Chapter 7. Life-Span Development of the Brain and Behavior
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
by Laura Sanders Young babies get a bad rap. They’re helpless, fickle and noisy. And even though they allegedly sleep for 16 hours a day, those hours come in 20-minute increments. Yet hidden in the chaos of a young infant’s life are some truly magnificent skills — perceptual feats that put adults to shame. So next time your baby loses it because she can’t get her thumb into her mouth, keep in mind that her strengths lie elsewhere. Six-month-old babies can spot subtle differences between two monkey faces easy as pie. But 9-month-olds — and adults — are blind to the differences. In a 2002 study of facial recognition, scientists pitted 30 6-month-old babies against 30 9-month-olds and 11 adults. First, the groups got familiar with a series of monkey and human faces that flashed on a screen. Then new faces showed up, interspersed with already familiar faces. The idea is that the babies would spend more time looking at new faces than ones they had already seen. When viewing human faces, all of the observers, babies and adults alike, did indeed spend more time looking at the new people, showing that they could easily pick out familiar human faces. But when it came to recognizing monkey faces, the youngsters blew the competition out of the water. Six-month-old babies recognized familiar monkey faces and stared at the newcomers longer. But both adults and 9-month-old babies were flummoxed, and looked at the new and familiar monkey faces for about the same amount of time. © Society for Science & the Public 2000 - 2015
Blocking the production of new immune cells in the brain could reduce memory problems seen in Alzheimer's disease, a study suggests. University of Southampton researchers said their findings added weight to evidence that inflammation in the brain is what drives the disease. A drug used to block the production of these microglia cells in the brains of mice had a positive effect. Experts said the results were exciting and could lead to new treatments. Up until now, most drugs used to treat dementia have targeted amyloid plaques in the brain which are a characteristic of people with the Alzheimer's disease. But this latest study, published in the journal Brain, suggests that in fact targeting inflammation in the brain, caused by a build-up of immune cells called microglia, could halt progression of the disease. Researchers found increased numbers of microglia in the post-mortem brains of people with Alzheimer's disease. Previous studies have also suggested that these cells could play an important role. Dr Diego Gomez-Nicola, lead study author from the university, said: "These findings are as close to evidence as we can get to show that this particular pathway is active in the development of Alzheimer's disease. "The next step is to work closely with our partners in industry to find a safe and suitable drug that can be tested to see if it works in humans." © 2016 BBC
Katherine Hobson Pregnant women worry about all kinds of things. Can I drink alcohol? (No.) Can I take antidepressants? (Maybe.) Can I do the downward dog? (Yes.) Now there's one less thing to fret about: harm to the baby when the mother takes birth control pill right before conceiving, or during the first few months of pregnancy. According to a study covering more than 880,000 births in Denmark, the overall rate of birth defects was consistent for women who had never taken the pill at all, for those who had used it before getting pregnant and for those who continued on the pill in early pregnancy. (There were about 25 birth defects per 1,000 births for all groups.) The study is important because so many women take the pill – about 16 percent of women of childbearing age in the U.S. When used perfectly, the failure rate of the pill is less than 1 percent, but that jumps to 9 percent under typical use because of missed pills, drug interactions or illness. That means a lot of embryos are exposed to the hormones used in the pill, which can linger for a few months after a woman stops taking it. "Our findings are really reassuring," says Brittany Charlton, an author of the study and a researcher in the Harvard T.H. Chan School of Public Health's epidemiology department. The results also confirm most of the previous research, which has pointed to no overall increase in major birth defects, she says. This study, published in the medical journal BMJ, used national birth, patient and prescription registry data to track contraceptive prescriptions among women who gave birth, then looked at whether birth defects were associated with pill use. © 2016 npr
Children conceived via infertility treatments are no more likely to have a developmental delay than children conceived without such treatments, according to a study by researchers at the National Institutes of Health, the New York State Department of Health and other institutions. The findings, published online in JAMA Pediatrics, may help to allay longstanding concerns that conception after infertility treatment could affect the embryo at a sensitive stage and result in lifelong disability. The authors found no differences in developmental assessment scores of more than 1,800 children born to women who became pregnant after receiving infertility treatment and those of more than 4,000 children born to women who did not undergo such treatment. “When we began our study, there was little research on the potential effects of conception via fertility treatments on U.S. children,” said Edwina Yeung, Ph.D., an investigator in the Division of Intramural Population Health Research at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “Our results provide reassurance to the thousands of couples who have relied on these treatments to establish their families.” Also taking part in the study were researchers from the University at Albany, New York; the New York State Department of Health, also in Albany; and CapitalCare Pediatrics in Troy, New York. The Upstate KIDS study enrolled infants born to women in New York State (except for New York City) from 2008 to 2010. Parents of infants whose birth certificates indicated infertility treatment were invited to enroll their children in the study, as were all parents of twins and other multiples. The researchers also recruited roughly three times as many singletons not conceived via infertility treatment. Four months after giving birth, the mothers indicated on a questionnaire the type of infertility treatment they received:
Keyword: Development of the Brain
Link ID: 21755 - Posted: 01.07.2016
Laura Sanders It didn’t take a lot of brainpower to come up with the name for a nerve cell that looks like a bushy, round tangle of fibers perched atop a nucleus. Meet the shrub cell. This botanically named cell, discovered in the brains of adult mice, made its formal debut in the Nov. 27 Science. The newly described cell lives in a particular nervy neighborhood — an area called layer 5 in the part of the brain that handles incoming visual information. Xiaolong Jiang of Baylor College of Medicine in Houston and colleagues defined shrub cells and other newcomers by their distinct shapes, their particular connections to other nerve cells or their similarities to nerve cells found elsewhere. Joining shrub cells are the freshly named horizontally elongated cells, deep-projecting cells, L5 basket cells and L5 neurogliaform cells. Each is an interneuron, a middleman that connects nerve cells to each other. The finding highlights the stunning variety of shapes and wiring patterns of cells in the brain. Citations X. Jiang et al. Principles of connectivity among morphologically defined cell types in adult neocortex. Science. Vol. 350, November 27, 2015. doi: 10.1126/science.aac9462 © Society for Science & the Public 2000 - 2015.
Keyword: Development of the Brain
Link ID: 21754 - Posted: 01.07.2016
By Debra W. Soh What should parents do if their little boy professes an intense desire to be a girl? Or if their daughter comes home from kindergarten and says she wants to be a boy? In recent years the dominant thinking has changed dramatically regarding children’s gender dysphoria. Previously, parents might hope that it would be a passing phase, as it usually is. But now they are under pressure from gender-identity politics, which asserts that children as young as 5 should be supported in wanting to live as the opposite sex. Any attempts to challenge this approach are deemed intolerant and oppressive. I myself was a gender-dysphoric child who preferred trucks and Meccano sets to Easy-Bake Ovens. I detested being female and all of its trappings. Yet when I was growing up in the 1980s, the concept of helping children transition to another sex was completely unheard of. My parents allowed me to wear boys’ clothing and shave my head, to live as a girl who otherwise looked and behaved like a boy. I outgrew my dysphoria by my late teens. Looking back, I am grateful for my parents’ support, which helped me work things out. Since then, research has established best-treatment practices for adolescents and adults with gender dysphoria: full transitioning, which includes treatment with hormones to suppress puberty and help the individual develop breasts or facial hair, as well as gender-reassignment surgery. But prepubescent children who identify with the opposite sex are another matter entirely. How best to deal with them has become so politicized that sexologists, who presumably would be able to determine the healthiest approach, are extremely reluctant to get involved. They have seen what happens when they deviate from orthodoxy. ©2016 Dow Jones & Company, Inc
Patricia Neighmond Losing your ability to think and remember is pretty scary. We know the risk of dementia increases with age. But if you have memory lapses, you probably needn't worry. There are pretty clear differences between signs of dementia and age-related memory loss. After age 50, it's quite common to have trouble remembering the names of people, places and things quickly, says Dr. Kirk Daffner, chief of the division of cognitive and behavioral neurology at Brigham and Women's Hospital in Boston. The brain ages just like the rest of the body. Certain parts shrink, especially areas in the brain that are important to learning, memory and planning. Changes in brain cells can affect communication between different regions of the brain. And blood flow can be reduced as arteries narrow. Simply put, this exquisitely complex organ just isn't functioning like it used to. Forgetting the name of an actor in a favorite movie, for example, is nothing to worry about. But if you forget the plot of the movie or don't remember even seeing it, that's far more concerning, Daffner says. When you forget entire experiences, he says, that's "a red flag that something more serious may be involved." Forgetting how to operate a familiar object like a microwave oven or forgetting how to drive to the house of a friend you've visited many times before can also be signs something is wrong. © 2016 npr
Jon Hamilton There's growing evidence that a lack of sleep can leave the brain vulnerable to Alzheimer's disease. "Changes in sleep habits may actually be setting the stage" for dementia, says Jeffrey Iliff, a brain scientist at Oregon Health & Science University in Portland. The brain appears to clear out toxins linked to Alzheimer's during sleep, Iliff explains. And, at least among research animals that don't get enough solid shut-eye, those toxins can build up and damage the brain. Iliff and other scientists at OHSU are about to launch a study of people that should clarify the link between sleep problems and Alzheimer's disease in humans. It has been clear for decades that there is some sort of link. Sleep disorders are very common among people with Alzheimer's disease. For a long time, researchers thought this was simply because the disease was "taking out the centers of the brain that are responsible for regulating sleep," Iliff says. But two recent discoveries have suggested the relationship may be more complicated. The first finding emerged in 2009, when researchers at Washington University in St. Louis showed that the sticky amyloid plaques associated with Alzheimer's develop more quickly in the brains of sleep-deprived mice. Then, in 2013, Iliff was a member of a team that discovered how a lack of sleep could be speeding the development of those Alzheimer's plaques: A remarkable cleansing process takes place in the brain during deep sleep, at least in animals. What happens, Iliff says, is "the fluid that's normally on the outside of the brain — cerebrospinal fluid, it's a clean, clear fluid — it actually begins to recirculate back into and through the brain along the outsides of blood vessels." This process, via what's known as the glymphatic system, allows the brain to clear out toxins, including the toxins that form Alzheimer's plaques, Iliff says. © 2016 npr
By Melinda Wenner Moyer There's a reason your mother told you to look people in the eye when you talk to them: eye contact conveys important social cues. Yet when someone holds your gaze for more than a few seconds, the experience can take on a different tenor. New work elucidates the factors that affect whether we like or loathe locking eyes for a lengthy period. Researchers have long known that eye contact is an important social signal. Our recognition of its import may even be hardwired. One study found that five-day-old babies prefer looking at faces that make direct eye contact compared with faces that have an averted gaze. “Eye contact provides some of the strongest information during a social interaction,” explains James Wirth, a social psychologist now at Ohio State University at Newark, because it conveys details about emotions and intentions. (Lack of eye contact is one of the early signs of autism in infants and toddlers.) The power of eye contact is so great that, according to a 2010 study co-authored by Wirth, if someone avoids your gaze for even a short period, you may feel ostracized. But what determines how we feel about prolonged eye contact? One recent study explored this question. In research presented in May 2015 at the Vision Sciences Society conference, psychologist Alan Johnston and his colleagues at University College London collected information from more than 400 volunteers about their personalities. Then the subjects indicated their comfort level while watching video clips of actors who appeared to be looking directly at them for varying lengths of time. © 2016 Scientific American
By NICHOLAS WADE After decades of disappointingly slow progress, researchers have taken a substantial step toward a possible treatment for Duchenne muscular dystrophy with the help of a powerful new gene-editing technique. Duchenne muscular dystrophy is a progressive muscle-wasting disease that affects boys, putting them in wheelchairs by age 10, followed by an early death from heart failure or breathing difficulties. The disease is caused by defects in a gene that encodes a protein called dystrophin, which is essential for proper muscle function. Because the disease is devastating and incurable, and common for a hereditary illness, it has long been a target for gene therapy, though without success. An alternative treatment, drugs based on chemicals known as antisense oligonucleotides, is in clinical trials. But gene therapy — the idea of curing a genetic disease by inserting the correct gene into damaged cells — is making a comeback. A new technique, known as Crispr-Cas9, lets researchers cut the DNA of chromosomes at selected sites to remove or insert segments. Three research groups, working independently of one another, reported in the journal Science on Thursday that they had used the Crispr-Cas9 technique to treat mice with a defective dystrophin gene. Each group loaded the DNA-cutting system onto a virus that infected the mice’s muscle cells, and excised from the gene a defective stretch of DNA known as an exon. Without the defective exon, the muscle cells made a shortened dystrophin protein that was nonetheless functional, giving all of the mice more strength. The teams were led by Charles A. Gersbach of Duke University, Eric N. Olson of the University of Texas Southwestern Medical Center and Amy J. Wagers of Harvard University. © 2016 The New York Times Company
By Elizabeth Pennisi Whether foraging for food, caring for young, or defending the nest, the worker castes of carpenter ants toil selflessly for their queen and colony. Now, biologists have figured out how to make some of those worker ants labor even harder, or change their very jobs in ant society, all by making small chemical modifications to their DNA. The finding calls attention to a new source of behavioral flexibility, and drives home the idea that so-called epigenetic modifications can connect genes to the environment, linking nature to nurture. The work is “a pioneering study establishing a causal link between epigenetics and complex social behavior,” says Ehab Abouheif, an evolutionary developmental biologist at McGill University, Montreal, in Canada. “These mechanisms may extend far beyond ants to other organisms with social behavior.” Insect biologists have long debated whether the division of labor in these sophisticated species with castes is driven by colony needs or is innate. Evidence in honey bees had pointed toward a genetic difference between queens and workers. In the past several years, however, work in both honey bees and ants had indicated that epigenetic modifications—changes to DNA other than to its sequence of bases (or DNA “letters”)—influence caste choices, indicating environmental factors can be pivotal. But subsequent research about one type of change, methylation, led to contradictory conclusions. © 2016 American Association for the Advancement of Science.
Link ID: 21744 - Posted: 01.02.2016
By Mitch Leslie Male mice bequeath an unexpected legacy to their progeny. Two studies published online this week in Science reveal that sperm from the rodents carry pieces of RNAs that alter the metabolism of their offspring. The RNAs spotlighted by the studies normally help synthesize proteins, so the findings point to an unconventional form of inheritance. The results are “exciting and surprising, but not impossible,” says geneticist Joseph Nadeau of the Pacific Northwest Diabetes Research Institute in Seattle, Washington. “Impossible” is exactly how biologists once described so-called epigenetic inheritance, in which something other than a DNA sequence passes a trait between generations. In recent years, however, researchers have found many examples. A male mouse’s diet and stress level, for instance, can tweak offspring metabolism. Researchers are still trying to determine how offspring inherit a father’s metabolic attributes and physiological condition. Some evidence implicates chemical modification of DNA. Other work by neuroscientist Tracy Bale of the University of Pennsylvania Perelman School of Medicine in Philadelphia and colleagues has found that mammalian sperm pack gene-regulating molecules called microRNAs. The new work highlights a different class of RNAs, transfer RNAs (tRNAs). In one study, genomicist Oliver Rando of the University of Massachusetts Medical School in Worcester and colleagues delved into a case of epigenetic inheritance in which the progeny of mice fed a low-protein diet show elevated activity of genes involved in cholesterol and lipid metabolism. When Rando’s group analyzed sperm from the protein-deprived males, they uncovered an increased abundance of fragments from several kinds of tRNAs. The researchers concluded the sperm acquired most of these fragments while passing through the epididymis, a duct from the testicle where the cells mature. © 2016 American Association for the Advancement of Science
Link ID: 21741 - Posted: 01.02.2016
By Gary Stix A lingering question asked by neuroscientists has to do with what, if anything, makes the male and female brain distinctive, whether in mice or (wo)men. There is still no concise answer. The best evidence from the most recent research suggests that both males and females share the same neural circuitry, but use it differently. Catherine Dulac, a professor of molecular and cellular biology at Harvard, and investigator at the Howard Hughes medical Institute, is a pioneer in exploring these questions. I talked to her briefly about her research, which also extends far beyond just the neurobiology of gender. Can you tell me in broad overview about what you study? I'm interested in understanding how the brain engages in instinctive social behaviors. There are a lot of instinctive behaviors such as eating and sleeping that are essential in animals and humans, but social behavior is a very distinctive and particularly interesting set of instinctive behaviors that we would like to understand at the neuronal level. What we would like to understand in mechanistic terms is how does an individual recognize other animals of its own species, for example how does an animal identifies a male, a female, or an infant, how does the brain processes these signals in order to trigger appropriate social behaviors such as mating, aggression or parenting. Can you tell me a little bit about your work of the last few years that relates to gender identification? © 2015 Scientific American
By Katrina Schwartz It has become a cultural cliché that raising adolescents is the most difficult part of parenting. It’s common to joke that when kids are in their teens they are sullen, uncommunicative, more interested in their phones than in their parents and generally hard to take. But this negative trope about adolescents misses the incredible opportunity to positively shape a kid’s brain and future life course during this period of development. “[Adolescence is] a stage of life when we can really thrive, but we need to take advantage of the opportunity,” said Temple University neuroscientist Laurence Steinberg at a Learning and the Brain conference in Boston. Steinberg has spent his career studying how the adolescent brain develops and believes there is a fundamental disconnect between the popular characterizations of adolescents and what’s really going on in their brains. Because the brain is still developing during adolescence, it has incredible plasticity. It’s akin to the first five years of life, when a child’s brain is growing and developing new pathways all the time in response to experiences. Adult brains are somewhat plastic as well — otherwise they wouldn’t be able to learn new things — but “brain plasticity in adulthood involves minor changes to existing circuits, not the wholesale development of new ones or elimination of others,” Steinberg said. Adolescence is the last time in a person’s life that the brain can be so dramatically overhauled. © 2015 KQED Inc.
By Karen Weintraub Mild cognitive impairment, or M.C.I., is not a disease in itself. Rather, it is a clinical description based on performance on a test of memory and thinking skills. Depending on its cause, mild cognitive impairment is potentially reversible. Poor performance on a cognitive test could be caused by certain medications, sleep apnea, depression or other problems, said Dr. Alvaro Pascual-Leone, a professor of neurology at Harvard Medical School and Beth Israel Deaconess Medical Center. In those cases, when the underlying disease is treated, cognitive abilities can bounce back. But in about half of people with M.C.I. – doctors are not sure of the exact number — memory problems are the first sign of impending Alzheimer’s disease. If M.C.I. progresses to Alzheimer’s, there is no recovery. Alzheimer’s is marked by an inexorable decline that is always fatal, although the path from the first signs of cognitive impairment to death may take three to 15 years, said Dr. David Knopman, a professor of neurology at the Mayo Clinic in Rochester, Minn. As many as 20 percent to 30 percent of those with M.C.I. who score below but near the cutoff for normal can cross back above in a subsequent cognitive test – perhaps because they are having a better day, he said. But someone whose score is borderline is at higher risk of developing Alzheimer’s than someone who scores higher, said Dr. Knopman, also vice chair of the medical and scientific advisory council of the Alzheimer’s Association. Doctors may be hesitant to label someone with early Alzheimer’s, which can be difficult to diagnose in the early stages, so they often call it mild cognitive impairment instead, said Dr. John C. Morris, a professor of neurology and the director of the Knight Alzheimer's Disease Research Center at Washington University School of Medicine in St. Louis. © 2015 The New York Times Company
Tim Radford British scientists believe they have made a huge step forward in the understanding of the mechanisms of human intelligence. That genetic inheritance must play some part has never been disputed. Despite occasional claims later dismissed, no-one has yet produced a single gene that controls intelligence. But Michael Johnson of Imperial College London, a consultant neurologist and colleagues report in Nature Neuroscience that they may have discovered a very different answer: two networks of genes, perhaps controlled by some master regulatory system, lie behind the human gift for lateral thinking, mental arithmetic, pub quizzes, strategic planning, cryptic crosswords and the ability to laugh at limericks. As usual, such research raises potentially politically-loaded questions about the nature of intelligence. “Intelligence is a composite measure of different cognitive abilities and how they are distributed in a population. It doesn’t measure any one thing. But it is measurable,” Dr Johnson said. About 40% of the variation in intelligence is explained by inheritance. The other factors are not yet certain. But the scientists raise the distant possibility that armed with the new information they may be able to devise ways to modify human intelligence. “The idea of ultimately using drugs to affect cognitive performance is not in any way new. We all drink coffee to improve our cognitive performance,” Dr Johnson said. “It’s about understanding the pathways that are related to cognitive ability both in health and disease, especially disease so one day we could help people with learning disabilities fulfill their potential. That is very important.” © 2015 Guardian News and Media Limited
Rae Ellen Bichell Ever notice the catnaps that older relatives take in the middle of the day? Or how grandparents tend to be early risers? You're not alone. Colleen McClung did, too. A neuroscientist at the University of Pittsburgh Medical Center, McClung wanted to know what was going on in the brain that changes people's daily rhythms as they age. We all have a set of so-called clock genes that keep us on a 24-hour cycle. In the morning they wind us up, and at night they help us wind down. A study out Monday in Proceedings of the National Academy of Sciences found that those genes might beat to a different rhythm in older folks. "When you think about the early bird dinner specials, it sort of fits in with their natural shift in circadian rhythms," says McClung. "There is a core set of genes that has been described in every animal — every plant all the way down from fungus to humans — and they're pretty much the same set of genes." The genes are the master controllers of a bunch of other genes that control processes ranging from metabolism to sleep. When you woke up this morning, the timekeeping genes told a gland in your brain to give a jolt of the stress hormone cortisol to wake up. Tonight, they'll tell a gland to spit out melatonin, a hormone that makes you sleepy. "You can think of them as sort of the conductor of an orchestra," says McClung. They make sure all the other genes keep time. © 2015 npr
A study of mice shows how proteasomes, a cell’s waste disposal system, may break down during Alzheimer’s disease, creating a cycle in which increased levels of damaged proteins become toxic, clog proteasomes, and kill neurons. The study, published in Nature Medicine and supported by the National Institutes of Health, suggests that enhancing proteasome activity with drugs during the early stages of Alzheimer’s may prevent dementia and reduce damage to the brain. “This exciting research advances our understanding of the role of the proteasomes in neurodegeneration and provides a potential way to alleviate symptoms of neurodegenerative disorders,” said Roderick Corriveau, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which provided funding for the study. The proteasome is a hollow, cylindrical structure which chews up defective proteins into smaller, pieces that can be recycled into new proteins needed by a cell. To understand how neurodegenerative disorders affect proteasomes, Natura Myeku, Ph.D., a postdoctoral fellow working with Karen E. Duff, Ph.D., professor of pathology and cell biology at Columbia University, New York City, focused on tau, a structural protein that accumulates into clumps called tangles in the brain cells of patients with Alzheimer’s disease and several other neurodegenerative disorders known as tauopathies. Using a genetically engineered mouse model of tauopathy, as well as looking at cells in a dish, the scientists discovered that as levels of abnormal tau increased, the proteasome activity slowed down.
Link ID: 21716 - Posted: 12.22.2015
Jon Hamilton Taking antidepressants during the second or third trimester of pregnancy may increase the risk of having a child with autism spectrum disorder, according to a study of Canadian mothers and children published Monday in JAMA Pediatrics. But scientists not involved in the research say the results are hard to interpret and don't settle the long-running debate about whether expectant mothers with depression should take antidepressants. "This study doesn't answer the question," says Bryan King, program director of the autism center at Seattle Children's Hospital and a professor of psychiatry and behavioral sciences at the University of Washington. "My biggest concern is that it will be over-interpreted," says King, who wrote an editorial that accompanied the study. "It kind of leaves you more confused," says Alan Brown, a professor of psychiatry and epidemiology at Columbia University who studies risk factors for autism. "Mothers shouldn't get super worried about it," he says. One reason it's confusing is that there's strong evidence that mothers with depression are more likely than other women to have a child with autism, whether or not they take antidepressants during pregnancy. King and Brown say that makes it very hard to disentangle the effects of depression itself from those of the drugs used to treat it. © 2015 npr
The clock is ticking for Ronald Cohn. He wants to use CRISPR gene editing to correct the genes of his friend’s 13-year-old son. The boy, Gavriel, has Duchenne muscular dystrophy, a genetic disease in which muscles degenerate. Breathing and heart problems often start by the time people with the condition are in their early twenties. Life expectancy is about 25 years. By the standards of science, the field of CRISPR gene editing is moving at a lightning fast pace. Although the technique was only invented a few years ago, it is already being used for research by thousands of labs worldwide to make extremely precise changes to DNA. A handful of people have already been treated using therapies enabled by the technology, and last week an international summit effectively endorsed the idea of gene editing embryos. It is too soon to try the technique out, but the summit concluded that basic research on embryos should be permitted, alongside a debate on how we should use the technology. But for people like Cohn, progress can’t come fast enough. Gavriel was diagnosed at age 4. He has already lost the use of his legs but still has some movement in his upper body, and uses a manual wheelchair. Cohn, a clinician at the Hospital for Sick Children in Toronto, estimates that he has three years to develop and test a CRISPR-based treatment if he is to help Gavriel. Muscular dystrophy is caused by a faulty gene for the protein dystrophin, which holds our muscles together. Gavriel has a duplicated version of the gene. This week, Cohn’s team published a paper describing how they grew Gavriel’s cells in a dish and used CRISPR gene-editing techniques to snip out the duplication. With the duplication removed, his cells produced normal dystrophin protein. © Copyright Reed Business Information Ltd.