Chapter 7. Life-Span Development of the Brain and Behavior
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By Kelly Servick Dean Hamer finally feels vindicated. More than 20 years ago, in a study that triggered both scientific and cultural controversy, the molecular biologist offered the first direct evidence of a “gay gene,” by identifying a stretch on the X chromosome likely associated with homosexuality. But several subsequent studies called his finding into question. Now the largest independent replication effort so far, looking at 409 pairs of gay brothers, fingers the same region on the X. “When you first find something out of the entire genome, you’re always wondering if it was just by chance,” says Hamer, who asserts that new research “clarifies the matter absolutely.” But not everyone finds the results convincing. And the kind of DNA analysis used, known as a genetic linkage study, has largely been superseded by other techniques. Due to the limitations of this approach, the new work also fails to provide what behavioral geneticists really crave: specific genes that might underlie homosexuality. Few scientists have ventured into this line of research. When the genetics of being gay comes up at scientific meetings, “sometimes even behavioral geneticists kind of wrinkle up their noses,” says Kenneth Kendler, a psychiatric geneticist at Virginia Commonwealth University in Richmond. That’s partially because the science itself is so complex. Studies comparing identical and fraternal twins suggest there is some heritable component to homosexuality, but no one believes that a single gene or genes can make a person gay. Any genetic predispositions probably interact with environmental factors that influence development of a sexual orientation. © 2014 American Association for the Advancement of Science.
By ALAN SCHWARZ CONCORD, Calif. — Every time Matthias is kicked out of a school or day camp for defying adults and clashing with other children, his mother, Joelle Kendle, inches closer to a decision she dreads. With each morning of arm-twisting and leg-flailing as she tries to get him dressed and out the door for first grade, the temptation intensifies. Ms. Kendle is torn over whether to have Matthias, just 6 and already taking the stimulant Adderall for attention deficit hyperactivity disorder, go on a second and more potent medication: the antipsychotic Risperdal. Her dilemma is shared by a steadily rising number of American families who are using multiple psychotropic drugs — stimulants, antipsychotics, antidepressants and others — to temper their children’s troublesome behavior, even though many doctors who mix such medications acknowledge that little is known about the overall benefits and risks for children. In 2012 about one in 54 youngsters ages 6 through 17 covered by private insurance was taking at least two psychotropic medications — a rise of 44 percent in four years, according to Express Scripts, which processes prescriptions for 85 million Americans. Academic studies of children covered by Medicaid have also found higher rates and growth. Combined, the data suggest that about one million children are currently taking various combinations of psychotropics. Risks of antipsychotics alone, for example, are known to include substantial weight gain and diabetes. Stimulants can cause appetite suppression, insomnia and, far more infrequently, hallucinations. Some combinations of medication classes, like antipsychotics and antidepressants, have shown improved benefits (for psychotic depression) but also heightened risks (for heart rhythm disturbances). But this knowledge has been derived substantially from studies in adults — children are rarely studied because of concerns about safety and ethics — leaving many experts worried that the use of multiple psychotropics in youngsters has not been explored fully. There is also debate over whether the United States Food and Drug Administration’s database of patients’ adverse drug reactions reliably monitors the hazards of psychotropic drug combinations, primarily because only a small fraction of cases are ever reported. Some clinicians are left somewhat queasy about relying mostly on anecdotal reports of benefit and harm. © 2014 The New York Times Company
By Emma Wilkinson Health reporter, BBC News Taking vitamin B12 and folic acid supplements does not seem to cut the risk of developing dementia in healthy people, say Dutch researchers. In one of the largest studies to date, there was no difference in memory test scores between those who had taken the supplements for two years and those who were given a placebo. The research was published in the journal Neurology. Alzheimer's Research UK said longer trials were needed to be sure. B vitamins have been linked to Alzheimer's for some years, and scientists know that higher levels of a body chemical called homocysteine can raise the risk of both strokes and dementia. Vitamin B12 and folic acid are both known to lower levels of homocysteine. That, along with studies linking low vitamin B12 and folic acid intake with poor memory, had prompted scientists to view the supplements as a way to ward off dementia. Yet in the study of almost 3,000 people - with an average age of 74 - who took 400 micrograms of folic acid and 500 micrograms of vitamin B12 or a placebo every day, researchers found no evidence of a protective effect. All those taking part in the trial had high blood levels of homocysteine, which did drop more in those taking the supplements. But on four different tests of memory and thinking skills taken at the start and end of the study, there was no beneficial effect of the supplements on performance. The researchers did note that the supplements might slightly slow the rate of decline but concluded the small difference they detected could just have been down to chance. Study leader Dr Rosalie Dhonukshe-Rutten, from Wageningen University in the Netherlands, said: "Since homocysteine levels can be lowered with folic acid and vitamin B12 supplements, the hope has been that taking these vitamins could also reduce the risk of memory loss and Alzheimer's disease. BBC © 2014
Link ID: 20313 - Posted: 11.15.2014
Sara Reardon Companies selling ‘probiotic’ foods have long claimed that cultivating the right gut bacteria can benefit mental well-being, but neuroscientists have generally been sceptical. Now there is hard evidence linking conditions such as autism and depression to the gut’s microbial residents, known as the microbiome. And neuroscientists are taking notice — not just of the clinical implications but also of what the link could mean for experimental design. “The field is going to another level of sophistication,” says Sarkis Mazmanian, a microbiologist at the California Institute of Technology in Pasadena. “Hopefully this will shift this image that there’s too much commercial interest and data from too few labs.” This year, the US National Institute of Mental Health spent more than US$1 million on a new research programme aimed at the microbiome–brain connection. And on 19 November, neuroscientists will present evidence for the link in a symposium at the annual Society for Neuroscience meeting in Washington DC called ‘Gut Microbes and the Brain: Paradigm Shift in Neuroscience’. Although correlations have been noted between the composition of the gut microbiome and behavioural conditions, especially autism1, neuroscientists are only now starting to understand how gut bacteria may influence the brain. The immune system almost certainly plays a part, Mazmanian says, as does the vagus nerve, which connects the brain to the digestive tract. Bacterial waste products can also influence the brain — for example, at least two types of intestinal bacterium produce the neurotransmitter γ-aminobutyric acid (GABA)2. © 2014 Nature Publishing Group
by Helen Thomson Could a futuristic society of humans with the power to control their own biological functions ever become reality? It's not as out there as it sounds, now the technical foundations have been laid. Researchers have created a link between thoughts and cells, allowing people to switch on genes in mice using just their thoughts. "We wanted to be able to use brainwaves to control genes. It's the first time anyone has linked synthetic biology and the mind," says Martin Fussenegger, a bioengineer at ETH Zurich in Basel, Switzerland, who led the team behind the work. They hope to use the technology to help people who are "locked-in" – that is, fully conscious but unable to move or speak – to do things like self-administer pain medication. It might also be able to help people with epilepsy control their seizures. In theory, the technology could be used for non-medical purposes, too. For example, we could give ourselves a hormone burst on demand, much like in the Culture – Iain M. Banks's utopian society, where people are able to secrete hormones and other chemicals to change their mood. Fussenegger's team started by inserting a light-responsive gene into human kidney cells in a dish. The gene is activated, or expressed, when exposed to infrared light. The cells were engineered so that when the gene activated, it caused a cascade of chemical reactions leading to the expression of another gene – the one the team wanted to switch on. © Copyright Reed Business Information Ltd.
By Abby Phillip If you're confused about what marijuana use really does to people who use it, you're not alone. For years, the scientific research on health effects of the drug have been all over the map. Earlier this year, one study suggested that even casual marijuana use could cause changes to the brain. Another found that marijuana use was also associated with poor sperm quality, which could lead to infertility in men. But marijuana advocates point to other research indicating that the drug is far less addictive than other drugs, and some studies have found no relationship between IQ and marijuana use in teens. Researchers at the Center for Brain Health at the University of Texas in Dallas sought to clear up some of the confusion with a study that looked at a relatively large group of marijuana users and evaluated their brains for a slew of different indicators. What they found was complex, but the pattern was clear: The brains of marijuana users were different than those of non-marijuana users. The area of the brain responsible for establishing the reward system that helps us survive and also keeps us motivated was smaller in users than in non-marijuana users. But there was also evidence that the brain compensated for this loss of volume by increasing connectivity and the structural integrity of the brain tissue. Those effects were more pronounced for marijuana users who started young. "The orbitofrontal cortex is one of the primary regions in a network of brain areas called the reward system," explained Francesca Filbey, lead author of the study and an associate professor of the neurogenetics of addictive behavior at the University of Texas in Dallas. "
Email David By David Grimm Place a housecat next to its direct ancestor, the Near Eastern wildcat, and it may take you a minute to spot the difference. They’re about the same size and shape, and, well, they both look like cats. But the wildcat is fierce and feral, whereas the housecat, thanks to nearly 10,000 years of domestication, is tame and adaptable enough to have become the world’s most popular pet. Now scientists have begun to pinpoint the genetic changes that drove this remarkable transformation. The findings, based on the first high-quality sequence of the cat genome, could shed light on how other creatures, even humans, become tame. “This is the closest thing to a smoking gun we’ve ever had,” says Greger Larson, an evolutionary biologist at the University of Oxford in the United Kingdom who has studied the domestication of pigs, dogs, and other animals. “We’re much closer to understanding the nitty-gritty of domestication than we were a decade ago.” Cats first entered human society about 9500 years ago, not long after people first took up farming in the Middle East. Drawn to rodents that had invaded grain stores, wildcats slunk out of the deserts and into villages. There, many scientists suspect, they mostly domesticated themselves, with the friendliest ones able to take advantage of human table scraps and protection. Over thousands of years, cats shrank slightly in size, acquired a panoply of coat colors and patterns, and (largely) shed the antisocial tendencies of their past. Domestic animals from cows to dogs have undergone similar transformations, yet scientists know relatively little about the genes involved. Researchers led by Michael Montague, a postdoc at the Washington University School of Medicine in St. Louis, have now pinpointed some of them. The scientists started with the genome of a domestic cat—a female Abyssinian—that had been published in draft form in 2007, then filled in missing sequences and identified genes. They compared the resulting genome with those of cows, tigers, dogs, and humans. © 2014 American Association for the Advancement of Science.
By Dr. Catherine A. Madison “Now why did I walk into this room? Oh, yes, looking for my …” This scenario, familiar to many, is most often a sign of normal aging — or of having too much on our minds. But when these events seem to be happening frequently, is it a more serious problem, such as Alzheimer’s disease or another dementia? Even more importantly, are there good health habits that can help lower the risk of these neurodegenerative conditions? Research continues to demonstrate that healthy lifestyles lower one’s risk of developing cognitive decline later in life. Wise food choices and lots of exercise are a good base, along with learning new material and keeping socially connected. But another key element to brain health is good sleep. We may take sleep for granted, but research suggests this is not a passive process. There is a growing consensus that sleep is linked to learning, memory, nerve cell remodeling and repair. Evidence also suggests lack of sleep can contribute to mood and immune disorders, as well as to a decline in overall health. Most of us have read the dos and don’ts of good sleep hygiene: avoid napping, don’t drink alcohol or caffeine close to bedtime, avoid late-evening exercise and sleep in a room that is quiet, dark and cool. We’ve also been told about sleep cycles, in which we typically progress from light sleep early in the night to slow wave sleep with rapid eye movement, or REM, later on. We need a balance of sleep cycles for optimal health.
By Tracy Jarrett Autism advocates on Friday applauded Jerry Seinfeld's disclosure that he may be autistic, while warning against making him the poster boy for a disorder that is no laughing matter. “I think, on a very drawn-out scale, I think I’m on the spectrum,” Seinfeld told NBC Nightly News’ Brian Williams. "Basic social engagement is really a struggle. I'm very literal, when people talk to me and they use expressions, sometimes I don't know what they're saying," he said. "But I don't see it as dysfunctional, I just think of it as an alternate mindset." Seinfeld's revelation sends a positive message that the autism community is much larger and more diverse than people often understand, Ari Ne’eman, president of the Autistic Advocacy Network, told NBC News. Ne’eman is living with autism and says that there is still a tremendous amount of stigma surrounding autism that hinders the opportunities available to those with the disorder. “Think about what this does for a closeted autistic person who goes into the workplace knowing that their co-workers have just seen somebody they know, respect, and have a positive opinion of, like Jerry Seinfeld, identify in this way — it’s a valuable and important step in building a greater tolerance for autism,” Ne’eman said. Liz Feld, president of Autism Speaks, agreed, pointing out that “there are many people on the autism spectrum who can relate to Jerry’s heartfelt comments about his own experiences.”
Link ID: 20289 - Posted: 11.08.2014
Sara Reardon Delivering medications to the brain could become easier, thanks to molecules that can escort drugs through the notoriously impervious sheath that separates blood vessels from neurons. In a proof-of-concept study in monkeys, biologists used the system to reduce levels of the protein amyloid-β, which accumulates in the brain plaques associated with Alzheimer's disease1. The blood–brain barrier is a layer of cells lining the inner surface of the capillaries that feed the central nervous system. It is nature's way of protecting the delicate brain from infectious agents and toxic compounds, while letting nutrients and oxygen in and waste products out. Because the barrier strictly regulates the passage of larger molecules and often prevents drug molecules from entering the brain, it has long posed one of the most difficult challenges in developing treatments for brain disorders. Several approaches to bypassing the barrier are being tested, including nanoparticles that are small enough to pass through the barrier's cellular membranes and deliver their payload; catheters that carry a drug directly into the brain; and ultrasound pulses that push microbubbles through the barrier. But no approach has yet found broad therapeutic application. Neurobiologist Ryan Watts and his colleagues at the biotechnology company Genentech in South San Francisco have sought to break through the barrier by exploiting transferrin, a protein that sits on the surface of blood vessels and carries iron into the brain. The team created an antibody with two ends. One end binds loosely to transferrin and uses the protein to transport itself into the brain. And once the antibody is inside, its other end targets an enzyme called β-secretase 1 (BACE1), which produces amyloid-β. Crucially, the antibody binds more tightly to BACE1 than to transferrin, and this pulls it off the blood vessel and into the brain. It locks BACE1 shut and prevents it from making amyloid-β. © 2014 Nature Publishing Group,
Link ID: 20286 - Posted: 11.06.2014
|By Lindsey Konkel and Environmental Health News New York City children exposed in the womb to high levels of pollutants in vehicle exhaust had a five times higher risk of attention problems at age 9, according to research by Columbia University scientists published Wednesday. The study adds to earlier evidence that mothers' exposures to polycyclic aromatic hydrocarbons (PAHs), which are emitted by the burning of fossil fuels and other organic materials, are linked to children's behavioral problems associated with Attention Deficit Hyperactivity Disorder (ADHD). “Our research suggests that environmental factors may be contributing to attention problems in a significant way,” said Frederica Perera, an environmental health scientist at Columbia’s Mailman School of Public Health who was the study's lead author. About one in 10 U.S. kids is diagnosed with ADHD, according to the Centers for Disease Control and Prevention. Children with ADHD are at greater risk of poor academic performance, risky behaviors and lower earnings in adulthood, the researchers wrote. “Air pollution has been linked to adverse effects on attention span, behavior and cognitive functioning in research from around the globe. There is little question that air pollutants may pose a variety of potential health risks to children of all ages, possibly beginning in the womb,” said Dr. Andrew Adesman, chief of developmental and behavioral pediatrics at Steven & Alexandra Cohen Children’s Medical Center of New York. He did not participate in the new study. © 2014 Scientific American
Kate Baggaley Much of the increase in autism diagnoses in recent decades may be tied to changes in how the condition is reported. Sixty percent of the increase in autism cases in Denmark can be explained by these changes, scientists report November 3 in JAMA Pediatrics. The researchers followed all 677,915 people born in Denmark in 1980 through 1991, monitoring them from birth through the end of 2011. Among children born in this period, diagnoses increased fivefold, until 1 percent of children born in the early 1990s were diagnosed with autism by age 20. During these decades, Denmark experienced two changes in the way autism is reported. In 1994, the criteria physicians rely on to diagnose autism were updated in both the International Classification of Diseases manual used by Denmark and in its American counterpart, the Diagnostic and Statistical Manual of Mental Disorders. Then in 1995, the Danish Psychiatric Register began reporting diagnoses where doctors had only outpatient contact with children, in addition to cases where autism was diagnosed after children had been kept overnight. The researchers estimated Danish children’s likelihood of being diagnosed with autism before and after the two reporting changes. These changes accounted for 60 percent of the increase in diagnoses. © Society for Science & the Public 2000 - 2014.
Link ID: 20280 - Posted: 11.05.2014
By SINDYA N. BHANOO BERKELEY, CALIF. — Lilith Sadil, 12, climbs into an examination chair here at the Myopia Control Center at the University of California. “Do you know why you are here?” asks Dr. Maria Liu, an optometrist. “Because my eyes are changing fast,” Lilith says. “Do you read a lot?” Dr. Liu asks. “Yes.” “Do you use the computer a lot?” “Yes.” Lilith is an active child who practices taekwondo. But like an increasing number of children, she has myopia — she can see close up but not farther away. Her mother, Jinnie Sadil, has brought her to the center because she has heard about a new treatment that could help. Eye specialists are offering young patients special contact lenses worn overnight that correct vision for the next day. Myopia has become something of a minor epidemic: More than 40 percent of Americans are nearsighted, a 16 percent increase since the 1970s. People with so-called high myopia — generally, blurry vision beyond about five inches — face an increased likelihood of developing cataracts and glaucoma, are at higher risk for retinal detachments that can result in blindness. Exactly what is causing the nationwide rise in nearsightedness is not known. “It can’t be entirely genetic, because genes don’t change that fast,” said Susan Vitale, an epidemiologist at the National Institutes of Health who studies myopia. “It’s probably something that’s environmental, or a combination of genetic and environmental factors.” Some research indicates that “near work” — reading, computer work, playing video games, and using tablets and smartphones — is contributing to the increase. A recent study found that the more educated a person is, the more likely he or she will be nearsighted. A number of other studies show that children who spend time outdoors are less likely to develop high myopia. But no one is certain whether the eye benefits from ultraviolet light or whether time outside simply means time away from near work. © 2014 The New York Times Company
Joan Raymond TODAY contributor It’s well established that baby talk plays a huge role in helping the wee widdle babies learn to tawk. And — no surprise — moms talk more to babies than dads do. But it seems that the baby's sex plays a role, too: Moms may be talking more to their infant daughters than their sons during the early weeks and months of a child’s life. In a new study published Monday in the online edition of Pediatrics, researchers looked at the language interactions between 33 late preterm and term infants and their parents by capturing 3,000 hours of recordings. Somewhat surprisingly, the researchers found that moms interacted vocally more with infant daughters rather than sons both at birth and 44 weeks post-menstrual age (equivalent to 1 month old.) Male adults responded more frequently to infant boys than infant girls, but the difference did not reach statistical significance, say the researchers. “We wanted to look more at gender and factors that affect these essentially mini-conversations that parents have with infants,” says lead author and neonatologist Dr. Betty Vohr, director of the Neonatal Follow-Up Program at Women & Infants Hospital of Rhode Island. “Infants are primed to vocalize and have reciprocal interactions.”
By CATHERINE SAINT LOUIS More than 50 children in 23 states have had mysterious episodes of paralysis to their arms or legs, according to data gathered by the Centers for Disease Control and Prevention. The cause is not known, although some doctors suspect the cases may be linked to infection with enterovirus 68, a respiratory virus that has sickened thousands of children in recent months. Concerned by a cluster of cases in Colorado, the C.D.C. last month asked doctors and state health officials nationwide to begin compiling detailed reports about cases of unusual limb weakness in children. Experts convened by the agency plan next week to release interim guidelines on managing the condition. That so many children have had full or partial paralysis in a short period is unusual, but officials said that the cases seemed to be extremely rare. “At the moment, it looks like whatever the chances are of getting this syndrome are less than one in a million,” said Mark A. Pallansch, the director of the division of viral diseases at the C.D.C. Some of the affected children have lost the use of a leg or an arm, and are having physical therapy to keep their muscles conditioned. Others have sustained more extensive damage and require help breathing. Marie, who asked to be identified by her middle name to protect her family’s privacy, said her 4-year-old son used to climb jungle gyms. But in late September, after the whole family had been sick with a respiratory illness, he started having trouble climbing onto the couch. He walked into Boston Children’s Hospital the day he was admitted. But soon his neck grew so weak, it “flopped completely back like he was a newborn,” Marie said. Typically, the time from when weakness begins until it reaches its worst is one to three days. But for her son, eight mornings in a row, he awoke with a "brand new deficit" until he had some degree of weakness in each limb and had trouble breathing. He was eventually transferred to a Spaulding rehabilitation center, where he is now. © 2014 The New York Times Company
By Virginia Morell Human fetuses are clever students, able to distinguish male from female voices and the voices of their mothers from those of strangers between 32 and 39 weeks after conception. Now, researchers have demonstrated that the embryos of the superb fairy-wren (Malurus cyaneus, pictured), an Australian songbird, also learn to discriminate among the calls they hear. The scientists played 1-minute recordings to 43 fairy-wren eggs collected from nests in the wild. The eggs were between days 9 and 13 of a 13- to 14-day incubation period. The sounds included white noise, a contact call of a winter wren, or a female fairy-wren’s incubation call. Those embryos that listened to the fairy-wrens’ incubation calls and the contact calls of the winter wrens lowered their heart rates, a sign that they were learning to discriminate between the calls of a different species and those of their own kind, the researchers report online today in the Proceedings of the Royal Society B. (None showed this response to the white noise.) Thus, even before hatching, these small birds’ brains are engaged in tasks requiring attention, learning, and possibly memory—the first time embryonic learning has been seen outside humans, the scientists say. The behavior is key because fairy-wren embryos must learn a password from their mothers’ incubation calls; otherwise, they’re less successful at soliciting food from their parents after hatching. © 2014 American Association for the Advancement of Science.
By Paula Span First, an acknowledgment: Insomnia bites. S. Bliss, a reader from Albuquerque, comments that even taking Ativan, he or she awakens at 4:30 a.m., can’t get back to sleep and suffers “a state of sleep deprivation and eventually a kind of walking exhaustion.” Molly from San Diego bemoans “confusion, anxiety, exhaustion, depression, loss of appetite, frankly a loss of will to go on,” all consequences of her sleeplessness. She memorably adds, “Give me Ambien or give me death.” Marciacornute reports that she’s turned to vodka (prompting another reader to wonder if Medicare will cover booze). After several rounds of similar laments here (and not only here; insomnia is prevalent among older adults), I found the results of a study by University of Chicago researchers particularly striking. What if people who report sleep problems are actually getting enough hours of sleep, overall? What if they’re not getting significantly less sleep than people who don’t complain of insomnia? Maybe there’s something else going on. It has always been difficult to ascertain how much people sleep; survey questions are unreliable (how can you tell when you’ve dozed off?), and wiring people with electrodes creates such an abnormal situation that the results may bear little resemblance to ordinary nightlife. Enter the actigraph, a wrist-motion monitor. “The machines have gotten better, smaller, less clunky and more reliable,” said Linda Waite, a sociologist and a co-author of the study. By having 727 older adults across the United States (average age: almost 72) wear actigraphs for three full days, Dr. Waite and her colleagues could tell when subjects were asleep and when they weren’t. Then they could compare their reported insomnia to their actual sleep patterns. Overall, in this random sample, taken from an ongoing national study of older adults, people didn’t appear sleep-deprived. They fell asleep at 10:27 p.m. on average, and awakened at 6:22 a.m. After subtracting wakeful periods during the night, they slept an average seven and a quarter hours. But averages don’t tell us much, so let’s look more closely at their reported insomnia. “What was surprising to us is that there’s very little association between people’s specific sleep problems and what the actigraph shows,” Dr. Waite said. © 2014 The New York Times Company
By Neuroskeptic A new paper threatens to turn the world of autism neuroscience upside down. Its title is Anatomical Abnormalities in Autism?, and it claims that, well, there aren’t very many. Published in Cerebral Cortex by Israeli researchers Shlomi Haar and colleagues, the new research reports that there are virtually no differences in brain anatomy between people with autism and those without. What makes Haar et al.’s essentially negative claims so powerful is that their study had a huge sample size: they included structural MRI scans from 539 people diagnosed with high-functioning autism spectrum disorder (ASD) and 573 controls. This makes the paper an order of magnitude bigger than a typical structural MRI anatomy study in this field. The age range was 6 to 35. The scans came from the public Autism Brain Imaging Data Exchange (ABIDE) database, a data sharing initiative which pools scans from 18 different neuroimaging centers. Haar et al. examined the neuroanatomy of the cases and controls using the popular FreeSurfer software package. What did they find? Well… not much. First off, the ASD group had no differences in overall brain size (intracranial volume). Nor were there any group differences in the volumes of most brain areas; the only significant finding here was an increased ventricle volume in the ASD group, but even this had a small effect size (d = 0.34). Enlarged ventricles is not specific to ASD by any means – the same thing has been reported in schizophrenia, dementia, and many other brain disorders.
by Neurobonkers A paper published in Nature Reviews Neuroscience last week addressed the prevalence of neuromyths among educators. The paper has been widely reported, but the lion's share of the coverage glossed over the impact that neuromyths have had in the real world. Your first thought after reading the neuromyths in the table below — which were widely believed by teachers — may well be, "so what?" It is true that some of the false beliefs are relatively harmless. For example, encouraging children to drink a little more water might perhaps result in the consumption of less sugary drinks. This may do little if anything to reduce hyperactivity but could encourage a more nutritious diet which might have impacts on problems such as Type II diabetes. So, what's the harm? The paper addressed a number of areas where neuromyths have had real world impacts on educators and policymakers, which may have resulted negatively on the provision of education. The graph above, reprinted in the Nature Reviews Neuroscience, paper has been included as empirical data in educational policy documents to provide evidence for an "allegedly scientific argument for withdrawing public funding of university education." The problem? The data is made up. The graph is in fact a model that is based on the false assumption that investment before the age of three will have many times the benefit of investment made in education later in life. The myth of three — the belief that there is a critical window to educate children before the age of three, after which point the trajectory is fixed — is one of the most persistent neuromyths. Viewed on another level, while some might say investment in early education can never be a bad thing, how about the implication that the potential of a child is fixed at such an early point in their life, when in reality their journey has just begun. © Copyright 2014, The Big Think, Inc
By CLIVE THOMPSON “You just crashed a little bit,” Adam Gazzaley said. It was true: I’d slammed my rocket-powered surfboard into an icy riverbank. This was at Gazzaley’s San Francisco lab, in a nook cluttered with multicolored skullcaps and wires that hooked up to an E.E.G. machine. The video game I was playing wasn’t the sort typically pitched at kids or even middle-aged, Gen X gamers. Indeed, its intended users include people over 60 — because the game might just help fend off the mental decline that accompanies aging. It was awfully hard to play, even for my Call of Duty-toughened brain. Project: Evo, as the game is called, was designed to tax several mental abilities at once. As I maneuvered the surfboard down winding river pathways, I was supposed to avoid hitting the sides, which required what Gazzaley said was “visual-motor tracking.” But I also had to watch out for targets: I was tasked with tapping the screen whenever a red fish jumped out of the water. The game increased in difficulty as I improved, making the river twistier and obliging me to remember turns I’d taken. (These were “working-memory challenges.”) Soon the targets became more confusing — I was trying to tap blue birds and green fish, but the game faked me out by mixing in green birds and blue fish. This was testing my “selective attention,” or how quickly I could assess a situation and react to it. The company behind Project: Evo is now seeking approval from the Food and Drug Administration for the game. If it gets that government stamp, it might become a sort of cognitive Lipitor or Viagra, a game that your doctor can prescribe for your aging mind. After only two minutes of play, I was making all manner of mistakes, stabbing frantically at the wrong fish as the game sped up. “It’s hard,” Gazzaley said, smiling broadly as he took back the iPad I was playing on. “It’s meant to really push it.” “Brain training” games like Project: Evo have become big business, with Americans spending an estimated $1.3 billion a year on them. They are also a source of controversy. © 2014 The New York Times Company