Chapter 13. Memory, Learning, and Development
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Ian Sample, science correspondent Children born to fathers over the age of 45 are at greater risk of developing psychiatric problems and more likely to struggle at school, according to the findings of a large-scale study. The research found that children with older fathers were more often diagnosed with disorders such as autism, psychosis, attention deficit hyperactivity disorder (ADHD), schizophrenia and bipolar disorder. They also reported more drug abuse and suicide attempts, researchers said. The children's difficulties seemed to affect school performance, leading to worse grades at the age of 15 and fewer years in education overall. "We were shocked when we saw the comparisons," said Brian D'Onofrio, the first author of the study at Indiana University in the US. But he added that it was impossible to be sure that older age was to blame for the problems. Scientists have reported links between fathers' age and children's cognitive performance and health before but this study suggests the risks may be more serious than previously thought. The increased risks might be caused by genetic mutations that build up in sperm as men age. Researchers at Indiana University and the Karolinska Institute in Stockholm studied medical and educational records of more than 2.6 million babies born to 1.4 million men. The group amounted to nearly 90% of births in Sweden from 1973 and 2001. Using the records, the scientists added up diagnoses for psychiatric disorders and educational achievements and compared the figures for children born to fathers of different ages. © 2014 Guardian News and Media Limited
by Emily Sohn Immediately after birth on many dairy farms, baby cows are separated from their mothers and housed in their own pens to protect them from getting sick. Two months later, they join the herd. But early-life isolation may be depriving baby cows of the opportunity to reach their full potential, found a new study. Compared to calves raised in pairs, isolated calves were much slower to learn new things and had a harder time adapting to changes in their environment. Aside from animal welfare concerns, the new findings suggest that dairy farmers have long been overlooking the brain development of their cows by depriving them of social interaction in their early weeks. “Imagine I said that instead of sending your child to kindergarten, I could put him in the classroom one-on-one with the teacher and all the same resources,” said Daniel Weary, a professor of animal welfare and dairy science at the University of British Columbia in Vancouver. “But at the end of the day, if we found that individuals in this system were showing cognitive deficits in relation to other individuals, we would feel bad about that.” For cows, he said, “it means we’re not keeping these animals in an environment that allows them to be what they can be and should be.” © 2014 Discovery Communications, LLC
Keyword: Development of the Brain
Link ID: 19298 - Posted: 02.27.2014
On 24 February, Uganda’s president, Yoweri Museveni, signed a draconian Anti-Homosexuality Bill into law, after 2 months of declining to do so. Science, he says, changed his mind—in particular, the findings of a special scientific committee his Health Ministry had appointed earlier in the month. “Their unanimous conclusion was that homosexuality, contrary to my earlier thinking, was behavioural and not genetic,” Museveni wrote to President Barack Obama on 18 February, in response to Obama’s pleas that he not sign the bill. “It was learnt and could be unlearnt.” But some scientists on the committee are crying foul, saying that Museveni and his ruling party—Uganda’s National Resistance Movement (NRM)—misrepresented their findings. “They misquoted our report,” says Paul Bangirana, a clinical psychologist at Makerere University in Kampala. “The report does not state anywhere that homosexuality is not genetic, and we did not say that it could be unlearnt.” Two other committee members have now resigned to protest the use of their report to justify the harsh legislation, which mandates life imprisonment for “aggravated homosexuality,” such as sexual acts with a minor, and prison terms of 7 to 14 years for attempted and actual homosexual acts, respectively. The law was first introduced into Uganda’s Parliament in 2009, but withdrawn after widespread objections to provisions that could have included the death penalty. As he signed the new version, passed by Parliament last 20 December, Museveni claimed that “mercenaries” were recruiting young people into gay activities. © 2014 American Association for the Advancement of Science
|By Beth Skwarecki Prions, the protein family notorious for causing "mad cow" and neurodegenerative diseases like Parkinson's, can play an important role in healthy cells. "Do you think God created prions just to kill?" mused Nobel laureate Eric Kandel. "These things must have evolved initially to have a physiological function." His work on memory helped reveal that animals make and use prions in their nervous systems as part of an essential function: stabilizing the synapses that constitute long-term memories. These natural prions aren't infectious but on a molecular level they chain up exactly the same way as their disease-causing brethren. (Some researchers call them "prionlike" to avoid confusion.) This week, work from neuroscientist Kausik Si of the Stowers Institute for Medical Research, one of Kandel's former students, shows that the prion's action is tightly controlled by the cell, and can be turned on when a new long-term memory needs to be formed. Prions are proteins with two unusual properties: First, they can switch between two possible shapes, one that is stable on its own and an alternate conformation that can form chains. Second, the chain-forming version has to be able to trigger others to change shape and join the chain. Say that in the normal version the protein is folded so that one portion of the protein structure—call it "tab A"—fits into its own "slot B." In the alternate form, though, tab A is available to fit into its neighbor's slot B. That means the neighbor can do the same thing to the next protein to come along, forming a chain or clump that can grow indefinitely. © 2014 Scientific American,
|By Jenni Laidman People born with Down syndrome have always been considered to be incurably developmentally delayed—until now. In the past few years a number of laboratories have uncovered critical drug targets within disabled chemical pathways in the brain that might be restored with medication. At least two clinical trials are currently studying the effects of such treatments on people with Down syndrome. Now geneticist Roger Reeves of Johns Hopkins University may have stumbled on another drug target—this one with the potential to correct the learning and memory deficits so central to the condition. Down syndrome occurs in about one in 1,000 births annually worldwide. It arises from an extra copy of chromosome 21 and the overexpression of each of the 300 to 500 genes the chromosome carries. “If you go back even as recently as 2004, researchers didn't have much of a clue about the mechanisms involved in this developmental disability,” says Michael Harpold, chief scientific officer with the Down Syndrome Research and Treatment Foundation. But all that has changed. “In the past six or seven years there have been several breakthroughs—and ‘breakthroughs’ is not by any means too big a word—in understanding the neurochemistry in Down syndrome,” Reeves says. This improved knowledge base has led to a series of discoveries with therapeutic promise, including the latest by Reeves. He and his team were attempting to restore the size of the cerebellum in mice engineered to show the hallmarks of Down syndrome. The cerebellum lies at the base of the brain and controls motor functions, motor learning and balance. In people with Down syndrome and in the Down mouse model the cerebellum is about 40 percent smaller than normal. By restoring its size, Reeves hoped to gain a clearer picture of the developmental processes that lead to anomalies in a brain with Down syndrome. © 2014 Scientific American
by Nathan Seppa Women who take acetaminophen during pregnancy are more likely to have a child with attention-deficit/hyperactivity disorder than are women who don’t, according to an analysis of nearly 41,000 pairs of mothers and children in a Danish birth registry. Researchers found that more than half of the women, who gave birth between 1996 and 2002, had used the pain reliever during pregnancy. Calls to the women when the children were 7 years old revealed that children whose moms used any acetaminophen during pregnancy were 37 percent more apt to be diagnosed with ADHD or a related disorder than children whose moms didn’t use the drug. If the women used it in all three trimesters, the apparent risk for offspring was 61 percent higher than for children whose mothers didn’t use the drug. Out of nearly 41,000 children, fewer than 1,000 were diagnosed with ADHD and related disorders. The data establish an association and not cause and effect. But the researchers note that acetaminophen, also sold as Tylenol or Panadol, can cross the placental barrier and may affect hormones in a fetus. Citations Z. Liew et al. Acetaminophen use during pregnancy, behavioral problems, and hyperkinetic disorders. JAMA Pediatrics. Online February 24, 2014. doi:10.1001/jamapediatrics.2013.4914. © Society for Science & the Public 2000 - 2013.
Brain cell regeneration has been discovered in a new location in human brains. The finding raises hopes that these cells could be used to help people recover after a stroke, or to treat other brain diseases. For years it was unclear whether or not we could generate new brain cells during our lifetime, as the process – neurogenesis – had only been seen in animals. Instead, it was thought that humans, with our large and complex brains, are born with all the required neurons. Then last year Jonas Frisén of the Karolinska Institute in Stockholm, Sweden, and his colleagues found that neurogenesis occurs in the hippocampi of the human brain. These structures are crucial for memory formation (Cell, DOI: 10.1016/j.cell.2013.05.002) Now they have found more new brain cells in a second location – golf-ball-sized structures called the striata. These seem to be involved in many different functions, including in learning and memory. These particular aspects, related as they are to the hippocampi, lead Frisén to speculate that these new brain cells may also be involved with learning. "New neurons may convey some sort of plasticity," he says, which might help people learn and adapt to new situations. To reveal the new brain cells, the team exploited the fact that there have been varying levels of a radioactive isotope of carbon – carbon-14 – in the atmosphere since nuclear bomb tests during the cold war. This means that the year of creation of many cells in the body can be found by measuring the ratio of carbon-14 to carbon-12 in its DNA. Analysis of 30 donated brains revealed which brain cells had been born during the lifetimes of the donors. © Copyright Reed Business Information Ltd.
Link ID: 19282 - Posted: 02.22.2014
National Institutes of Health researchers have identified gene variants that cause a rare syndrome of sporadic fevers, skin rashes and recurring strokes, beginning early in childhood. The team’s discovery coincides with findings by an Israeli research group that identified an overlapping set of variants of the same gene in patients with a similar type of blood vessel inflammation. The NIH group first encountered a patient with the syndrome approximately 10 years ago. The patient, then 3 years old, experienced fevers, skin rash and strokes that left her severely disabled. Because there was no history of a similar illness in the family, the NIH group did not at first suspect a genetic cause, and treated the patient with immunosuppressive medication. However, when the NIH team evaluated a second patient with similar symptoms two years ago — a child who had experienced recurrent fevers and six strokes by her sixth birthday — they began to suspect a common genetic cause and embarked on a medical odyssey that has led not only to a diagnosis, but to fundamental new insights into blood vessel disease. In their study, which appears in the Feb. 19, 2014, advance online edition of the New England Journal of Medicine, the researchers describe how next-generation genome sequencing, only recently available, facilitated a molecular diagnosis for patients in their study. The researchers found that harmful variants in the CECR1 gene impede production of a protein vital to the integrity of healthy blood vessel walls. The researchers showed that faulty variants in their patients’ DNA that encode the CECR1 gene cause a loss of function of the gene’s ability to produce of an enzyme called adenosine deaminase 2 (ADA2). Without it, abnormalities and inflammation in blood vessel walls result. The researchers call the new syndrome, deficiency of ADA2, or DADA2.
James Hamblin Brain training is becoming big business. Everywhere you look, someone is talking about neuroplasticity and trying to train your brain. Soon there will be no wild brains left. At the same time, everyone who spends more than two continuous hours using a computer is, according to the American Optometric Association, ruining their eyes with Computer Vision Syndrome. So, Dr. Aaron Seitz might be onto something with his new brain-training program that promises better vision. UltimEyes is a game-based app that's sold as "fun and rewarding" as it improves your vision and "reverse[s] the effects of aging eyes." It doesn't claim to work on the eyes themselves, but on the brain cortex that processes vision—the part that takes blurry puzzle pieces from the eyes and arranges them into a sweet puzzle. (Brain training for memory, the kind we hear about the most on TV, would be the part that lacquers the finished puzzle, frames it, and hangs it on the wall.) A standard 25-minute session using UltimEyes forces your eyes to work in ways they probably don't in everyday life, and its website warns that after the first use, "just like the first time that you go to the gym, your eyes may feel a bit tired. This experience typically goes away by your third session as your visual system adjusts to its new work-out routine." Seitz is a neuroscientist at the University of California, Riverside. To test out his vision-training game, he had players on the university's baseball team use the app. Half the team trained for 30 sessions. For comparison, the other half did no training. © 2014 by The Atlantic Monthly Group
Ian Sample, science correspondent, in Chicago Regular brisk walks can slow down the shrinking of the brain and the faltering mental skills that old age often brings, scientists say. Studies on men and women aged 60 to 80 found that taking a short walk three times a week increased the size of brain regions linked to planning and memory over the course of a year. The prefrontal cortex and hippocampus increased in size by only 2% or 3%, but that was enough to offset the steady shrinkage doctors expected to see over the same period. "It may sound like a modest amount but that's actually like reversing the age clock by about one to two years," said Professor Kirk Erickson, a neuroscientist at the University of Pittsburgh. "While the brain is shrinking, we actually saw not a levelling out but an increase in the size of these regions. It was better than before we started the study." People who took part in the study scored higher on spatial memory tests, and some reported feeling more mentally alert, according to Erickson. "They feel better, they feel as if the fog has lifted. Anecdotally, it seems to benefit these cognitive functions," he said. Erickson recruited more than 100 adults who confessed to doing little if any exercise in their daily lives. Half were randomly assigned to walk for 30 to 45 minutes three days a week. The rest spent a similar amount of time doing stretching exercises. Medical scans showed minor increases in the two brain regions in both groups. But the effect was greater in the walkers, Erickson said at the annual meeting of the American Association for the Advancement of Science. © 2014 Guardian News and Media Limited
Link ID: 19271 - Posted: 02.20.2014
By ALAN SCHWARZ Jerry, 9 years old, dissolved into his Game Boy while his father described his attentional difficulties to the family pediatrician. The child began flitting around the room distractedly, ignoring the doctor’s questions and squirming in his chair — but then he leapt up and yelled: “Freeze! What do you think is the problem here?” Nine-year-old Jerry was in fact being played by Dr. Peter Jensen, one of the nation’s most prominent child psychiatrists. On this Sunday in January in New York, Dr. Jensen was on a cross-country tour, teaching pediatricians and other medical providers how to properly evaluate children’s mental health issues — especially attention deficit hyperactivity disorder, which some doctors diagnose despite having little professional training. One in seven children in the United States — and almost 20 percent of all boys — receives a diagnosis of A.D.H.D. by the time they turn 18, according to the Centers for Disease Control and Prevention. It narrowly trails asthma as the most common long-term medical condition in children. Increasing concern about the handling of the disorder has raised questions about the training doctors receive before diagnosing the condition and prescribing stimulants like Adderall or Concerta, sometimes with little understanding of the risks. The medications can cause sleep problems, loss of appetite and, in rare cases, delusions. Because the disorder became a widespread national health concern only in the past few decades, many current pediatricians received little formal instruction on it, sometimes only several hours, during their seven years of medical school and residency. But the national scarcity of child psychiatrists has placed much of the burden for evaluating children’s behavioral problems on general pediatricians and family doctors, a reality that Dr. Jensen and others are trying to address through classes that emphasize role-playing exercises and spirited debate. © 2014 The New York Times Company
By GRETCHEN REYNOLDS Watching participants in slopestyle and half-pipe skiing and snowboarding flip, curl, cartwheel and otherwise contort themselves in the air during the Winter Olympics competition, many of us have probably wondered not only how the athletes managed to perform such feats but also why. Helpfully, a recent study of the genetics of risk-taking intimates that their behavior may be motivated, at least in part, by their DNA. For some time, scientists and many parents have suspected that certain children are born needing greater physical stimulation than others, suggesting that sensation seeking, as this urge is known in psychological terms, has a genetic component. A thought-provoking 2006 study of twins, for instance, concluded that risk-taking behavior was shared by the pairs to a much greater extent than could be accounted for solely by environmental factors. If one twin sought out risks, the other was likely to do so as well. But finding which genes or, more specifically, which tiny snippets of DNA within genes, might be influencing the desire to huck oneself off of a snow-covered slope has proven to be troublesome. In recent years, scientists zeroed in on various sections of genes that affect the brain’s levels of or response to the neurotransmitter dopamine, a substance that is known to influence our feelings of pleasure, reward and gratification. People who engage in and enjoy extreme, daredevil conduct, researchers presumed, would likely process dopamine differently than those of us content to watch. But the results of some early genetic studies comparing dopamine-related portions of genes with sensation seeking were inconsistent. Some found that people with certain variations within genes, including a gene called DRD4 that is believed to be closely involved in the development and function of dopamine receptors in our brain, gravitated toward risky behavior. Others, though, found no such links. But most of these studies focused on so-called deviant risk-taking, such as gambling and drug addiction. © 2014 The New York Times Company
By Geoffrey Mohan Stress can damage the brain. The hormones it releases can change the way nerves fire, and send circuits into a dangerous feedback loop, leaving us vulnerable to anxiety, depression and post-traumatic stress disorder. But how stress accomplishes its sinister work on a cellular level has remained mysterious. Neuroscientists at a UC Berkeley lab have uncovered evidence that a well-known stress hormone trips a switch in stem cells in the brain, causing them to produce a white matter cell that ultimately can change the way circuits are connected in the brain. This key step toward hardening wires, the researchers found, may be at the heart of the hyper-connected circuits associated with prolonged, acute stress, according to the study published online Tuesday in the journal Molecular Psychiatry. The findings strengthen an emerging view that cells once written off as little more than glue, insulation and scaffolding may regulate and reorganize the brain's circuitry. Researchers examined a population of stem cells in the brain’s hippocampus, an area critical to fusing emotion and memory, and one that has been known to shrink under the effects of prolonged acute stress. Under normal circumstances, these cells form new neurons or glia, a type of white matter. Los Angeles Times Copyright 2014
By GREGORY COWLES David Stuart MacLean’s first book, “The Answer to the Riddle Is Me,” opens with a scene out of Robert Ludlum: The protagonist wakes from a blackout to find himself on a crowded train platform in India, with no idea who he is or what he’s doing in a foreign country. The catch is that the protagonist is Mr. MacLean himself, and his book isn’t an international thriller but a “memoir of amnesia,” as his agreeably paradoxical subtitle puts it — the true story of how his memory was wiped clean and how that condition has subsequently affected his life. It is all the more thrilling for that. In 2002, Mr. MacLean was a 28-year-old Fulbright scholar visiting India to research a novel. It wasn’t his first trip; he had gone a few years earlier and stayed for months. But this time around, his anti-malaria medication touched off a break with reality as sudden as it was severe. He hallucinated angels and demons, and felt his thoughts “puddling in the carpet near the doorway and sloshing down the hall.” Delirious, he agreed with the police officer who surmised he must be a drug addict, and apologized profusely for misdeeds he had never committed. At the hospital, a nurse called him “the most entertaining psychotic that they’d ever had.” As harrowing as this territory is, Mr. MacLean makes an affable, sure-footed guide. In his descriptions, you can recognize the good fiction writer he must have been even before amnesia forced him to view the world anew; if the writer’s task is to “make it new,” then losing your memory turns out to be an unexpected boon. An avid drinker before his breakdown, he recoils the first time he tries Scotch again, thinking it smells “like Band-Aids.” He can’t remember his girlfriend of a year, but her voice is “faintly familiar, like the smell of the car heater the first time you turn it on in the fall.” He grasps at hope when his parents arrive to take him home: “I still didn’t have my memory, but I now had an outline of myself, like a tin form waiting for batter.” © 2014 The New York Times Company
Keyword: Learning & Memory
Link ID: 19262 - Posted: 02.18.2014
Ian Sample, science correspondent, in Chicago A woman's diet in early life has more impact on her baby's birth weight than the food she eats as an adult, researchers say. The surprise finding suggests that you are what your mother ate, and that a woman's diet in her adult life has less influence on her baby's health than previously thought. Prof Christopher Kuzawa at Northwestern University in Illinois said that women's bodies seemed to "buffer" the supply of nutrients to their unborn babies, meaning that foetuses were partly protected from changes in women's diets. Kuzawa advised pregnant women to follow a healthy diet, but said they need not worry about every calorie because their health and diet as a toddler could be more important for their baby. "There is some good news here for expectant mothers. Although there certainly are some harmful things to avoid during pregnancy, and some supplements to take to make sure some important bases are covered, the mother's body seems to do a good job of buffering overall nutritional supply to her growing baby," he said. "Within the bounds of a healthy balanced diet, the overall quantity of food that a mother eats is unlikely to have large effects on her baby's birth weight," he added. The findings emerged from a 30-year study that followed more than 3,000 pregnant women in the Philippines whose children have now begun to have babies of their own. Kuzawa said that while there was good evidence that unborn children benefit from their mothers taking extra folate and that they are harmed by toxins such as lead, mercury, excessive alcohol and bisphenol A, which is used to make some plastics, the picture was less clear on the roles of calories, protein, fat and carbohydrates. © 2014 Guardian News and Media Limited
by Ashley Yeager Humans aren’t the only ones to suffer from obsessive-compulsive disorder. Dogs can suffer from the disorder as well, with particular breeds compulsively chewing their feet, chasing their tails or sucking blankets. Now scientists say they have identified several of the genes that trigger the behavior in Doberman pinschers, bullterriers, sheepdogs and German shepherds. Four genes, CDH2, CTNNA2, ATXN1 and PGCP, involved in the communication between brain cells appear to play a role in dog OCD, researchers report February 16 in Genome Biology. The results could be used to better understand the disorder in people. © Society for Science & the Public 2000 - 2013.
Kids with ADHD may be able to learn better focus through a computer game that trains the brain to pay attention, a new study suggests. The game was part of a neurofeedback system that used bicycle helmets wired to measure brain waves and gave immediate feedback when kids were paying attention, researchers reported Monday in Pediatrics. Giving kids feedback on what their brains are doing is "like turning on a light switch," said Dr. Naomi Steiner, the study's lead author and a developmental and behavioral pediatrician at the Floating Hospital for Children at Tufts Medical Center. "Kids said 'Oh, this is what people mean when they tell me to pay attention.'" To test the system, Steiner and her colleagues randomly assigned 104 Boston area elementary school children to one of three groups: no treatment, 40 half-hour sessions of neurofeedback or 40 sessions of cognitive therapy. The kids getting neurofeedback wore standard bicycle helmets fitted with brain wave sensors while they performed a variety of exercises on the computer. In one exercise, kids were told to focus on a cartoon dolphin. When people pay attention, theta wave activity goes down while beta waves increase, Steiner explained. If the kids' brains showed they were paying attention, the dolphin would dive to the bottom of the sea. Parents' reports on ADHD symptoms six months later showed a lasting improvement in kids who had done neurofeedback.
CHICAGO, ILLINOIS—Chances are, your baby won’t respond to questions like, “How was your day, honey?” Or, “What do you want to be when you grow up?” But just because infants can’t form sentences until toddlerhood doesn’t mean that they don’t benefit from early conversations with their parents. It’s long been observed that the better children perform in school and the more successful their careers, the higher the socioeconomic status (SES) of their family—and, according to Stanford University’s Anne Fernald, this has a lot to do with how parents of different SES speak to their babies. Those babies that are spoken to frequently in an engaging and nurturing way—generally from a higher SES—tend to develop faster word-processing skills, or the ability to follow a sentence from one object or setting to another. This word processing speed, in turn, directly relates to the development not just of vocabulary and language skills, but also memory and nonverbal cognitive abilities. In a new study, Fernald and colleagues measured parent-baby banter from round-the-clock recordings in babies’ homes, then tested those babies’ word-processing speed using retinal-following experiments that tracked how long it took them to follow a prompt to an image like a dog or juice. The researchers found that the differences in word-processing speed between high and low SES were stark: By 2 years of age, high SES children were 6 months ahead of their low SES counterparts; and by age 3, the differences in processing abilities were highly predictive of later performance in and out of school, the team reported here today at the annual meeting of AAAS, which publishes Science. Fernald hopes that this research will lead to interventions that help to shrink the language gap between kids on either side of the income gap. © 2014 American Association for the Advancement of Science
by Laura Sanders Some of the human brain’s wrinkles are forged by the behavior of a single gene, scientists report in the Feb. 14 Science. By scanning more than 1,000 people’s brains, researchers identified five with malformed wrinkles in a specific region. The abnormalities — numerous shallow dips surrounding an unusually wide brain furrow called the Sylvian fissure — were linked with intellectual and language disabilities and seizures in these people. All five people had mutations that dampened the behavior of a gene named GPR56. Curbing this gene’s behavior results in diminished production of cells that eventually become neurons in the affected brain region, mouse experiments revealed. Boosting the gene’s behavior had the opposite effect. The results might clarify how wrinkles allow human brains to cram lots of neurons into a small space, Christopher Walsh of Boston Children’s Hospital and colleagues suggest. © Society for Science & the Public 2000 - 2013
Katherine Sharpe Ben Harkless could not sit still. At home, the athletic ten-year-old preferred doing three activities at once: playing with his iPad, say, while watching television and rolling on an exercise ball. Sometimes he kicked the walls; other times, he literally bounced off them. School was another story, however. Ben sat in class most days with his head down on his desk, “a defeated heap”, remembers his mother, Suzanne Harkless, a social worker in Berkeley, California. His grades were poor, and his teacher was at a loss for what to do. Harkless took Ben to a therapist who diagnosed him with attention deficit hyperactivity disorder (ADHD). He was prescribed methylphenidate, a stimulant used to improve focus in people with the condition. Harkless was reluctant to medicate her child, so she gave him a dose on a morning when she could visit the school to observe. “He didn't whip through his work, but he finished his work,” she says. “And then he went on and helped his classmate next to him. My jaw dropped.” ADHD diagnoses are rising rapidly around the world and especially in the United States, where 11% of children aged between 4 and 17 years old have been diagnosed with the disorder. Between half and two-thirds of those are put on medication, a decision often influenced by a child's difficulties at school. And there are numerous reports of adolescents and young adults without ADHD using the drugs as study aids. © 2014 Nature Publishing Group,