Chapter 13. Memory, Learning, and Development

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Scientists believe injections of a natural protein may lessen the symptoms and progress of Alzheimer's dementia after promising early trials in mice. The treatment - IL 33 - appeared to improve memory and help clear and prevent brain deposits similar to those seen in people with Alzheimer's. Tentative human studies of the treatment will soon begin, but experts say it will take many years to know if it could help patients in real life. The work is published in PNAS journal. Interleukin 33, or IL 33 for short, is made by the body as part of its immune defence against infection and disease, particularly within the brain and spinal cord. And patients with Alzheimer's have been found to have lower amounts of IL 33 in their brains than healthy adults. The researchers from the University of Glasgow and the Hong Kong University of Science and Technology tested what effect a boost of IL 33 might have on mice bred to have brain changes akin to Alzheimer's. The rodents rapidly improved their memory and cognitive function to that of the age-matched normal mice within a week of having the injections. Prof Eddy Liew, who led the work at the University of Glasgow, is excited but cautious about his findings. "Exciting as it is, there is some distance between laboratory findings and clinical applications. There have been enough false 'breakthroughs' in the medical field to caution us not to hold our breath until rigorous clinical trials have been done." © 2016 BBC.

Keyword: Alzheimers
Link ID: 22115 - Posted: 04.19.2016

For the first time, scientists have scanned the brains of subjects taking LSD, and found that the LSD state mimics that of infants. NPR's Rachel Martin speaks with researcher Robin Carhart-Harris. RACHEL MARTIN, HOST: Picture yourself in a boat on a river with tangerine trees and marmalade skies. Now picture yourself as a baby. You gaze up at your mother. She's got those kaleidoscope eyes. Pretty trippy, right? Turns out in a new study of brain scans, that the minds of people on LSD function in a similar way to babies' brains. Dr. Robin Carhart-Harris from Imperial College London's Center for Neuropsychopharmacology joins us from the studios of the BBC to talk about this study. So I understand this was the first time that brain scans like this have ever been done, looking specifically at the brains of people who have used LSD. How much LSD had your subjects taken? I mean, what were the prerequisites for a brain that you were going to scan? CARHART-HARRIS: Yeah, so they had to have had at least one experience with a psychedelic drug. So that includes LSD. It also includes magic mushrooms, other concoctions like ayahuasca, which is an Amazonian brew that has psychedelic properties. We gave them a moderate dose of LSD, roughly equivalent to what you might call a hit of LSD or one blotter of LSD if it was to be taken recreationally. MARTIN: So what kind of vetting did you have to do of the participants in your study because we should say different people respond to LSD in different ways? There are risks associated with this drug. CARHART-HARRIS: That's quite right. All drugs have risks, and LSD's no exception. One of the risks is that you might recruit someone who has a psychological vulnerability. So we're very, very careful when we recruit our volunteers to ensure that they have a solid mental health background. They don't have any personal or family history of any psychotic disorders - so those are things like schizophrenia. We have a psychiatrist assess them. We also evaluate their health. So they are very thoroughly screened. © 2016 npr

Keyword: Drug Abuse; Brain imaging
Link ID: 22112 - Posted: 04.18.2016

Eleanor Ainge Roy in Dunedin An octopus has made a brazen escape from the national aquarium in New Zealand by breaking out of its tank, slithering down a 50-metre drainpipe and disappearing into the sea. In scenes reminiscent of Finding Nemo, Inky – a common New Zealand octopus – made his dash for freedom after the lid of his tank was accidentally left slightly ajar. Staff believe that in the middle of the night, while the aquarium was deserted, Inky clambered to the top of his cage, down the side of the tank and travelled across the floor of the aquarium. Rob Yarrell, national manager of the National Aquarium of New Zealand in Napier, said: “Octopuses are famous escape artists. “But Inky really tested the waters here. I don’t think he was unhappy with us, or lonely, as octopus are solitary creatures. But he is such a curious boy. He would want to know what’s happening on the outside. That’s just his personality.” One theory is that Inky slid across the aquarium floor – a journey of three or four metres – and then, sensing freedom was at hand, into a drainpipe that lead directly to the sea. The drainpipe was 50 metres long, and opened on to the waters of Hawke’s Bay, on the east coast of New Zealand’s North Island. Another possible escape route could have involved Inky squeezing into an open pipe at the top of his tank, which led under the floor to the drain. © 2016 Guardian News and Media Limited

Keyword: Intelligence; Evolution
Link ID: 22103 - Posted: 04.14.2016

By Gareth Cook What are the most intelligent creatures on the planet? Humans come first. (Though there are days when we have to wonder.) After Homo sapiens, most people might answer chimpanzees, and then maybe dogs and dolphins. But what of birds? The science writer Jennifer Ackerman offers a lyrical testimony to the wonders of avian intelligence in her new book, “The Genius of Birds.” There have long been hints of bird smarts, but it’s become an active field of scientific inquiry, and Ackerman serves as tour guide. She answered questions from Mind Matters editor Gareth Cook. What drew you to birds? I’ve watched birds for most of my life. I admire all the usual things about them. Their plumage and song. Their intense way of living. Their flight. I also admire their resourcefulness and pluck. I’ve always been intrigued by their apparently smart behavior, whether learned or innate. I grew up in Washington, D.C. — the second youngest in a gaggle of five girls. My parents had precious little time for one-on-one. Especially my dad, who had a demanding government job. So when he asked me if I wanted to go birdwatching with him one spring morning when I was seven or eight, I jumped at the chance. It was magical, going out in the dark woods along the C&O canal and listening for bird song. My father had learned his calls and songs in Boy Scout camp from an expert, an elderly Greek man named Apollo, so he was pretty good at identifying birds, even the shy woodland species. Eventually he gave me my own copy of Peterson’s Field Guide, along with a small pair of binoculars. I’ve loved birds ever since. My first run in with a clever bird was on our dining room table. We had a pet parakeet, a budgerigar named Gre-Gre, who was allowed to fly around the dining room and perch on our head or shoulders. He had a kind of social genius. He made you love him. But at breakfast, it was impossible to eat your cereal without his constant harassment. He liked to perch on the edge of my bowl and peck at the cereal, flapping his wings frantically to keep his balance, splashing my milk. I’d build a barricade of boxes around my place setting, but he always found a way in, moving a box or popping over the top. He was a good problem-solver. © 2016 Scientific American

Keyword: Intelligence; Evolution
Link ID: 22101 - Posted: 04.13.2016

Dr. Perri Klass First of all, nobody takes a small child on an airplane for the fun of it. I have been there and I know. Don’t get me wrong, I’m no airplane saint; you won’t generally catch me offering to hold someone else’s kid, or making friends around the seatback. I don’t usually admit to being a pediatrician, for fear of hearing a medical saga. But I have put in my time on airplanes with my own infants and toddlers and small children, and I certainly know how it feels. Probably the best thing that can be said for traveling with young children is that it teaches you to appreciate traveling without them, however puzzling the inflight announcements, however long the delays, however tightly spaced the seats. I did enough economy-class traveling with children while my own were young that my reflexive reaction to all flight cancellations, turbulence or the moment when the person in front of me reclines the seat very suddenly, knocking my laptop closed, is now: At least I don’t have a small child with me – thank heavens. Babies do not cry on airplanes for the fun of it either. Nor do they cry, by and large, to let you know that their parents are neglectful or callous. They cry for infant versions of the same reasons that adults snap at one another about reclining seats, or elbow each other with quiet savagery over the armrest. They cry because their ears hurt and they’re being made to stay in a certain position when they don’t want to or the air smells strange and the noises are loud, or their stomachs feel upset or the day has been too long and they still aren’t there yet or they’re just plain cranky. As are we all. Crying is an evolutionary strategy to summon adult aid; over millennia, crying has probably evolved to be hard to ignore. I don’t know if it’s any comfort, but when you’re the parent with the crying baby, it doesn’t particularly help to be an expert. “I remember one flight where my daughter screamed the whole way and kept trying to get out of her seatbelt,” said my old friend, Dr. Elizabeth Barnett, a professor of pediatrics at Boston University and a travel medicine specialist. “As a parent, you feel two things — you’re in distress because you’re trying to comfort your child and not succeeding, so you feel bad for your child, and you also feel guilty because you know your child is disturbing everybody else.” © 2016 The New York Times Company

Keyword: Pain & Touch; Development of the Brain
Link ID: 22094 - Posted: 04.12.2016

Sam Doernberg and Joe DiPietro It’s the first day of class, and we—a couple of instructors from Cornell—sit around a table with a few of our students as the rest trickle in. Anderson, one of the students seated across from us, smiles and says, “I’m going to get an A+ in your class.” “No,” VanAntwerp retorts, “I’m getting the A+.” You might think that this scene is typical of classes at a school like Cornell University, where driven students compete for top marks. But this didn’t happen on a college campus: It took place in a maximum-security prison. To the outside world, they are inmates, but in the classroom, they are students enrolled in the Cornell Prison Education Program, or “CPEP.” Per New York State Department of Corrections rules, we have permission to use the inmates’ last names only—which is also often how we know them best. Those who graduate from the program—taught by Cornell instructors—will receive an associate’s degree from Cayuga Community College. Before teaching neuroscience to prison inmates, we taught it to Cornell undergraduates as part of the teaching staff for Cornell’s Introduction to Neuroscience course. Most Cornell neuroscience students are high-achieving biology majors and premeds, who are well prepared to succeed in a demanding course. They generally have gone from one academic success to another, and it is no secret that they expect a similar level of success in a neuroscience class. © 2016 by The Atlantic Monthly Group

Keyword: Learning & Memory
Link ID: 22093 - Posted: 04.12.2016

By Jordana Cepelewicz The brain relies on a system of chemical messengers, known as neurotransmitters, to carry missives from cell to cell. When all is well, these communications enable the brain to coordinate various functions, from complex thought to quick, knee-jerk reactions—but when the system is out of whack, serious disease or disorder can ensue. A team of researchers at the Technical University of Denmark (D.T.U.) and University of Oxford have for the first time identified the molecular structure of dopamine beta-hydroxylase (DBH), the enzyme that controls the conversion between dopamine and norepinephrine, two major neurotransmitters. Understanding the crystal structure of the enzyme could provide an ideal target for drug development. Dopamine and norepinephrine play key roles in many brain functions such as learning, memory, movement and the fight-or-flight response. Imbalances in the levels of these neurotransmitters—and the role DBH plays in regulating them—have been implicated in a wide range of disorders, including hypertension, congestive heart failure, anxiety, depression, post-traumatic stress disorder, Alzheimer’s, schizophrenia, Parkinson’s and even cocaine addiction. DBH has long intrigued biochemists but it has been challenging to perform the analyses needed to determine the protein’s structure. “This enzyme has been particularly difficult,” says Hans Christensen, a chemist at D.T.U. and the study’s lead researcher. “We tried many different expression systems before we finally succeeded. Now that we have the structure it is clear why—[it] is very intricate, with different parts of the enzyme interacting very tightly.” © 2016 Scientific American,

Keyword: Alzheimers; Schizophrenia
Link ID: 22087 - Posted: 04.09.2016

By Melinda Wenner Moyer What if you could pop a pill that made you smarter? It sounds like a Hollywood movie plot, but a new systematic review suggests that the decades-long search for a safe and effective “smart drug” (see below) might have notched its first success. Researchers have found that modafinil boosts higher-order cognitive function without causing serious side effects. Modafinil, which has been prescribed in the U.S. since 1998 to treat sleep-related conditions such as narcolepsy and sleep apnea, heightens alertness much as caffeine does. A number of studies have suggested that it could provide other cognitive benefits, but results were uneven. To clear up the confusion, researchers then at the University of Oxford analyzed 24 studies published between 1990 and 2014 that specifically looked at how modafinil affects cognition. In their review, which was published last year in European Neuropsychopharmacology, they found that the methods used to evaluate modafinil strongly affected the outcomes. Research that looked at the drug's effects on the performance of simple tasks—such as pressing a particular button after seeing a certain color—did not detect many benefits. Yet studies that asked participants to do complex and difficult tasks after taking modafinil or a placebo found that those who took the drug were more accurate, which suggests that it may affect “higher cognitive functions—mainly executive functions but also attention and learning,” explains study co-author Ruairidh Battleday, now a medical doctor and Ph.D. student at the University of California, Berkeley. But don't run to the pharmacy just yet. Although many doctors very likely prescribe the drug off-label to help people concentrate—indeed, a 2008 survey by the journal Nature found that one in five of its readers had taken brain-boosting drugs, and half those people had used modafinil—trials have not yet been done on modafinil's long-term effectiveness or safety. © 2016 Scientific American

Keyword: Drug Abuse; Learning & Memory
Link ID: 22085 - Posted: 04.09.2016

Laura Sanders NEW YORK — Cells in a brain structure known as the hippocampus are known to be cartographers, drawing mental maps of physical space. But new studies show that this seahorse-shaped hook of neural tissue can also keep track of social space, auditory space and even time, deftly mapping these various types of information into their proper places. Neuroscientist Rita Tavares described details of one of these new maps April 2 at the annual meeting of the Cognitive Neuroscience Society. Brain scans had previously revealed that activity in the hippocampus was linked to movement through social space. In an experiment reported last year in Neuron, people went on a virtual quest to find a house and job by interacting with a cast of characters. Through these social interactions, the participants formed opinions about how much power each character held, and how kindly they felt toward him or her. These judgments put each character in a position on a “social space” map. Activity in the hippocampus was related to this social mapmaking, Tavares and colleagues found. It turns out that this social map depends on the traits of the person who is drawing it, says Tavares, of Icahn School of Medicine at Mount Sinai in New York City. People with more social anxiety tended to give more power to characters they interacted with. What’s more, these people's social space maps were smaller overall, suggesting that they explored social space less, Tavares says. Tying these behavioral traits to the hippocampus may lead to a greater understanding of social behavior — and how this social mapping may go awry in psychiatric conditions, Tavares said. © Society for Science & the Public 2000 - 2016.

Keyword: Learning & Memory
Link ID: 22076 - Posted: 04.06.2016

by Daniel Galef Footage from a revolutionary behavioural experiment showed non-primates making and using tools just like humans. In the video, a crow is trying to get food out of a narrow vessel, but its beak is too short for it to reach through the container. Nearby, the researchers placed a straight wire, which the crow bent against a nearby surface into a hook. Then, holding the hook in its beak, it fished the food from the bottle. Corvids—the family of birds that includes crows, ravens, rooks, jackdaws, and jays—are pretty smart overall. Although not to the level of parrots and cockatoos, ravens can also mimic human speech. They also have a highly developed system of communication and are believed to be among the most intelligent non-primate animals in existence. McGill Professor Andrew Reisner recalls meeting a graduate student studying corvid intelligence at Oxford University when these results were first published in 2015. “I had read early in the year that some crows had been observed making tools, and I mentioned this to him,” Reisner explained. “He said that he knew about that, as it had been he who had first observed it happening. Evidently the graduate students took turns watching the ‘bird box,’ […] and the tool making first occurred there on his shift.”

Keyword: Evolution; Intelligence
Link ID: 22072 - Posted: 04.06.2016

By Roni Caryn Rabin Alzheimer’s disease is a progressive brain disorder that causes dementia, destroying memory, cognitive skills, the ability to care for oneself, speak and walk, said Ruth Drew, director of family and information services at the Alzheimer’s Association. “And since the brain affects everything, Alzheimer’s ultimately affects everything,” she said, “including the ability to swallow, cough and breathe.” Once patients reach the advanced stages of Alzheimer’s, they may stop eating and become weak and susceptible to infections, said Dr. Jason Karlawish, a professor of medicine at the University of Pennsylvania. Unable to swallow or cough, they are at high risk of choking, aspirating food particles or water into the lungs and developing pneumonia, which is often the immediate cause of death, he said. “You see a general decline in the contribution the brain makes, not just in thinking, but in maintaining the body’s homeostasis,” Dr. Karlawish said. Using a feeding tube to nourish patients and hospitalizing them for infections does not significantly extend life at the advanced stages of the disease and is discouraged because it can prolong suffering with no hope of recovery, he said. Alzheimer's is the sixth leading cause of death in the United States, according to the Centers for Disease Control and Prevention, but that figure may underestimate the actual number of cases, Dr. Karlawish said, since some deaths may be attributed to other causes like pneumonia. © 2016 The New York Times Company

Keyword: Alzheimers
Link ID: 22071 - Posted: 04.06.2016

Laura Sanders NEW YORK — Sometimes forgetting can be harder than remembering. When people forced themselves to forget a recently seen image, select brain activity was higher than when they tried to remember that image. Forgetting is often a passive process, one in which the memory slips out of the brain, Tracy Wang of the University of Texas at Austin said April 2 at the annual meeting of the Cognitive Neuroscience Society. But in some cases, forgetting can be deliberate. Twenty adults saw images of faces, scenes and objects while an fMRI scanner recorded their brains’ reactions to the images. If instructed to forget the preceding image, people were less likely to remember that image later. Researchers used the scan data to build a computer model that could infer how strongly the brain responds to each particular kind of image. In the ventral temporal cortex, a part of the brain above the ear, brain patterns elicited by a particular image were stronger when a participant was told to forget the sight than when instructed to remember it. Of course, everyone knows that it’s easy to forget something without even trying. But these results show that intentional forgetting isn’t a passive process — the brain has to actively work to wipe out a memory on purpose. Citations T.H. Wang et al. Forgetting is more work than remembering. Annual meeting of the Cognitive Neuroscience Society, New York City, April 2, 2016. © Society for Science & the Public 2000 - 2016

Keyword: Learning & Memory
Link ID: 22068 - Posted: 04.05.2016

Mo Costandi This spectacular image – which took the best part of a year to create – shows the fine structure of a nerve terminal at high resolution, revealing, for the very first time, an intricate network of fine filaments that controls the movements of synaptic vesicles. The brain is soft and wet, with the consistency of a lump of jelly. Yet, it is the most complex and highly organized structure that we know of, containing hundreds of billions of neurons and glial cells, and something on the order of one quadrillion synaptic connections, all of which are arranged in a very specific manner. This high degree of specificity extends down to the deepest levels of brain organization. Just beneath the membrane at the nerve terminal, synaptic vesicles store neurotransmitter molecules, and await the arrival of a nervous impulse, whereupon they fuse with the membrane and release their contents into the synaptic cleft, the miniscule gap at the junction between nerve cells, and diffuse across it to bind to receptor protein molecules embedded at the surface of the partner cell. 3D model of a nerve terminal in atomic detail The process of neurotransmitter release is tightly orchestrated. Ready vesicles are ‘docked’ in the ‘active zone’ lying beneath the cell membrane, and are depleted when they fuse with the membrane, only to be replenished from a reservoir of pre-prepared vesicles located further inside the cell. Spent vesicles are quickly pulled back out of the membrane, reformed, refilled with neurotransmitter molecules, and then returned to the reservoir, so that they can be shuttled into the active zone when needed. An individual nerve cell may use up hundreds, or perhaps thousands, of vesicles every second, and so this recycling process occurs continuously to maintain the signalling between nerve cells. © 2016 Guardian News and Media Limited

Keyword: Development of the Brain
Link ID: 22067 - Posted: 04.04.2016

By DONALD G. McNEIL Jr The World Health Organization said on Thursday that there is “strong scientific consensus” that Zika virus is a cause of microcephaly, unusually small heads with brain damage in infants, as well as other neurological disorders. Yet a surge in microcephaly has been reported only in Brazil; a small increase was reported in French Polynesia, and a cluster of 32 cases is now under investigation in Colombia. For proof of the connection between infection with the virus and birth defects, scientists are waiting for the results of a large study of 5,000 pregnant women, most of them in Colombia. Women with past Zika infections will be compared with similar women without infections to see if they have more microcephalic children. The epidemic peaked in Colombia in early February, according to the W.H.O. Most of the women in the study are due to give birth in May and June. Virtually all public health agencies already believe the virus is to blame for these birth defects and are giving medical advice based on that assumption. Here are the lines of evidence they cite. As early as last August, hospitals in northeast Brazil realized that something unheard of was happening: Neonatal wards that normally saw one or two microcephalic babies a year were seeing five or more at the same time. Doctors learned from the mothers that many of them had had Zika symptoms months earlier. © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22065 - Posted: 04.04.2016

The mystery is starting to untangle. It has long been known that twisted fibres of a protein called tau collect in the brain cells of people with Alzheimer’s, but their exact role in the disease is unclear. Now a study in mice has shown how tau interferes with the strengthening of connections between neurons – the key mechanism by which we form memories. In healthy cells, the tau protein helps to stabilise microtubules that act as rails for transporting materials around the cell. In people with Alzheimer’s, these proteins become toxic, but an important unanswered question is what forms of tau are toxic: the tangles may not be the whole story. In the new study, Li Gan and her colleagues at the Gladstone Institute of Neurological Disease in San Francisco found that the brains of those with Alzheimer’s have high levels of tau with a particular modification, called acetylated tau. They then looked at what acetylated tau does in a mouse model of Alzheimer’s, finding that it accumulates at synapses – the connections between neurons. When we form memories, synapses become strengthened through extra receptors inserted into the cell membranes, and this heightens their response. But acetylated tau depletes another protein called KIBRA, which is essential for this synapse-strengthening mechanism. “We’re excited because we think we now have a handle on the link between tau and memory,” says Gan. “We’re also cautious because we know this may not be the only link. It’s still early days in understanding the mechanism.” © Copyright Reed Business Information Ltd.

Keyword: Alzheimers; Learning & Memory
Link ID: 22064 - Posted: 04.04.2016

By Emily Underwood More than 99% of clinical trials for Alzheimer’s drugs have failed, leading many to wonder whether pharmaceutical companies have gone after the wrong targets. Now, research in mice points to a potential new target: a developmental process gone awry, which causes some immune cells to feast on the connections between neurons. “It is beautiful new work,” which “brings into light what’s happening in the early stage of the disease,” says Jonathan Kipnis, a neuroscientist at the University of Virginia School of Medicine in Charlottesville. Most new Alzheimer’s drugs aim to eliminate β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. Those with Alzheimer’s tend to have more of these deposits in their brains than do healthy people, yet more plaques don’t always mean more severe symptoms such as memory loss or poor attention, says Beth Stevens of Boston Children’s Hospital, who led the new work. What does track well with the cognitive decline seen in Alzheimer’s disease—at least in mice that carry genes that confer high risk for the condition in people—is a marked loss of synapses, particularly in brain regions key to memory, Stevens says. These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity. Stevens has spent much of her career studying a normal immune mechanism that prunes weak or unnecessary synapses as the brain matures from the womb through adolescence, allowing more important connections to become stronger. In this process, a protein called C1q sets off a series of chemical reactions that ultimately mark a synapse for destruction. After a synapse has been “tagged,” immune cells called microglia—the brain’s trash disposal service—know to “eat” it, Stevens says. © 2016 American Association for the Advancement of Science

Keyword: Alzheimers; Neuroimmunology
Link ID: 22062 - Posted: 04.01.2016

By Nicholas Bakalar Stress in childhood may be linked to hardening of the arteries in adulthood, new research suggests. Finnish researchers studied 311 children 12 to 18 years old, scoring their levels of stress according to a variety of components, including the family’s economic circumstances, the emotional environment in the home, whether parents engaged in healthy behaviors, stressful events (such as divorce, moves or death of a family member) and parental concerns about the child’s social adjustment. Using these criteria, they calculated a stress score. When the members of the group were 40 to 46 years old, they used computed tomography to measure coronary artery calcification, a marker of atherosclerosis and a risk factor for cardiovascular disease. The study, in JAMA Pediatrics, controlled for sex, cholesterol, body mass index and other factors, but still found that the higher the childhood stress score, the greater the risk for coronary artery calcification. The study is observational, and the data is based largely on parental reports, which can be biased. Still, its long follow-up time and careful control of other variables gives it considerable strength. There are plausible mechanisms for the connection, including stress-induced increases in inflammation, which in animal models have been linked to a variety of ailments. “I think that economic conditions are important here,” said the lead author, Dr. Markus Juonala, a professor of internal medicine at the University of Turku in Finland. “Public health interventions should focus on how to intervene in better ways with people with higher stress and lower socioeconomic status.” © 2016 The New York Times Company

Keyword: Stress; Development of the Brain
Link ID: 22057 - Posted: 04.01.2016

By Matthew Hutson Earlier this month, a computer program called AlphaGo defeated a (human) world champion of the board game Go, years before most experts expected computers to rival the best flesh-and-bone players. But then last week, Microsoft was forced to silence its millennial-imitating chatbot Tay for blithely parroting Nazi propaganda and misogynistic attacks after just one day online, her failure a testimony to the often underestimated role of human sensibility in intelligent behavior. Why are we so compelled to pit human against machine, and why are we so bad at predicting the outcome? As the number of jobs susceptible to automation rises, and as Stephen Hawking, Elon Musk, and Bill Gates warn that artificial intelligence poses an existential threat to humanity, it’s natural to wonder how humans measure up to our future robot overlords. But even those tracking technology’s progress in taking on human skills have a hard time setting an accurate date for the uprising. That’s in part because one prediction strategy popular among both scientists and journalists—benchmarking the human brain with digital metrics such as bits, hertz, and million instructions per section, or MIPS—is severely misguided. And doing so could warp our expectations of what technology can do for us and to us. Since their development, digital computers have become a standard metaphor for the mind and brain. The comparison makes sense, in that brains and computers both transform input into output. Most human brains, like computers, can also manipulate abstract symbols. (Think arithmetic or language processing.) But like any metaphor, this one has limitations.

Keyword: Brain imaging; Robotics
Link ID: 22052 - Posted: 03.31.2016

By David Z. Hambrick Nearly a century after James Truslow Adams coined the phrase, the “American dream” has become a staple of presidential campaign speeches. Kicking off her 2016 campaign, Hillary Clinton told supporters that “we need to do a better job of getting our economy growing again and producing results and renewing the American dream.” Marco Rubio lamented that “too many Americans are starting to doubt” that it is still possible to achieve the American dream, and Ted Cruz asked his supporters to “imagine a legal immigration system that welcomes and celebrates those who come to achieve the American dream.” Donald Trump claimed that “the American dream is dead” and Bernie Sanders quipped that for many “the American dream has become a nightmare.” But the American dream is not just a pie-in-the-sky notion—it’s a scientifically testable proposition. The American dream, Adams wrote, “is not a dream of motor cars and high wages merely, but a dream of social order in which each man and each woman shall be able to attain to the fullest stature of which they are innately capable…regardless of the fortuitous circumstances of birth or position.” In the parlance of behavioral genetics—the scientific study of genetic influences on individual differences in behavior—Adams’ idea was that all Americans should have an equal opportunity to realize their genetic potential. A study just published in Psychological Science by psychologists Elliot Tucker-Drob and Timothy Bates reveals that this version of the American dream is in serious trouble. Tucker-Drob and Bates set out to evaluate evidence for the influence of genetic factors on IQ-type measures (aptitude and achievement) that predict success in school, work, and everyday life. Their specific question was how the contribution of genes to these measures would compare at low versus high levels of socioeconomic status (or SES), and whether the results would differ across countries. The results reveal, ironically, that the American dream is more of a reality for other countries than it is for America: genetic influences on IQ were uniform across levels of SES in Western Europe and Australia, but, in the United States, were much higher for the rich than for the poor. © 2016 Scientific American

Keyword: Genes & Behavior; Intelligence
Link ID: 22051 - Posted: 03.30.2016

Chris French The fallibility of human memory is one of the most well established findings in psychology. There have been thousands of demonstrations of the unreliability of eyewitness testimony under well-controlled conditions dating back to the very earliest years of the discipline. Relatively recently, it was discovered that some apparent memories are not just distorted memories of witnessed events: they are false memories for events that simply never took place at all. Psychologists have developed several reliable methods for implanting false memories in a sizeable proportion of experimental participants. It is only in the last few years, however, that scientists have begun to systematically investigate the phenomenon of non-believed memories. These are subjectively vivid memories of personal experiences that an individual once believed were accurate but now accepts are not based upon real events. Prior to this, there were occasional anecdotal reports of non-believed memories. One of the most famous was provided by the influential developmental psychologist Jean Piaget. He had a clear memory of almost being kidnapped at about the age of two and of his brave nurse beating off the attacker. His grateful family were so impressed with the nurse that they gave her a watch as a reward. Years later, the nurse confessed that she had made the whole story up. Even after he no longer believed that the event had taken place, Piaget still retained his vivid and detailed memory of it. © 2016 Guardian News and Media Limited

Keyword: Learning & Memory
Link ID: 22050 - Posted: 03.30.2016