Chapter 13. Memory, Learning, and Development
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By Emilie Reas Think back to your first childhood beach vacation. Can you recall the color of your bathing suit, the softness of the sand, or the excitement of your first swim in the ocean? Early memories such as this often arise as faded snapshots, remarkably distinct from newer memories that can feel as real as the present moment. With time, memories not only lose their rich vividness, but they can also become distorted, as our true experiences tango with a fictional past. The brain’s ability to preserve or alter memories lies at the heart of our basic human experience. The you of today is molded not only by your personal history, but also by your mental visits to that past, prompting you to laugh over a joke heard yesterday, reminisce about an old friend or cringe at the thought of your awkward adolescence. When we lose those pieces of the past we lose pieces of our identity. But just where in the brain do those old memories go? Despite decades studying how the brain transforms memories over time, neuroscientists remain surprisingly divided over the answer. Some of the best clues as to how the brain processes memories have come from patients who can’t remember. If damage to a particular brain area results in memory loss, researchers can be confident that the region is important for making or recalling memories. Such studies have reliably shown that damage to the hippocampus, a region nestled deep inside the brain, prevents people from creating new memories. But a key question, still open to debate, is what happens to a memory after it’s made. Does it stay in the hippocampus or move out to other areas of the brain? To answer this, scientists have studied old memories formed before brain damage, only to discover a mix of inconsistent findings that have given rise to competing theories. © 2013 Scientific American
Keyword: Learning & Memory
Link ID: 18792 - Posted: 10.16.2013
By SINDYA N. BHANOO Hungry babies instinctively open their mouths as their mother’s breast or a bottle draws near. Now, researchers from England and France report that this instinct — the anticipation of touch — is a skill fetuses teach themselves in the womb. Studying scans at monthly intervals between 24 and 36 weeks of pregnancy, the scientists found that the youngest fetuses were more likely to touch their heads and that as they matured, they began to touch their mouths more. And by 36 weeks, the fetuses began to open their mouths before they touched them. The anticipation of touch is a skill a baby uses during feeding, said Nadja Reissland, a psychologist at Durham University in England, who reports the findings along with colleagues in the journal Developmental Psychobiology. “We can’t say it’s a precursor to feeding, but it’s one element of feeding,” she said. “You actually need to open your mouth in order to feed.” Premature babies may not have fully grasped this skill, Dr. Reissland said. The study could provide more information about what premature babies can do and what special care they need. “The fetus might actually be learning the limits of its body, the texture of the body and what it feels like to be a person in the womb,” she said. © 2013 The New York Times Company
Keyword: Development of the Brain
Link ID: 18786 - Posted: 10.15.2013
By JANE E. BRODY Fifty years ago, a revolution began in neonatal care that has preserved the physical and mental health, and often the lives, of thousands of babies: screening of newborns for inherited and congenital disorders. On Oct. 15, 1963, the first law requiring that all newborns be screened for phenylketonuria, or PKU, took effect in Massachusetts. PKU, an inherited metabolic disorder, afflicts one in 20,000 of the four million babies born each year in the United States. Children with PKU are missing an enzyme that converts the amino acid phenylalanine to tyrosine, and unless they remain on a special protein-restricted diet, the resulting buildup of phenylketone damages the brain and causes mental retardation and physical disabilities. Today every state tests babies at birth for PKU — and not just that. There are now more than 50 disorders that can be picked up through screening, 31 of which comprise the “core conditions” of the government’s Recommended Uniform Screening Panel. Other conditions are likely to be added to the panel in the future. All but two of them — hearing loss and critical congenital heart disease — can be detected by automated analysis of a few drops of dried blood from a heel stick done within a few days of birth. Giana Swift, a fifth grader in Sherman Oaks, Calif., was one of more than 12,500 babies who benefit from newborn screening each year. The story of her birth in October 2002 was recounted in The Times. Through a pilot screening program, Giana was found to have an inherited metabolic disorder called 3-MCC (3-methylcrotonyl-CoA carboxylase deficiency). It afflicts about 100 babies a year, rendering them unable to process the amino acid leucine. As with PKU, toxic byproducts of the unprocessed amino acid build up in the blood and damage the brain. Because she was tested at birth, Giana thrived, first on a special leucine-free baby formula, then on a diet nearly free of protein. Her grateful father, David Swift, 44, recently described Giana as “very bright, precocious, happy and a top athlete.” Copyright 2013 The New York Times Company
Kashmira Gander A team in Bristol have created an implant that encourages cells damaged by the disease to grow again. It does this through a system of tubes and catheters that pump proteins into patients’ brain once a month, potentially stopping the disease from progressing by encouraging the damaged cells to grow again. The port located behind a patient’s ear releases a protein called glial cell line-derived neurotrophic factor (GDNF). Six patients at Frenchay Hospital, Bristol, have trialled the system, and doctors are now looking for another 36 to help them continue their research. Dr Kieran Breen, director of research and innovation at Parkinson's UK, said: “For years, the potential of GDNF as a treatment for Parkinson's has remained one of the great unanswered research questions. ”This new study will take us one step closer to finally answering this question once and for all. “We believe GDNF could have the potential to unlock a new approach for treating Parkinson's that may be able to slow down and ultimately stop the progression of the condition all together. ”Currently there are very few treatments available for people with Parkinson's and none capable of stopping the condition from advancing.“ More than 127,000 people in the UK currently have the disease, which is caused when nerve cells in the brain die due to a lack of the chemical dopamine. Symptoms include slowness of movement, stiffness and tremors. © independent.co.uk
by Laura Sanders After Baby V joined our team, one of the first things people would ask is, “Are you getting any sleep?” (The answer was, and is, no.) The recurring question highlights how sorely lacking sleep is for new parents. Capitalism noticed us tired parents, too: Countless products beckon exhausted families with promises of eight, 10, even 12 hours of blissful, uninterrupted sleep. You can buy special swaddles, white noise machines, swings that sway like a moving car and books upon books that whisper contradictory secrets of how to get your baby to sleep through the night. (If you don’t have time to read them all, mother-of-twins Ava Neyer helpfully breaks down all of the advice for you.) As the owner of a stack of such books, I was intrigued by this recent review: “Behavioral sleep interventions in the first six months of life do not improve outcomes for mothers or infants: A systematic review.” Excuse me? The Sleep Sheep, the Baby Whisperer and the Sleep Lady lied to me? At the behest of the United Kingdom’s National Institute for Health Research, Australians Pamela Douglas and Peter Hill combed through the existing scientific literature on sleep interventions looking for benefits. These interventions included delaying responses to infant cues (also known by its cold-hearted name of “crying it out”), sticking to a feeding or sleeping schedule and other ways that aim to teach a baby how to fall asleep without the need to eat or be held. After analyzing 43 studies on infant sleep interventions, the team concluded that these methods weren’t beneficial for babies younger than six months, or their mothers. The studies didn’t convincingly show that interventions curb infant crying, prevent sleep or behavioral problems later or protect against maternal depression, Douglas and Hill write in the September Journal of Developmental & Behavioral Pediatrics. © Society for Science & the Public 2000 - 2013.
Children whose mothers are depressed during pregnancy have a small increased risk of depression in adulthood, according to a UK study. Medical treatment during pregnancy could lower the risk of future mental health problems in the child, say researchers at Bristol University. The study followed the offspring of more than 8,000 mothers who had postnatal or antenatal depression. The risk is around 1.3 times higher than normal at age 18, it found. The study is published in JAMA Psychiatry. Lead researcher Dr Rebecca Pearson told the BBC: "Depression in pregnancy should be taken seriously and treated in pregnancy. It looks like there is a long-term risk to the child, although it is small." She said it was an association, not a causal link, and needed further investigation. Prof Carmine Pariante of King's College London's Institute of Psychiatry said the development of an individual's mental health did not start at birth but in the uterus. "The message is clear - helping women who are depressed in pregnancy will not only alleviate their suffering but also the suffering of the next generation." Prof Celso Arango of Gregorio Maranon General University Hospital, Madrid, said stress hormones may affect the child's development in the womb. "Women with depression would ideally be treated before getting pregnant, but if they are already pregnant when diagnosed with depression it is even more important that they are treated as it will impact on the mother and child." The researchers think different factors may be involved in antenatal and postnatal depression, with environmental factors such as social support having a bigger impact in postnatal depression. BBC © 2013
Charlie Cooper Scientists have hailed an historic “turning point” in the search for a medicine that could beat Alzheimer's disease, after a drug-like compound was used to halt brain cell death in mice for the first time. Although the prospect of a pill for Alzheimer's remains a long way off, the landmark British study provides a major new pathway for future drug treatments. The compound works by blocking a faulty signal in brains affected by neurodegenerative diseases, which shuts down the production of essential proteins, leading to brain cells being unprotected and dying off. It was tested in mice with prion disease - the best animal model of human neurodegenerative disorders - but scientists said they were confident the same principles would apply in a human brain with debilitating brain diseases such as Alzheimer's or Parkinson's. The study, published today in the journal Science Translational Medicine, was carried out at the Medical Research Council's (MRC) Toxicology Unit at the University of Leicester. “It's a real step forward,” team leader Professor Giovanna Mallucci told The Independent. “It's the first time a substance has been given to mice that prevents brain disease. The fact that this is a compound that can be given orally, that gets into the brain and prevents brain disease, is a first in itself… We can go forward and develop better molecules and I can't see why preventing this process should only be restricted to mice. I think this probably will translate into other mammalian brains.” © independent.co.uk
Link ID: 18775 - Posted: 10.10.2013
By MICHAEL TORTORELLO SONOMA, Calif. — Here is a truth about children with autism: they grow up to become adults with autism. Advocates estimate that over the next decade some 500,000 such individuals will come of age in the United States. No one can say for sure what adulthood will hold for them. To start, where will everyone live and work? A 2008 Easter Seals study found that 79 percent of young adults with autism spectrum disorders continue to reside with their parents. A solid majority of them have never looked for a job. And yet the life expectancy of people with autism is more or less average. Here is another truth, then, about children with autism: they can’t stay at home forever. This realization — as obvious as it is worrying — has recently stirred the beginnings of a response from researchers, architects and, not least, parents. In 2009, a pair of academics, Kim Steele and Sherry Ahrentzen, collaborated on “Advancing Full Spectrum Housing,” a comprehensive design guideline for housing adults with autism. (An expanded book on the topic is scheduled to come out next year.) Perhaps the first development to closely follow their template is Sweetwater Spectrum, a residence for 16 adults whose abilities and disabilities span the full range of autism. The innovative $10.4 million project opened in January in the heart of California wine country, and its founding families and board hope to make Sweetwater a model for like-minded experiments across the country. “You hear about different organizations planning to do these things,” said Dr. Ahrentzen, a professor in the Shimberg Center for Housing Studies at the University of Florida, in Gainesville. But “it takes time to get all these different funding sources in place.” © 2013 The New York Times Company
Link ID: 18774 - Posted: 10.10.2013
By Scott Barry Kaufman Brain training: yay or nay? It’s not so simple. As we all know, people differ quite a bit from one another in how much information they can maintain, manipulate, and transform in their heads at one time. Crucially, these differences relate to important outcomes, such as abstract reasoning, academic performance, reading comprehension, and the acquisition of new skills. The most consistent and least controversial finding in the literature is that working memory training programs produce reliable short-term improvements in both verbal and visuospatial working memory skills. On average, the effect sizes range from moderate to large, although the long-term sustainability of these effects is much more ambiguous. These effects are called near transfer effects, because they don’t transfer very far beyond the trained domain of cognitive functioning. What are far more controversial (and far more interesting) are far transfer effects. One particular class of far transfer effects that cognitive psychologists are particularly interested in are those that show increases in fluid intelligence: the deliberate but flexible control of attention to solve novel “on the spot” problems that cannot be perfomed by relying exclusively on previously learned habits, schemas, and scripts. Here is where we enter the swamp. Some studies have reported absolutely no effect of working memory training on fluid intelligence, whereas others have found an effect. The results are mixed and inconclusive. Various critics have rightfully listed a number of methodological flaws and alternative explanations that could explain the far transfer effects. © 2013 Scientific American
Keyword: Learning & Memory
Link ID: 18773 - Posted: 10.10.2013
by Bruce Bower Babies may start to learn their mother tongues even before seeing their mothers’ faces. Newborns react differently to native and foreign vowel sounds, suggesting that language learning begins in the womb, researchers say. Infants tested seven to 75 hours after birth treated spoken variants of a vowel sound in their home language as similar, evidence that newborns regard these sounds as members of a common category, say psychologist Christine Moon of Pacific Lutheran University in Tacoma, Wash., and her colleagues. Newborns deemed different versions of a foreign vowel sound to be dissimilar and unfamiliar, the scientists report in an upcoming Acta Paediatrica. “It seems that there is some prenatal learning of speech sounds, but we do not yet know how much,” Moon says. Fetuses can hear outside sounds by about 10 weeks before birth. Until now, evidence suggested that prenatal learning was restricted to the melody, rhythm and loudness of voices (SN: 12/5/09, p. 14). Earlier investigations established that 6-month-olds group native but not foreign vowel sounds into categories. Moon and colleagues propose that, in the last couple months of gestation, babies monitor at least some vowels — the loudest and most expressive speech sounds — uttered by their mothers. © Society for Science & the Public 2000 - 2013
By Helen Briggs BBC News The brain has a critical window for language development between the ages of two and four, brain scans suggest. Environmental influences have their biggest impact before the age of four, as the brain's wiring develops to process new words, say UK and US scientists. The research in The Journal of Neuroscience suggests disorders causing language delay should be tackled early. It also explains why young children are good at learning two languages. The scientists, based at King's College London, and Brown University, Rhode Island, studied 108 children with normal brain development between the ages of one and six. They used brain scans to look at myelin - the insulation that develops from birth within the circuitry of the brain. To their surprise, they found the distribution of myelin is fixed from the age of four, suggesting the brain is most plastic in very early life. Any environmental influences on brain development will be strongest in infanthood, they predict. This explains why immersing children in a bilingual environment before the age of four gives them the best chance of becoming fluent in both languages, the research suggests. BBC © 2013
Alison Abbott In a sign that psychiatric-disease research is entering a new era, the pharmaceutical giant Novartis has hired an expert in neural circuitry, rather than pharmacology, to head its relaunched neuroscience division. The appointment of 42-year-old Ricardo Dolmetsch, who has spent his entire career in academic research, signifies a radical policy shift for the company, as it moves away from conventional neurotransmitter research to concentrate on analysing the neural circuitry that causes brain diseases. The decision suggests Novartis is confident that after years of fruitless research in the field, revolutionary advancements in, for example, genetic and stem-cell technologies will pay dividends. The company intends to hire 100 new staff members for the department over the next 3 years. But the move is risky: even if it pans out, new drugs for common disorders such as schizophrenia could be decades away from reaching the market. Dolmetsch, a former senior director at the Allen Institute for brain Science in Seattle, Washington, who has also worked at Stanford University School of Medicine in California, says that his new role gives him access to previously unimaginable resources. “I had this idea that big pharma was a slow, plodding, conservative giant,” he says. “I was surprised by the depth of science at Novartis.” An expert in autism spectrum disorder, he was also attracted by the prospect of contributing to the development of therapies — something that academic institutions are poorly equipped to do — particularly because one of his own sons has autism. There was “not much enthusiasm” for studying disease at the Allen Institute, which focuses instead on basic research into brain science, he says. © 2013 Nature Publishing Group
by Linda Geddes There's little doubt that smoking during pregnancy is bad for the baby. But besides stunting growth and boosting the risk of premature birth, it seems that tobacco smoke leaves a lasting legacy on the brain. Children whose mothers smoked during pregnancy have altered brain growth, which may put them at greater risk of anxiety and depression. Hanan El Marroun at Erasmus Medical Center in Rotterdam, the Netherlands, and her colleagues had previously seen impaired brain growth in babies born to women who smoked throughout their pregnancy, although no differences were seen if women stopped smoking soon after learning that they were pregnant. The question was whether these changes were permanent, or would correct themselves as the child developed. So El Marroun's team used MRI to look at the brains of 113 children aged between 6 and 8 years old whose mothers smoked during pregnancy, and another 113 children whose mums did not. The children's behavioural and emotional functioning was also tested. Depression link Those whose mothers smoked throughout pregnancy had smaller total brain volumes and reduced amounts of grey and white matter in the superior frontal cortex, an area involved in regulating moods. What's more, these structural differences correlated with symptoms of depression and anxiety in the children. Not every child whose mother smoked showed these symptoms, and the study could not definitively prove cause and effect. However, because we already know that smoking is bad for babies, pregnant women should continue to be advised not to smoke, El Marroun says. © Copyright Reed Business Information Ltd.
By Scicurious When most of us hear birds twittering away in the trees, we hear it as background noise. It’s often hard to separate out one bird from another. But when you can, you begin to hear just how complex birdsong can be, a complex way of male signaling to a female how THEY are the best, and THEY are the one they should clearly pick. You hear ups and downs and trills and repeating themes. We used to think that birdsong was a relatively simple gene by environment interaction. The big males with the big songs get the best females, and then it’s a matter of also getting the best food, and the then healthy bird teaches its offspring to sing, and the health offspring goes on to display the best song. The song is therefore an “honest signal” of the bird’s fitness, it’s got good genes and good food and it is ready to MATE, baby! But how much of it is really training and how much is genetic? To find out, we go to what may possibly be the cutest of research subjects…the zebra finch. To look at the relationship between genes and environment in song learning, the authors turned to the zebra finch. Many other studies have also looked at the zebra finch and how it learns song, and how environmental pressures (like say, not enough food) change the way the song is displayed. But those experiments usually bred the birds and looked at the environment…they didn’t look at the teachers. The father birds, who were “teaching” their offspring to sing. © 2013 Scientific American
By Rebecca Lanning, Everywhere I went, people asked me about my son Will. They knew he’d graduated from high school, and they wanted to know what he was doing. Smiling politely, I told them that Will had been accepted to his first-choice college. But, I always added — in case someone saw him around town — that he had deferred enrollment. He was taking a gap year, I’d say. “So what’s your son doing with his windfall of free time? Traveling abroad? Doing research?” My cheeks burned as I played along, offering sound bites. A start-up venture. A film project. Independent study. Anything to avoid the truth: that my handsome, broad-shouldered son was, probably, at that very moment, home in bed with the shutters drawn, covers pulled over his head. Officially, Will was taking a gap year. But after 13 years of school, what he needed, what he’d earned, was a nap year. Will has long suffered from learning difficulties. It took years to pinpoint a diagnosis — and even when we did, figuring out how to manage it wasn’t easy. He needed a break. So did I. Will’s problems began to surface when he was in kindergarten. “He’s not where the other children are,” his teacher whispered to me one morning. I knew what she meant. Clumsy and slow to read, Will rested his head on his desk a lot. His written work, smudgy from excessive erasing, looked like bits of crumpled trash. School was torture for Will. He couldn’t take notes, failed to turn in homework, forgot when tests were coming up. Yet on standardized tests, his verbal scores consistently exceeded the 99th percentile. I wondered why he struggled, when clearly he was bright. © 1996-2013 The Washington Post
by Linda Geddes They are identical in almost every way, except one twin is fat and the other is thin. Now a study of this rare group is shedding light on a medical mystery: how some people can be obese and perfectly healthy. Obesity usually goes hand in hand with metabolic syndrome – high blood pressure, high cholesterol and type 2 diabetes – but a minority of obese people escape this fate. To probe the fit fat phenomenon, Jussi Naukkarinen at the University of Helsinki in Finland and his colleagues turned to a registry of identical twins, picking 16 pairs whose body weight differed by 17 kilograms on average. They are a perfect model for studying such differences because they are genetically identical and have usually been raised in very similar environments. Naukkarinen's team started by looking at the siblings' body fat distribution and quickly saw that the fat twins fell into two groups: those that tended to accumulate fat within their livers, and those whose liver fat resembled that of their thin twin. Suppressed activity Next, they looked at other markers of ill-health, including insulin resistance, cholesterol, inflammation and blood pressure. These measures also divided the group. "Basically all the hallmarks of the metabolic syndrome were lacking in the group where there was no liver fat," Naukkarinen says. Researchers also compared samples of the twins' abdominal fat, or adipose tissue. In unhealthy obese twins, genes involved in inflammation were activated – genes that were not activated in their thin twin. The activity of cellular powerhouses called mitochondria seemed to be suppressed as well. But in healthy obese twins, gene expression was similar to that of the thin twin. © Copyright Reed Business Information Ltd.
By John Horgan Last spring, I kicked up a kerfuffle by proposing that research on race and intelligence, given its potential for exacerbating discrimination, should be banned. Now Nature has expanded this debate with “Taboo Genetics.” The article “looks at four controversial areas of behavioral genetics”—intelligence, race, violence and sexuality—”to find out why each field has been a flashpoint, and whether there are sound scientific reasons for pursuing such studies.” Behavioral genetics has failed to produce robust evidence linking complex traits and disorders to specific genes. The essay provides a solid overview, including input from both defenders of behavioral genetics and critics. The author, Erika Check Hayden, quotes me saying that research on race and intelligence too often bolsters “racist ideas about the inferiority of certain groups, which plays into racist policies.” I only wish that Hayden had repeated my broader complaint against behavioral genetics, which attempts to explain human behavior in genetic terms. The field, which I’ve been following since the late 1980s, has a horrendous track record. My concerns about the potential for abuse of behavioral genetics are directly related to its history of widely publicized, erroneous claims. I like to call behavioral genetics “gene whiz science,” because “advances” so often conform to the same pattern. Researchers, or gene-whizzers, announce: There’s a gene that makes you gay! That makes you super-smart! That makes you believe in God! That makes you vote for Barney Frank! The media and the public collectively exclaim, “Gee whiz!” © 2013 Scientific American
The discovery of "missing" genes could help scientists understand how autism develops, a study suggests. US researchers looked at the genetic profiles of more than 431 people with an autistic spectrum disorder (ASD) and 379 without. They found those with an ASD were more likely to have just one copy of certain genes, when they should have had two. UK experts said genetic factors were one promising area of research into the causes of autism. About 1% of the population has an ASD. They can run in families - but scientists have not identified a cause. Gene deletions or additions happen in everyone - it is why people are different. It is which genes are affected that determines what the effect is. 'Mis-wiring' There were far more gene deletions in the ASD group, and they were more likely to have multiple deletions. Writing in the American Journal of Human Genetics, the team from Mount Sinai suggests this "mis-wiring" could alter the activity of nerve cells in the brain. Prof Joseph Buxbaum, who led the research team, said: "This is the first finding that small deletions impacting one or two genes appear to be common in autism, and that these deletions contribute to risk of development of this disorder." BBC © 2013
Figuring out the next 99,999,999,900 neurons “We have a hundred billion neurons in each human brain,” said Nicholas Spitzer, a neurobiologist and co-director of the Kavli Institute for Brain and Mind at the University of California-San Diego (which is partnering with The Atlantic on this event). “Right now, the best we can do is to record the electrical activity of maybe a few hundred of those neurons. Gee, that’s not very impressive.” Spitzer and his team are trying to figure out what’s going on in the rest of those neurons, or brain cells – specifically, what "jobs" they have in the body. But first, a bit of Neuroscience 101: “As your readers may know, the nerve cells or neurons in the brain communicate with each other through the release of chemicals, called neurotransmitters,” Spitzer said. “This allows a motor neuron that makes a muscle contract signal to the muscle to say, ‘time to contract.’ It seems like kind of a clumsy way to organize a signaling system.” But sometimes, those neurons change "jobs" – a motor neuron might start signaling another function in the body, for example. "These issues have their origins in the Greek and Roman and Chinese philosophers." “We thought for a long time that the wiring of the brain was a little bit like the wiring of some sort of electronic device in that the connection of the wires in the ‘device,’ the brain, are fairly fixed. What we’re finding is that the wires can remain in place, but the function of the circuit and the connection of the wires can change,” Spitzer said. “This is something of a heresy.” © 2013 by The Atlantic Monthly Group
Intelligence tests were first devised in the early twentieth century as a way to identify children who needed extra help in school. It was only later that the growing eugenics movement began to promote use of the tests to weed out the less intelligent and eliminate them from society, sparking a debate over the appropriateness of the study of intelligence that carries on to this day. But it was not the research that was problematic: it was the intended use of the results. As the News Feature on page 26 details, this history is never far from the minds of scientists who work in the most fraught areas of behavioural genetics. Although the ability to investigate the genetic factors that underlie the heritability of traits such as intelligence, violent behaviour, race and sexual orientation is new, arguments and attitudes about the significance of these traits are not. Scientists have a responsibility to do what they can to prevent abuses of their work, including the way it is communicated. Here are some pointers. First: be patient. Do not speculate about the possibility of finding certain results, or about the implications of those results, before your data have even been analysed. The BGI Cognitive Genomics group in Shenzhen, China, is studying thousands of people to find genes that underlie intelligence, but group members sparked a furore by predicting that studies such as theirs could one day let parents select embryos with genetic predispositions to high intelligence. Many other geneticists are sceptical that the project will even find genes linked to this trait. © 2013 Nature Publishing Group