It could come down to the way parents talk to their daughters, as compared to their sons, when the children are developing memory skills. To understand this apparent gender divide in recalling memories, it helps to start with early childhood—specifically, ages 2 to 6. Whether you knew it or not, during these years, you learned how to form memories, and researchers believe this happens mostly through conversations with others, primarily our parents. These conversations teach us how to tell our own stories, essentially; when a mother asks her child for more details about something that happened that day in school, for example, she is implicitly communicating that these extra details are essential parts to the story. © 2014 The Slate Group LLC
By Maria Konnikova At the turn of the twentieth century, Ivan Pavlov conducted the experiments that turned his last name into an adjective. By playing a sound just before he presented dogs with a snack, he taught them to salivate upon hearing the tone alone, even when no food was offered. That type of learning is now called classical—or Pavlovian—conditioning. Less well known is an experiment that Pavlov was conducting at around the same time: when some unfortunate canines heard the same sound, they were given acid. Just as their luckier counterparts had learned to salivate at the noise, these animals would respond by doing everything in their power to get the imagined acid out of their mouths, each “shaking its head violently, opening its mouth and making movements with its tongue.” For many years, Pavlov’s classical conditioning findings overshadowed the darker version of the same discovery, but, in the nineteen-eighties, the New York University neuroscientist Joseph LeDoux revived the technique to study the fear reflex in rats. LeDoux first taught the rats to associate a certain tone with an electric shock so that they froze upon hearing the tone alone. In essence, the rat had formed a new memory—that the tone signifies pain. He then blunted that memory by playing the tone repeatedly without following it with a shock. After multiple shock-less tones, the animals ceased to be afraid. Now a new generation of researchers is trying to figure out the next logical step: re-creating the same effects within the brain, without deploying a single tone or shock. Is memory formation now understood well enough that memories can be implanted and then removed absent the environmental stimulus?
By Filipa Ioannou Per the Associated Press, the Food and Drug Administration is considering a ban on electric-shock devices that are used to punish unwanted behavior by patients with autism and other developmental disabilities. If it comes as a surprise to you that any involuntary electric shocks are administered to autism patients in the United States, that's because the devices are only used at one facility in the country—the Judge Rotenberg Educational Center in Canton, Mass. The school has been a target of media attention in the past; in 2012, video leaked of 18-year-old patient Andre McCollins being restrained face-down and shocked 31 times. McCollins’ mother sued the center, and the lawsuit was settled outside of court. Rotenberg must get a court’s approval to begin administering skin shocks to a student. The center uses a graduated electronic decelerator, or GED, that is attached to the arms or legs. If the student acts aggressively – head-banging, throwing furniture, attacking someone – then a center worker can press a button to activate the electrode, delivering a two-second shock to the skin. The amount of pain generated by the device is a contentious subject. The Rotenberg Center's Glenda Crookes compared the sensation to “a bee sting” in comments to CBS News, and some Rotenberg parents are strong proponents of the device. But a U.N. official in 2010 said the shocks constituted “torture." An FDA report also addresses the widely held belief that autistic individuals have a high pain threshold, pointing out the possibility that “not all children with ASD express their pain in the same way as a ‘neurotypical child’ would (e.g., cry, moan, seek comfort, etc.), which may lead to misinterpretation by caregivers and medical professionals that patients are insensitive or to an incorrect belief that the child is not in pain.” © 2014 The Slate Group LLC.
By Megan Allison Diagnoses of Attention Hyperactivity Disorder are on the rise. The Centers for Disease Control and Prevention calculated that by 2011, 11 percent of children had been diagnosed with ADHD, and 6.1 percent of all US children were taking an ADHD medication. But could a solution be as simple as exercise? A study published this month in the Journal of Abnormal Child Psychology found that aerobic activity sessions before school helped children with ADHD with their moods and attention spans. The study involved a group of just over 200 students in kindergarten through second grade at schools in Indiana and Vermont. For 12 weeks, the students did 31 minutes of physical activity. The control group participated in classroom activities during this time. Although the results showed that all students showed improvement, authors noted that the exercise especially helped kids with ADHD. “It benefits all the kids, but I definitely see where it helps the kids with ADHD a lot,” said Jill Fritz, a fourth-grade teacher in Jacksonville, Fla. in an interview with The Wall Street Journal. “It really helps them get back on track and get focused.” In the Boston area, Dr. Sarah Sparrow Benes, Program Director of Physical and Health Education Programs at Boston University, teaches elementary and special educators how to use movement as a strategy in their classroom for learning. She finds that all students can benefit from exercise.
By Elizabeth Pennisi "What's for dinner?" The words roll off the tongue without even thinking about it—for adults, at least. But how do humans learn to speak as children? Now, a new study in mice shows how a gene, called FOXP2, implicated in a language disorder may have changed between humans and chimps to make learning to speak possible—or at least a little easier. As a uniquely human trait, language has long baffled evolutionary biologists. Not until FOXP2 was linked to a genetic disorder that caused problems in forming words could they even begin to study language’s roots in our genes. Soon after that discovery, a team at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, discovered that just two bases, the letters that make up DNA, distinguished the human and chimp versions of FOXP2. To try to determine how those changes influenced the gene's function, that group put the human version of the gene in mice. In 2009, they observed that these "humanized" mice produced more frequent and complex alarm calls, suggesting the human mutations may have been involved in the evolution of more complex speech. Another study showed that humanized mice have different activity in the part of the brain called the striatum, which is involved in learning, among other tasks. But the details of how the human FOXP2 mutations might affect real-world learning remained murky. To solve the mystery, the Max Planck researchers sent graduate student Christiane Schreiweis to work with Ann Graybiel, a neuroscientist at the Massachusetts Institute of Technology in Cambridge. She's an expert in testing mouse smarts by seeing how quickly they can learn to find rewards in mazes. © 2014 American Association for the Advancement of Science
By Linda Searing THE QUESTION Benzodiazepines such as Valium, Xanax and Ativan, widely prescribed to relieve anxiety and alleviate insomnia, are known to affect memory and cognition in the short term. Might they also have a more serious, longer-term effect on the brain? THIS STUDY analyzed data on 8,990 adults older than 66, including 1,796 with Alzheimer’s disease. In a five-to-10-year span before the start of the study, 3,767 of the participants (52 percent) had taken benzodiazepines. Overall, those who had taken the drugs were 51 percent more likely to have Alzheimer’s than were those who had never taken benzodiazepines. The longer people took the drugs, the greater their risk for Alzheimer’s. Those who took the drugs for less than 90 days had essentially the same risk as those who never took them. But risk nearly doubled for people who took them for longer than six months. Risk also was greater for longer-acting vs. shorter-acting benzodiazepines. WHO MAY BE AFFECTED? Adults, especially older people, who take benzodiazepines. The drugs have a calming effect on the body and work quickly, unlike antidepressants, which can take weeks to have an effect. The American Geriatrics Society lists benzodiazepines as inappropriate for treating older people for insomnia or agitation because of their negative effect on cognition seen in that age group and an increased likelihood of falls and accidents. However, some recent estimates note that roughly half of older adults take benzodiazepines. CAVEATS Some study participants may have been prescribed benzodiazepines to treat early symptoms of unrecognized dementia, which can include depression, anxiety and sleep disorders; the study authors noted that use of the drugs “might be an early marker of a condition associated with an increased risk of dementia and not the cause.”
By ANDREW POLLACK New York State’s attorney general filed an antitrust lawsuit on Monday seeking to stop a pharmaceutical company from forcing patients with Alzheimer’s disease to switch to a new version of a widely used drug. The lawsuit contends that the switch is designed to blunt competition from low-priced generic versions of the medication. Forest Laboratories, now owned by Actavis, announced in February that it would stop selling the existing tablet form of the drug, Namenda, in favor of new extended-release capsules called Namenda XR that can be taken once a day instead of twice. While the company said that patients preferred the newer drug, it has made little secret of its desire to switch all patients to the newer form, which has a longer patent life, before the old tablets face generic competition in July. The strategy would make it much harder for the generics to gain traction. The lawsuit, filed in Federal District Court in Manhattan, says the step is an illegal attempt by Forest to maintain its monopoly even after its patent expires. “A drug company manipulating vulnerable patients and forcing physicians to alter treatment plans unnecessarily, simply to protect corporate profits, is unethical and illegal,” the attorney general, Eric T. Schneiderman, said in a statement. A spokesman for Actavis said the company did not comment on pending litigation as a matter of policy. The company said that the once-a-day drug had “significant advantages” for patients and their caregivers. The lawsuit argues that the benefit of switching is not very great. It says the company decided to force the switch because it feared that not enough patients would switch voluntarily. © 2014 The New York Times Company
Link ID: 20078 - Posted: 09.16.2014
by Michael Slezak It's one of the biggest mysteries of Alzheimer's. The disease is associated with the formation of protein plaques in the brain, but why is it that some people with plaques seem not to have the disease? Research suggests that some people's brains are able to reorganise during the early stages of Alzheimer's, delaying the appearance of initial symptoms. The plaques in question are small mounds of a protein called beta-amyloid, and are found in the brains of people with Alzheimer's disease. Whether these plaques are a cause of the disease has been hotly debated. One reason for doubt is the appearance of plaques in many older people who have no symptoms Movie Cameraof dementia at all. Using fMRI to measure changes in blood flow around the brain, William Jagust from the University of California in Berkley and colleagues compared brain function in three groups of people without symptoms of dementia: 22 young people, 16 older people with beta-amyloid plaques and 33 older people without the plaques. He asked each of them to memorise a photographed scene while inside the machine. Jagust found that older people with plaques had increased blood flow – which means stronger activation of that brain area – in the regions of the brain that are usually activated during memory formation, compared with the older people who did not have plaques. The team then analysed whether this extra brain activation might be helping to compensate for the plaques. © Copyright Reed Business Information Ltd.
by Simon Makin Talking in your sleep might be annoying, but listening may yet prove useful. Researchers have shown that sleeping brains not only recognise words, but can also categorise them and respond in a previously defined way. This could one day help us learn more efficiently. Sleep appears to render most of us dead to the world, our senses temporarily suspended, but sleep researchers know this is a misleading impression. For instance, a study published in 2012 showed that sleeping people can learn to associate specific sounds and smells. Other work has demonstrated that presenting sounds or smells during sleep boosts performance on memory tasks – providing the sensory cues were also present during the initial learning. Now it seems the capabilities of sleeping brains stretch even further. A team led by Sid Kouider from the Ecole Normale Supérieur in Paris trained 18 volunteers to classify spoken words as either animal or object by pressing buttons with their right or left hand. Brain activity was recorded using EEG, allowing the researchers to measure the telltale spikes in activity that indicate the volunteers were preparing to move one of their hands. Since each hand is controlled by the motor cortex on the opposite side of the brain, these brainwaves can be matched to the intended hand just by looking at which side of the motor cortex is active. © Copyright Reed Business Information Ltd.
David Cyranoski A Japanese patient with a debilitating eye disease is about to become the first person to be treated with induced pluripotent stem cells, which have generated enthusiastic expectations and earned their inventor a Nobel Prize. A health-ministry committee has vetted researchers' safety tests and cleared the team to begin the experimental procedure. Masayo Takahashi, an ophthalmologist at the RIKEN Center for Developmental Biology (CDB) in Kobe, has been using induced pluripotent stem (iPS) cells to prepare a treatment for age-related macular degeneration. Unlike embryonic stem cells, iPS cells are produced from adult cells, so they can be genetically tailored to each recipient. They are capable of becoming any cell type in the body, and have the potential to treat a wide range of diseases. The CDB trial will be the first opportunity for the technology to prove its clinical value. In age-related macular degeneration, extra blood vessels form in the eye, destabilizing a supportive base layer of the retina known as the retinal pigment epithelium. This results in the loss of the light-sensitive photoreceptors that are anchored in the epithelium, and often leads to blindness. Takahashi took skin cells from people with the disease and converted them to iPS cells. She then coaxed these cells to become retinal pigment epithelium cells, and then to grow into thin sheets that can be transplanted to the damaged retina. Takahashi and her collaborators have shown in monkey studies1 that iPS cells generated from the recipients' own cells do not provoke an immune reaction that causes them to be rejected. There have been concerns that iPS cells could cause tumours, but Takahashi's team has found that to be unlikely in mice2 and monkeys1. © 2014 Nature Publishing Group