Chapter 16. None
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By JOHN BRANCH When the N.F.L. agreed in 2012 to donate tens of millions of dollars to concussion research overseen by the National Institutes of Health, it was widely seen as a positive turning point in football’s long history of playing down the long-term effects of brain injuries on players. At the time, the league said that it would have no influence over how the money was used. But the league and its head, neck and spine committee worked to improperly influence the government research, trying to steer the study toward a doctor with ties to the league, according to a study conducted by a congressional committee and released on Monday. “Our investigation has shown that while the N.F.L. had been publicly proclaiming its role as funder and accelerator of important research, it was privately attempting to influence that research,” the study concluded. “The N.F.L. attempted to use its ‘unrestricted gift’ as leverage to steer funding away from one of its critics.” The N.F.L., in a statement, said it rejected the accusations laid out in the study, which was conducted by Democratic members of the House Committee on Energy and Commerce. “There is no dispute that there were concerns raised about both the nature of the study in question and possible conflicts of interest,” the league said. “These concerns were raised for review and consideration through the appropriate channels.” It is the latest in a long history of instances in which the N.F.L. has been found to mismanage concussion research, dating to the league’s first exploration of the crisis when it used deeply flawed data to produce a series of studies. In this case, some of the characters are the same, including Dr. Elliot Pellman, who led the league’s concussion committee for years before he was discredited for his questionable credentials and his role as a longtime denier of the effects of concussions on players. © 2016 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 22241 - Posted: 05.24.2016
By Andy Coghlan It’s a tear-jerker worthy of Hollywood – and one of the first examples of compassionate care and grief in a wild monkey. The alpha male of a group of snub-nosed monkeys and his dying partner spent a final, tender hour together beneath the tree from which she had fallen minutes earlier, cracking her head on a rock. Before she succumbed, he gently touched and groomed her. And after she was dead he remained by her side for 5 minutes, touching her and pulling gently at her hand, as if to try and revive her (for a full account of what happened, see “A monkey tends to his dying mate – as it unfolded”, below). “The case we’ve reported is particularly important because of the exclusively gentle nature of the interactions, and the special treatment of the dying female shown by the adult male,” says James Anderson of Kyoto University, Japan. “The events suggest that in the case of strongly bonded individuals at least, monkeys may show compassionate behaviour to ailing or dying individuals.” Together, the reports add to evidence that humans may not be the only species to display grieving behaviour following bereavement, or to show respect for dead individuals with whom they have forged ties. They also hint that animals have some recognition of the finality of death. “It seems likely that in long-lived species such as many primates, repeated exposure to death within the group leads to an understanding of the irreversibility of death,” says Anderson. “I believe the adult male and other members of his unit understood the dead female was no longer alive.” © Copyright Reed Business Information Ltd.
“I understand how the appearance and texture of food can change the experience,” says food writer and Great British Bake Off finalist Tamal Ray, “but I never really considered how the other senses might have a role to play.” An anaesthetist by day, Ray is best-known for creating spectacular tiered cakes and using a syringe to inject extra, syrupy deliciousness into them. Which is why we introduced him to Oxford psychologist Charles Spence and chef Jozef Youssef – and turned what they taught him about the science of taste into the video above. Part mad professor, part bon vivant, Spence has spent the past 15 years discovering that little of how we experience flavour is to do with our taste buds – smell, vision, touch and even sound dictate how we perceive flavours. Youssef, meanwhile, sharpened his culinary skills at the Fat Duck, the Connaught and the Dorchester, before starting experimental dining outfit Kitchen Theory, where he applies science to meals that play with the multisensory experience of eating. When Spence started studying the sensory science behind flavour perception, it was a deeply unfashionable subject. “There’s some ancient Roman notion that eating and drinking involve lower senses,” he says, “not higher, rational senses like hearing and vision.” Now, the fruits of the research field he calls “gastrophysics” can be seen everywhere from the world’s top restaurants to airline food, via progressive hospital kitchens and multisensory cocktail bars. Spence heads the Crossmodal Research Laboratory at the University of Oxford. “Crossmodal”, in this context, means the investigation of how all the senses interact. Although we’re often unaware of it, when it comes to flavour perception, we all have synaesthesia. That is, our senses intermingle so that our brains combine shapes, textures, colours and even sounds with corresponding tastes.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 22239 - Posted: 05.23.2016
Aaron E. Carroll I don’t eat breakfast. It’s not that I dislike what’s offered. Given the choice of breakfast food or lunch food, I’d almost always choose eggs or waffles. It’s just that I’m not hungry at 7:30 a.m., when I leave for work. In fact, I’m rarely hungry until about lunchtime. So, other than a morning cup of coffee, I don’t eat much before noon. This habit has forced me to be subjected to more lectures on how I’m hurting myself, my diet, my work and my health than almost any other. Only a fool would skip the most important meal of the day, right? As with many other nutritional pieces of advice, our belief in the power of breakfast is based on misinterpreted research and biased studies. It does not take much of an effort to find research that shows an association between skipping breakfast and poor health. A 2013 study published in the journal Circulation found that men who skipped breakfast had a significantly higher risk of coronary heart disease than men who ate breakfast. But, like almost all studies of breakfast, this is an association, not causation. More than most other domains, this topic is one that suffers from publication bias. In a paper published in The American Journal of Clinical Nutrition in 2013, researchers reviewed the literature on the effect of breakfast on obesity to look specifically at this issue. They first noted that nutrition researchers love to publish results showing a correlation between skipping breakfast and obesity. They love to do so again and again. At some point, there’s no reason to keep publishing on this. However, they also found major flaws in the reporting of findings. People were consistently biased in interpreting their results in favor of a relationship between skipping breakfast and obesity. They improperly used causal language to describe their results. They misleadingly cited others’ results. And they also improperly used causal language in citing others’ results. People believe, and want you to believe, that skipping breakfast is bad. © 2016 The New York Times Company
Link ID: 22238 - Posted: 05.23.2016
By Lucas Powers, CBC News You're standing on the side of the road, with traffic whizzing past. The police officer who pulled you over suspects you may have smoked the reefer before departing for McDonald's. But she's in a bit of a quagmire, because, really, there's no reliable way to know for sure. Are you high? If you are high, how high are you, really? Or really did you just want those little cheeseburgers (no ketchup and extra pickles)? So she does the most logical thing: a field sobriety test. Tried and true. Walk the line. Touch the tip your nose. Can't do it? That's... suspicious. Maybe a night in the clink? Some Canadian cops also have roadside saliva swabs that can be used to test for the presence of drugs, but they are useless, legally speaking (for now.) Now, had you been quaffing ales before the drive, a breathalyzer — controversial as they can be in terms of accuracy and reliability — would have cleared up the situation pretty quickly. Of course, no such roadside device exists for cannabis and its psychotropic ingredient THC. There's growing evidence that cannabis can impair driving by slowing reaction times and encouraging perplexing moves by drivers, like slowing way down and being reluctant to change lanes. Doctors at Toronto's Centre for Addiction and Mental Health are doing the world's biggest-ever clinical study, asking exactly what causes this behaviour, and how dangerous it is. Either way, an innovation war worth billions to the victor has been declared over developing a cannabis breathalyzer. ©2016 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 22236 - Posted: 05.23.2016
Bret Stetka We've all been caught in that hazy tug of war between wakefulness and sleep. But the biology behind how our brains drive us to sleep when we're sleep-deprived hasn't been entirely clear. For the first time scientists have identified the neurons in the brain that appear to control sleep drive, or the growing pressure we feel to sleep after being up for an extended period of time. The findings, published online Thursday by the journal Cell, could lead to better understanding of sleep disorders in humans. And perhaps, one day, if the work all pans out, better treatments for chronic insomnia could be developed. To explore which brain areas might be involved in sleep drive, Johns Hopkins neuroscientist Dr. Mark Wu and his colleagues turned to fruit flies, that long tinkered-with subject of scientific inquiry. Despite our rather obvious physical distinctions, humans and fruit flies – or Drosophila – have a good deal in common when it comes to genes, brain architecture and even behaviors. Included in the study were over 500 strains of fly, each with unique brain activation profiles (meaning certain circuits are more active in certain flies). By employing a genetic engineering technique in which specific groups of neurons can be activated with heat, the researchers were able to monitor the firing of nearly all the major circuits in the fruit fly brain and monitor the resulting effects on sleep. Moreover, the neurons of interest were engineered to glow green when activated allowing specific cells to be identified with fluorescent microscopy. Wu found that activating a group of cells called R2 neurons, which are found in a brain region known as the ellipsoid body, put fruit flies to sleep, even for hours after the neurons were "turned off." © 2016 npr
By D. T. Max When a spinal cord is damaged, location is destiny: the higher the injury, the more severe the effects. The spine has thirty-three vertebrae, which are divided into five regions—the coccygeal, the sacral, the lumbar, the thoracic, and the cervical. The nerve-rich cord traverses nearly the entire length of the spine. The nerves at the bottom of the cord are well buried, and sometimes you can walk away from damage to these areas. In between are insults to the long middle region of the spine, which begins at the shoulders and ends at the midriff. These are the thoracic injuries. Although they don’t affect the upper body, they can still take away the ability to walk or feel below the waist, including autonomic function (bowel, bladder, and sexual control). Injuries to the cord in the cervical area—what is called “breaking your neck”—can be lethal or leave you paralyzed and unable to breathe without a ventilator. Doctors who treat spinal-cord-injury patients use a letter-and-number combination to identify the site of the damage. They talk of C3s (the cord as it passes through the third cervical vertebra) or T8s (the eighth thoracic vertebra). These morbid bingo-like codes help doctors instantly gauge the severity of a patient’s injury. Darek Fidyka, who is forty-one years old, is a T9. He was born and raised in Pradzew, a small farming town in central Poland, not far from Lodz. ... Several of the wounds punctured his lungs, and one nearly cut his spinal cord in half. As Fidyka lay on the ground, he felt his body change. “I can remember very vividly losing feeling in my legs, bit by bit,” he says. “It started in the upper part of the spine and was moving down slowly while I lay waiting for the ambulance to arrive.”
Link ID: 22230 - Posted: 05.19.2016
Stephen Cave For centuries, philosophers and theologians have almost unanimously held that civilization as we know it depends on a widespread belief in free will—and that losing this belief could be calamitous. Our codes of ethics, for example, assume that we can freely choose between right and wrong. In the Christian tradition, this is known as “moral liberty”—the capacity to discern and pursue the good, instead of merely being compelled by appetites and desires. The great Enlightenment philosopher Immanuel Kant reaffirmed this link between freedom and goodness. If we are not free to choose, he argued, then it would make no sense to say we ought to choose the path of righteousness. Today, the assumption of free will runs through every aspect of American politics, from welfare provision to criminal law. It permeates the popular culture and underpins the American dream—the belief that anyone can make something of themselves no matter what their start in life. As Barack Obama wrote in The Audacity of Hope, American “values are rooted in a basic optimism about life and a faith in free will.” So what happens if this faith erodes? The sciences have grown steadily bolder in their claim that all human behavior can be explained through the clockwork laws of cause and effect. This shift in perception is the continuation of an intellectual revolution that began about 150 years ago, when Charles Darwin first published On the Origin of Species. Shortly after Darwin put forth his theory of evolution, his cousin Sir Francis Galton began to draw out the implications: If we have evolved, then mental faculties like intelligence must be hereditary. But we use those faculties—which some people have to a greater degree than others—to make decisions. So our ability to choose our fate is not free, but depends on our biological inheritance. © 2016 by The Atlantic Monthly Group.
Link ID: 22228 - Posted: 05.18.2016
George Johnson At the Science of Consciousness conference last month in Tucson, I was faced with a quandary: Which of eight simultaneous sessions should I attend? In one room, scientists and philosophers were discussing the physiology of brain cells and how they might generate the thinking mind. In another, the subject was free will — real or an illusion? Next door was a session on panpsychism, the controversial (to say the least) idea that everything — animal, vegetable and mineral — is imbued at its subatomic roots with mindlike qualities. Running on parallel tracks were sessions titled “Phenomenal Consciousness,” the “Neural Correlates of Consciousness” and the “Extended Mind.” For much of the 20th century, the science of consciousness was widely dismissed as an impenetrable mystery, a morass of a problem that could be safely pursued only by older professors as they thought deep thoughts in their endowed chairs. Beginning in the 1990s, the field slowly became more respectable. There is, after all, a gaping hole in science. The human mind has plumbed the universe, concluding that it is precisely 13.8 billion years old. With particle accelerators like the Large Hadron Collider at CERN, scientists have discovered the vanishingly tiny particles, like the Higgs boson, that underpin reality. But there is no scientific explanation for consciousness — without which none of these discoveries could have been made. © 2016 The New York Times Company
Link ID: 22227 - Posted: 05.18.2016
Andrea Hsu Scientists and doctors say the case is clear: The best way to tackle the country's opioid epidemic is to get more people on medications that have been proven in studies to reduce relapses and, ultimately, overdoses. Yet, only a fraction of the more than 4 million people believed to abuse prescription painkillers or heroin in the U.S. are being given what's called medication-assisted treatment. One reason is the limited availability of the treatment. But it's also the case that stigma around the addiction drugs has inhibited their use. Methadone and buprenorphine, two of the drugs used for treatment, are themselves opioids. A phrase you often hear about medication-assisted treatment is that it's merely replacing one drug with another. While doctors and scientists strongly disagree with that characterization, it's a view that's widespread in recovery circles. Now, the White House is pushing to change the landscape for people seeking help. In his 2017 budget, President Obama has asked Congress for $1.1 billion in new funding to address the opioid epidemic, with almost all of it geared toward expanding access to medication-assisted treatment. The White House is also highlighting success stories. At the National Prescription Drug Abuse and Heroin Summit held in Atlanta in March, President Obama appeared on stage with Crystal Oertle, a 35-year-old mother of two from Ohio. Oertle spoke of her spiral into addiction, which began with prescription painkillers and progressed to heroin. She tried unsuccessfully to quit on her own several times, before being prescribed buprenorphine a year ago. © 2016 npr
Keyword: Drug Abuse
Link ID: 22226 - Posted: 05.18.2016
By Sarah Kaplan You probably wouldn't be surprised if a scientist told you that your genes influence when you hit puberty, how tall you are, what your BMI will be and whether you're likely to develop male pattern baldness. But what if he said that the same gene could hold sway over all four things? That finding comes from a study published Monday in the journal Nature Genetics. Using data from dozens of genome-wide association studies (big scans of complete sets of DNA from many thousands of people), researchers at the New York Genome Center and the genetic analysis company 23andMe found examples of single "multitasking" genes that influence diverse and sometimes seemingly disparate traits. The scientists say that the links they uncovered could help researchers understand how certain genes work, and figure out better ways of treating some of the health problems they might control. "Most studies tend to go one disease at a time," said Joseph Pickrell, a professor at Columbia University and the New York Genome Center's lead investigator on the project. "But if we can try to make these sorts of connections between what you might think of as unrelated traits ... that gives us another angle of attack to understand the connections between these different diseases." To start, Pickrell and his team sought out genome-wide association studies (GWAS) identifying particular genetic variants associated with 42 different traits. Many had to do with diseases (for example, studies that linked certain genes to the risk of developing Alzheimer's or type 2 diabetes) and other personal health traits (body mass index, blood type, cholesterol levels).
Keyword: Genes & Behavior
Link ID: 22225 - Posted: 05.18.2016
A bionic body is closer than you think By Dwayne Godwin, Jorge Cham Dwayne Godwin is a neuroscientist at the Wake Forest University School of Medicine. Jorge Cham draws the comic strip Piled Higher and Deeper at www.phdcomics.com. © 2016 Scientific American
Link ID: 22222 - Posted: 05.17.2016
By JONATHAN BALCOMBE Washington — IN March, two marine biologists published a study of giant manta rays responding to their reflections in a large mirror installed in their aquarium in the Bahamas. The two captive rays circled in front of the mirror, blew bubbles and performed unusual body movements as if checking their reflection. They made no obvious attempt to interact socially with their reflections, suggesting that they did not mistake what they saw as other rays. The scientists concluded that the mantas seemed to be recognizing their reflections as themselves. Mirror self-recognition is a big deal. It indicates self-awareness, a mental attribute previously known only among creatures of noted intelligence like great apes, dolphins, elephants and magpies. We don’t usually think of fishes as smart, let alone self-aware. As a biologist who specializes in animal behavior and emotions, I’ve spent the past four years exploring the science on the inner lives of fishes. What I’ve uncovered indicates that we grossly underestimate these fabulously diverse marine vertebrates. The accumulating evidence leads to an inescapable conclusion: Fishes think and feel. Because fishes inhabit vast, obscure habitats, science has only begun to explore below the surface of their private lives. They are not instinct-driven or machinelike. Their minds respond flexibly to different situations. They are not just things; they are sentient beings with lives that matter to them. A fish has a biography, not just a biology. Those giant manta rays have the largest brains of any fish, and their relative brain-to-body size is comparable to that of some mammals. So, an exception? Then you haven’t met the frillfin goby. © 2016 The New York Times Company
Dara Mohammadi As the small motorboat chugs to a halt, three travellers, wind-beaten from the three-hour journey along the Atrato river, step on to the muddy banks of Bellavista, an otherwise inaccessible town in the heart of the heavily forested north-west of Colombia. They swing their hessian bags – stuffed with bedsheets, dried beans and cuddly toys – to their shoulders and clamber up a dusty path. Tucked inside the bag of one of the travellers, neuropsychologist Sonia Moreno, is the reason they are here: a wad of unfinished, hand-drawn charts of family trees. The people whose names are circled on the charts have Huntington’s disease, an incurable genetic brain disorder that usually starts between the ages of 35 and 45 years. It begins with personality changes that can make them aggressive, violent, uninhibited, anxious and depressed. The disease progresses slowly, robbing them first of the control of their body, which jerks and twists seemingly of its own will, and then their ability to walk, talk and think until, about 20 years after the symptoms first begin, they die. Their children, each of whom has a 50% chance of inheriting the disease, watch and wait to see if it will happen to them. It is in this way that the disease strangles families. With Moreno is Ignacio Muñoz-Sanjuan, vice president of translational biology at CHDI Foundation, a US nonprofit research organisation that aims to find ways to prevent or slow down the progression of the disease. The foundation spent $140m–$150m (£97m-£104m) on research last year, but Muñoz-Sanjuan is not here on official business. He’s here for Factor-H, an initiative he founded four years ago to help with the other end of the problem – poor families with Huntington’s struggling in Latin America. © 2016 Guardian News and Media Limited o
By Julia Shaw You see a crime take place. You are interviewed about it. You give a statement about what you saw. Do you think that at a later date you would be able to detect whether someone had tampered with your statement? Or re-written parts of it? This is currently a hot topic in the UK, where a very recently published inquiry into the so-called Hillsborough disaster, in which 96 people were crushed to death during a soccer match in 1989, found that testimonies had been deliberately altered by police. Research published earlier this year by the false memory dream team at the University of California, looked directly into the implications of such police (mis)conduct. They found that it is possible that changed statements can go unnoticed by the person who gave the original testimony, and may even develop into a false memory that accommodates the false account. To describe this effect, the researchers came up with the term "memory blindness"—the phenomenon of failing to recognize our own memories. The term was intended to mirror the ‘choice blindness’ literature. Choice blindness is forgetting choices that we have made. The researchers wanted to know “Can choice blindness have lasting effects on eyewitness memory?” To examine this, PhD Student Kevin Cochran and his colleagues conducted two experiments. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22218 - Posted: 05.16.2016
By John Horgan Speakers at the 2016 Tucson consciousness conference suggested that “temporal nonlocality” or other quantum effects in the brain could account for free will. But what happens when the brain is immersed in a hot tub? This is the second of four posts on “The Science of Consciousness” in Tucson, Arizona, which lasted from April 26 to April 30. (See Further Reading for links to other posts.) Once again, I’m trying to answer the question: What is it like to be a skeptical journalist at a consciousness conference? -- John Horgan DAY 2, THURSDAY, APRIL 28. HOT TUBS AND QUANTUM INCOHERENCE Breakfast on the patio with Stuart Kauffman, who has training in… almost everything. Philosophy, medicine, science. We’ve bumped heads in the past, but we’re friendly now. In his mid-70s, Stu is still obsessed with--and hacking away at--the biggest mysteries. We talk about… almost everything. Quantum mechanics, the origin of life, materialism, free will, God, the birth and death of his daughter, the death of his wife, his re-marriage, predictability versus possibility. As Stu speaks, his magnificent, weathered face looks happy/sad, arrogant/anxious. Superposition of emotions. He tells me about his brand-new book, Humanity in a Creative Universe, in which he outlines a perspective that can help lift us out of our spiritual crisis. Who saves the savior? I scoot to a morning session, “Consciousness and Free Will.” I hope it will supply me with ammo for my defenses of free will. I can do without God, but not free will. © 2016 Scientific American, a Division of Nature America, Inc.
Link ID: 22216 - Posted: 05.16.2016
By Adam Gopnik On a bitter, soul-shivering, damp, biting gray February day in Cleveland—that is to say, on a February day in Cleveland—a handless man is handling a nonexistent ball. Igor Spetic lost his right hand when his forearm was pulped in an industrial accident six years ago and had to be amputated. In an operation four years ago, a team of surgeons implanted a set of small translucent “interfaces” into the neural circuits of his upper arm. This afternoon, in a basement lab at a Veterans Administration hospital, the wires are hooked up directly to a prosthetic hand—plastic, flesh-colored, five-fingered, and articulated—that is affixed to what remains of his arm. The hand has more than a dozen pressure sensors within it, and their signals can be transformed by a computer into electric waves like those natural to the nervous system. The sensors in the prosthetic hand feed information from the world into the wires in Spetic’s arm. Since, from the brain’s point of view, his hand is still there, it needs only to be recalled to life. Now it is. With the “stimulation” turned on—the electronic feed coursing from the sensors—Spetic feels nineteen distinct sensations in his artificial hand. Above all, he can feel pressure as he would with a living hand. “We don’t appreciate how much of our behavior is governed by our intense sensitivity to pressure,” Dustin Tyler, the fresh-faced principal investigator on the Cleveland project, says, observing Spetic closely. “We think of hot and cold, or of textures, silk and cotton. But some of the most important sensing we do with our fingers is to register incredibly minute differences in pressure, of the kinds that are necessary to perform tasks, which we grasp in a microsecond from the feel of the outer shell of the thing. We know instantly, just by touching, whether to gently squeeze the toothpaste or crush the can.”
Keyword: Pain & Touch
Link ID: 22215 - Posted: 05.14.2016
By JONAH BROMWICH It’s relatively easy to determine when someone is too drunk to drive. If a driver’s blood-alcohol level is 0.08 percent or higher, that person is considered legally impaired. But a study says that measuring the effects of marijuana on drivers is far trickier, and that blood tests are an unreliable indication of impairment by cannabis. As more states consider legalizing the substance, that presents a challenge to legislators seeking to create laws on driving while impaired by marijuana. The study, commissioned by the AAA Foundation for Traffic Safety, found that laws in six states that legally assess impairment by measuring how much THC (the active ingredient in marijuana) is in a person’s blood are not supported by science. “There is no concentration of the drug that allows us to reliably predict that someone is impaired behind the wheel in the way that we can with alcohol,” said Jake Nelson, AAA’s director of traffic safety advocacy and research. Lawmakers in those states looked to policies on drunken driving for cues on how to legislate against driving while high. But the body absorbs alcohol and cannabis in different ways, the study said. While drunkenness directly correlates to alcohol in the bloodstream, cannabis impairment takes place only when THC makes its way into the fatty tissue of the brain. Regular marijuana users, including those who take the drug medicinally, often show no signs of impairment after using, according to Jolene Forman, a staff lawyer for the Drug Policy Alliance, a drug-reform advocacy group. She also said that marijuana can stay in the blood for hours, days and even weeks after its effects wear off. © 2016 The New York Times Company
Keyword: Drug Abuse
Link ID: 22214 - Posted: 05.14.2016
By Hazem Zohny Here is a picture of the nine-dot problem. The task seems simple enough: connect all nine dots with four straight lines, but, do so without lifting the pen from the paper or retracing any line. If you don’t already know the solution, give it a try – although your chances of figuring it out within a few minutes hover around 0 percent. In fact, even if I were to give you a hint like “think outside of the box,” you are unlikely to crack this deceptively (and annoyingly!) simple puzzle. And yet, if we were to pass a weak electric current through your brain (specifically your anterior temporal lobe, which sits somewhere between the top of your ear and temple), your chances of solving it may increase substantially. That, at least, was the finding from a study where 40 percent of people who couldn’t initially solve this problem managed to crack it after 10 minutes of transcranial direct current stimulation (tDCS) – a technique for delivering a painlessly weak electric current to the brain through electrodes on the scalp. How to explain this? It is an instance of the alleged power of tDCS and similar neurostimulation techniques. These are increasingly touted as methods that can “overclock” the brain in order to boost cognition, improve our moods, make us stronger, and even alter our moral dispositions. The claims are not completely unfounded: there is evidence that some people become slightly better at holding and manipulating information in their minds after a bout of tDCS. It also appears to reduce some people’s likelihood of formulating false memories, and seems to have a lasting improvement on some people’s ability to work with numbers. It can even appear to boost creativity, enhancing the ability of some to make abstract connections between words to come up with creative analogies. But it goes further, with some evidence that it can help people control their urges as well improve their mood. And beyond these psychological effects, tDCS of the part of the brain responsible for movement seems to improve muscular endurance and reduce fatigue. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22205 - Posted: 05.11.2016
By PAM BELLUCK BALTIMORE — Leave it to the youngest person in the lab to think of the Big Idea. Xuyu Qian, 23, a third-year graduate student at Johns Hopkins, was chatting in late January with Hongjun Song, a neurologist. Dr. Song was wondering how to test their three-dimensional model of a brain — well, not a brain, exactly, but an “organoid,” essentially a tiny ball of brain cells, grown from stem cells and mimicking early brain development. “We need a disease,” Dr. Song said. Mr. Qian tossed out something he’d seen in the headlines: “Why don’t we check out this Zika virus?” Within a few weeks — a nanosecond compared with typical scientific research time — that suggestion led to one of the most significant findings in efforts to answer a central question: How does the Zika virus cause brain damage, including the abnormally small heads in babies born to infected mothers? The answer could spur discoveries to prevent such devastating neurological problems. And time is of the essence. One year after the virus was first confirmed in Latin America, with the raging crisis likely to reach the United States this summer, no treatment or vaccine exists. “We can’t wait,” said Dr. Song, at the university’s Institute for Cell Engineering, where he and his wife and research partner, Dr. Guo-Li Ming, provided a pipette-and-petri-dish-level tour. “To translate our work for the clinic, to the public, normally it takes years. This is a case where we can make a difference right away.” The laboratory’s initial breakthrough, published in March with researchers at two other universities, showed that the Zika virus attacked and killed so-called neural progenitor cells, which form early in fetal development and generate neurons in the brain. © 2016 The New York Times Company