Andrea Hsu Intuitively, we tend to think of forgetting as failure, as something gone wrong in our ability to remember. Now, Canadian neuroscientists with the University of Toronto are challenging that notion. In a paper published Wednesday in the journal Neuron, they review the current research into the neurobiology of forgetting and hypothesize that our brains purposefully work to forget information in order to help us live our lives. I spoke with Blake Richards, one of the co-authors of the paper, who applies artificial intelligence theories to his study of how the brain learns. He says that in the AI world, there's something called over-fitting — a phenomenon in which a machine stores too much information, hindering its ability to behave intelligently. He hopes that greater understanding of how our brains decide what to keep and what to forget will lead to better AI systems that are able to interact with the world and make decisions in the way that we do. We hear a lot about the study of memory. Is the study of forgetting a relatively new thing? Within psychology, there's a long history of work examining forgetting. So that's not a new field of study. But the neuroscientists — those of us who work with the biology of how the brain works — have not really examined forgetting much in the past. Generally, the focus for the last few decades in neuroscience has been the question of how do the cells in our brains change themselves in order to store information and remember things. It's only been in the last few years that there's been an upswing in scientific studies looking at what's happening inside our brains at the cellular level that might actually produce forgetting. © 2017 npr

Keyword: Learning & Memory
Link ID: 23771 - Posted: 06.24.2017

By Sam Wong People who have had amputations can control a virtual avatar using their imagination alone, thanks to a system that uses a brain scanner. Brain-computer interfaces, which translate neuron activity into computer signals, have been advancing rapidly, raising hopes that such technology can help people overcome disabilities such as paralysis or lost limbs. But it has been unclear how well this might work for people who have had limbs removed some time ago, as the brain areas that previously controlled these may become less active or repurposed for other uses over time. Ori Cohen at IDC Herzliya, in Israel, and colleagues have developed a system that uses an fMRI brain scanner to read the brain signals associated with imagining a movement. To see if it can work a while after someone has had a limb removed, they recruited three volunteers who had had an arm removed between 18 months and two years earlier, and four people who have not had an amputation. While lying in the fMRI scanner, the volunteers were shown an avatar on a screen with a path ahead of it, and instructed to move the avatar along this path by imagining moving their feet to move forward, or their hands to turn left or right. The people who had had arm amputations were able to do this just as well with their missing hand as they were with their intact hand. Their overall performance on the task was almost as good as of those people who had not had an amputation. © Copyright New Scientist Ltd.

Keyword: Robotics
Link ID: 23770 - Posted: 06.24.2017

By Chris Brown, Chris Corday, All it took was a single beer for Murray's Shaw life to unravel. The moment came on a bike holiday in January 2016 in San Diego while he was with some friends from the Vancouver area. After almost 20 years sober, the community college instructor from New Westminster, B.C., cracked open a cold one at the end of a long ride. Fourteen months later, he died alone in a hotel room in Vancouver's Downtown Eastside. Fentanyl overdose was the coroner's conclusion. "He wasn't making a choice with a rational mind. He was depressed and he was battling this impulse to use," said his wife, Sasha Wood, who offered to tell her husband's story to CBC News in the hopes it might help other families dealing with substance abuse issues. Fentanyl has become a scourge across the country, but B.C. has been hit the hardest: an average of four people have died of drug overdose every day in 2017. Wood said the events that led to Shaw's death illustrate much that's wrong with how the Canadian health care system treats those with an addiction. 'I just thought he could stop' Shaw had problems with alcohol in his 20s and got into trouble with the law. But Wood, 49, says he sought treatment and turned his life around. He stopped drinking completely, went to university and worked toward a PhD. ©2017 CBC/Radio-Canada.

Keyword: Drug Abuse
Link ID: 23769 - Posted: 06.24.2017

By KATIE THOMAS Nolan and Jack Willis, twins from upstate New York, and just 10 other boys took part in a clinical trial that led to the approval last fall of the very first drug to treat their rare, deadly muscle disease. Now the Willis boys are again test cases as a different type of medical question comes to the fore: whether insurers will cover the controversial drug, Exondys 51, which can cost more than $1 million a year even though it’s still unclear if it works. The boys’ insurer, Excellus BlueCross BlueShield, refused to cover the cost of the drug because the twins, who are 15, can no longer walk. Their disease, Duchenne muscular dystrophy, overwhelmingly affects boys and causes muscles to deteriorate, killing many of them by the end of their 20s. “I’m cycling between rage and just sadness,” their mother, Alison Willis Hoke, said recently, on the day she learned that an appeal for coverage had been denied. For now, the company that sells the drug, Sarepta Therapeutics, is covering the treatment’s costs, but Mrs. Hoke does not know how long that will last. The desperation in Mrs. Hoke’s voice reflects a sobering reality for families of boys with the disease since their elation last fall over the drug’s approval. Because the Food and Drug Administration overruled its own experts — who weren’t convinced the Exondys 51 had shown sufficiently good results — and gave the drug conditional approval, many insurers are now declining to cover it or are imposing severe restrictions that render patients ineligible. The story of Exondys 51 raises complex and emotionally charged questions about what happens when the F.D.A. approves an expensive drug based on a lower bar of proof. In practice, health insurers have taken over as gatekeeper in determining who will get the drug. © 2017 The New York Times Company

Keyword: Muscles; Movement Disorders
Link ID: 23768 - Posted: 06.23.2017

By Kat McGowan Doctors at Zuckerberg San Francisco General Hospital could not figure out what was wrong with the 29-year-old man sitting before them. An otherwise healthy construction worker from Nicaragua, the patient was suffering from a splitting headache, double vision and ringing in his ears. Part of his face was also numb. The cause could have been anything—from an infection to a stroke, a tumor or some kind of autoimmune disease. The Emergency Department (ED) staff took a magnetic resonance imaging scan of the man’s brain, performed a spinal tap and completed a series of other tests that did not turn up any obvious reason for the swelling in his brain—a condition that is formally known as encephalitis. Most likely, it was some kind of infection. But what kind? Nineteen standard tests are available to help clinicians try to pin down the source of encephalitis, but they test for the presence of only the most common infections; more than 60 percent of cases go unsolved each year. Physicians looked in the patient’s cerebrospinal fluid (which surrounds the brain and protects it) for evidence of Lyme disease, syphilis and valley fever, among other things. Nothing matched. So the S.F. General ED staff settled on the most likely culprit as a diagnosis: a form of tuberculosis (TB) that causes brain inflammation but cannot always be detected with typical tests. Doctors gave the man a prescription for some steroids to reduce the swelling plus some anti-TB drugs and sent him home. © 2017 Scientific American,

Keyword: Miscellaneous
Link ID: 23767 - Posted: 06.23.2017

by Laura Sanders When we brought our first baby home from the hospital, our pediatrician advised us to have her sleep in our room. We put our tiny new roommate in a crib near our bed (though other containers that were flat, firm and free of blankets, pillows or stuffed animals would have worked, too). The advice aims to reduce the risk of sleep-related deaths, including sudden infant death syndrome, or SIDS. Studies suggest that in their first year of life, babies who bunk with their parents (but not in the same bed) are less likely to die from SIDS than babies who sleep in their own room. The reasons aren’t clear, but scientists suspect it has to do with lighter sleep: Babies who sleep near parents might more readily wake themselves up and avoid the deep sleep that’s a risk factor for SIDS. That’s an important reason to keep babies close. Room sharing also makes sense from a logistical standpoint. Middle of the night feedings and diaper changes are easier when there’s less distance between you and the babe. But babies get older. They start snoring a little louder and eating less frequently, and it’s quite natural to wonder how long this room sharing should last. That’s a question without a great answer. In November 2016, the American Academy of Pediatrics task force on SIDS updated its sleep guidelines. The earlier recommendation was that babies ought to sleep in parents’ bedrooms for an entire year. The new suggestion softens that a bit to say infants should be there for “ideally for the first year of life, but at least for the first 6 months.” © Society for Science & the Public 2000 - 2017

Keyword: Sleep; Drug Abuse
Link ID: 23766 - Posted: 06.23.2017

Jon Hamilton Thanks to Sigmund Freud, we all know what it means to dream about swords, sticks and umbrellas. Or maybe we don't. "For 100 years, we got stuck into that Freudian perspective on dreams, which turned out to be not scientifically very accurate," says Robert Stickgold, a sleep researcher and associate professor of psychiatry at Harvard Medical School. "So it's only been in the last 15 to 20 years that we've really started making progress." Today, most brain scientists reject Freud's idea that dreams are highly symbolic representations of unconscious (and usually sexual) desire. That dream umbrella, they say, is probably just an umbrella. But researchers are still trying to figure out what dreams do represent, and what their purpose is. "There's not really a solid theory about why dreaming is there," says Benjamin Baird, a postdoctoral fellow at the Center for Sleep and Consciousness at the University of Wisconsin ­– Madison. "It's a big mystery." We all have a future self, a version of us that is better, more successful. It can inspire us to achieve our dreams, or mock us for everything we have failed to become. In this episode of the NPR podcast Invisibilia, hosts Alix Spiegel and Hanna Rosin talk to a woman who believes she can connect with her younger self in dreams. © 2017 npr

Keyword: Sleep
Link ID: 23765 - Posted: 06.23.2017

Staring down a packed room at the Hyatt Regency Hotel in downtown San Francisco this March, Randy Gallistel gripped a wooden podium, cleared his throat, and presented the neuroscientists sprawled before him with a conundrum. “If the brain computed the way people think it computes," he said, "it would boil in a minute." All that information would overheat our CPUs. Humans have been trying to understand the mind for millennia. And metaphors from technology—like cortical CPUs—are one of the ways that we do it. Maybe it’s comforting to frame a mystery in the familiar. In ancient Greece, the brain was a hydraulics system, pumping the humors; in the 18th century, philosophers drew inspiration from the mechanical clock. Early neuroscientists from the 20th century described neurons as electric wires or phone lines, passing signals like Morse code. And now, of course, the favored metaphor is the computer, with its hardware and software standing in for the biological brain and the processes of the mind. In this technology-ridden world, it’s easy to assume that the seat of human intelligence is similar to our increasingly smart devices. But the reliance on the computer as a metaphor for the brain might be getting in the way of advancing brain research. As Gallistel continued his presentation to the Cognitive Neuroscience Society, he described the problem with the computer metaphor. If memory works the way most neuroscientists think it does—by altering the strength of connections between neurons—storing all that information would be way too energy-intensive, especially if memories are encoded in Shannon information, high fidelity signals encoded in binary.

Keyword: Learning & Memory; Consciousness
Link ID: 23764 - Posted: 06.23.2017

By Sharon Begley, STAT To anyone who’s aware that efforts to develop Alzheimer’s drug treatments have met failure after failure, and to have therefore decided that prevention is the only hope, a U.S. panel of experts issued a sobering message on Thursday: Don’t count on it. From physical activity to avoiding high blood pressure to brain training, a 17-member committee assembled by the National Academies of Sciences concluded, no interventions are “supported by high-strength evidence.” Instead, some high-quality studies found that one or another intervention worked, but other equally rigorous studies found they didn’t. 1. Cognitive training The evidence for programs aimed at boosting reasoning, problem-solving, memory, and speed of processing does include randomized trials that reported benefits from brain training, but the report calls that evidence “low to moderate strength.” One problem: There seemed to be benefits for two years, but not after five or 10. Results in other randomized studies were even more equivocal. There are also data from studies that are less rigorous, leading the committee to conclude that brain training (computer-based or not) can delay or slow age-related cognitive decline—but not Alzheimer’s. 2. Controlling blood pressure Evidence that this helps is weaker still. © 2017 Scientific American

Keyword: Alzheimers
Link ID: 23763 - Posted: 06.23.2017

Cassie Martin Long typecast as the strong silent type, bones are speaking up. In addition to providing structural support, the skeleton is a versatile conversationalist. Bones make hormones that chat with other organs and tissues, including the brain, kidneys and pancreas, experiments in mice have shown. “The bone, which was considered a dead organ, has really become a gland almost,” says Beate Lanske, a bone and mineral researcher at Harvard School of Dental Medicine. “There’s so much going on between bone and brain and all the other organs, it has become one of the most prominent tissues being studied at the moment.” At least four bone hormones moonlight as couriers, recent studies show, and there could be more. Scientists have only just begun to decipher what this messaging means for health. But cataloging and investigating the hormones should offer a more nuanced understanding of how the body regulates sugar, energy and fat, among other things. Of the hormones on the list of bones’ messengers — osteocalcin, sclerostin, fibroblast growth factor 23 and lipocalin 2 — the last is the latest to attract attention. Lipocalin 2, which bones unleash to stem bacterial infections, also works in the brain to control appetite, physiologist Stavroula Kousteni of Columbia University Medical Center and colleagues reported in the March 16 Nature. After mice eat, their bone-forming cells absorb nutrients and release a hormone called lipocalin 2 (LCN2) into the blood. LCN2 travels to the brain, where it gloms on to appetite-regulating nerve cells, which tell the brain to stop eating, a recent study suggests. © Society for Science & the Public 2000 - 2017.

Keyword: Hormones & Behavior
Link ID: 23762 - Posted: 06.22.2017

Researchers have identified structural changes in two genes that increase the risk of developing Tourette syndrome, a neurological disorder characterized by involuntary motor and vocal tics. The study, published in the journal Neuron, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our study is the tip of the iceberg in understanding the complex biological mechanisms underlying this disorder. With recent advancements in genetic research, we are at the cusp of identifying many genes involved in Tourette syndrome,” said Jeremiah Scharf, M.D., Ph.D., assistant professor of neurology and psychiatry at Harvard Medical School and Massachusetts General Hospital, Boston, and co-corresponding author of the study. The research was part of an international collaboration co-led by Dr. Scharf; Giovanni Coppola, M.D., professor of psychiatry and neurology at the University of California, Los Angeles; Carol Mathews, M.D., professor of psychiatry at the University of Florida in Gainesville; and Peristera Paschou, Ph.D., associate professor in the department of biological sciences at Purdue University, West Lafayette, Indiana. The scientific team conducted genetic analyses on 2,434 individuals with Tourette syndrome and compared them to 4,093 controls, focusing on copy number variants, changes in the genetic code resulting in deletions or duplications in sections of genes. Their results determined that deletions in the NRXN1 gene or duplications in the CNTN6 gene were each associated with an increased risk of Tourette syndrome. In the study, approximately 1 in 100 people with Tourette syndrome carried one of those genetic variants.

Keyword: Tourettes; Genes & Behavior
Link ID: 23761 - Posted: 06.22.2017

By Alice Klein EVIDENCE that Parkinson’s disease may be an autoimmune disorder could lead to new ways to treat the illness. Parkinson’s begins with abnormal clumping of a protein called synuclein in the brain. Neighbouring dopamine-producing neurons then die, causing tremors and difficulty moving. The prevailing wisdom has been that these neurons die from a toxic reaction to synuclein deposits. However, Parkinson’s has been linked to some gene variants that affect how the immune system works, leading to an alternative theory that synuclein causes Parkinson’s by triggering the immune system to attack the brain. An argument against this theory has been that brain cells are safe from immune system attack, because most neurons don’t have antigens – the markers immune cells use to recognise a target. But by studying postmortem brain tissue samples, David Sulzer at Columbia University and his team have discovered that dopamine-producing neurons do display antigens. The team has now conducted blood tests to reveal that people with Parkinson’s show an immune response to these antigens, while people who don’t have the condition do not (Nature, DOI: 10.1038/nature22815). These findings suggest Parkinson’s may be an autoimmune disorder, in which the immune system mistakenly attacks part of the body. There have been hints before that the immune system is involved in Parkinson’s, but this is the first evidence that it plays a major pathological role, says Roger Barker at the University of Cambridge. “It would be an attractive target for therapeutic intervention,” he says. However, it isn’t clear yet if the immune response directly causes neuron death, or if it is merely a side effect of the disease. Sulzer’s team plans to try blocking the autoimmune response in Parkinson’s, to see if this can stop the disease progressing. © Copyright New Scientist Ltd.

Keyword: Parkinsons; Neuroimmunology
Link ID: 23760 - Posted: 06.22.2017

Parkinson’s disease is commonly thought of as a movement disorder, but after years of living with the disease, approximately 25 percent of patients also experience deficits in cognition that impair function. A newly developed research tool may help predict a patient’s risk for developing dementia and could enable clinical trials aimed at finding treatments to prevent the cognitive effects of the disease. The research was published in Lancet Neurology and was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This study includes both genetic and clinical assessments from multiple groups of patients, and it represents a significant step forward in our ability to effectively model one of the most troublesome non-motor aspects of Parkinson’s disease,” said Margaret Sutherland, Ph.D., program director at the NINDS. For the study, a team of researchers led by Clemens Scherzer, M.D., combined data from 3,200 people with Parkinson’s disease, representing more than 25,000 individual clinical assessments and evaluated seven known clinical and genetic risk factors associated with developing dementia. From this information, they built a computer-based risk calculator that may predict the chance that an individual with Parkinson’s will develop cognitive deficits. Dr. Scherzer is head of the Neurogenomics Lab and Parkinson Personalized Medicine Program at Harvard Medical School and a member of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital, Boston.

Keyword: Parkinsons
Link ID: 23759 - Posted: 06.22.2017

By Matthew Hutson Artificial neural networks, computer algorithms that take inspiration from the human brain, have demonstrated fancy feats such as detecting lies, recognizing faces, and predicting heart attacks. But most computers can’t run them efficiently. Now, a team of engineers has designed a computer chip that uses beams of light to mimic neurons. Such “optical neural networks” could make any application of so-called deep learning—from virtual assistants to language translators—many times faster and more efficient. “It works brilliantly,” says Daniel Brunner, a physicist at the FEMTO-ST Institute in Besançon, France, who was not involved in the work. “But I think the really interesting things are yet to come.” Most computers work by using a series of transistors, gates that allow electricity to pass or not pass. But decades ago, physicists realized that light might make certain processes more efficient—for example, building neural networks. That’s because light waves can travel and interact in parallel, allowing them to perform lots of functions simultaneously. Scientists have used optical equipment to build simple neural nets, but these setups required tabletops full of sensitive mirrors and lenses. For years, photonic processing was dismissed as impractical. Now, researchers at the Massachusetts Institute of Technology (MIT) in Cambridge have managed to condense much of that equipment to a microchip just a few millimeters across. © 2017 American Association for the Advancement of Science

Keyword: Robotics
Link ID: 23758 - Posted: 06.21.2017

Ian Sample Science editor Older men tend to have “geekier” sons who are more aloof, have higher IQs and a more intense focus on their interests than those born to younger fathers, researchers claim. The finding, which emerged from a study of nearly 8,000 British twins, suggests that having an older father may benefit children and boost their performance in technical subjects at secondary school. Researchers in the UK and the US analysed questionnaires from 7,781 British twins and scored them according to their non-verbal IQ at 12 years old, as well as parental reports on how focused and socially aloof they were. The scientists then combined these scores into an overall “geek index”. Magdalena Janecka at King’s College London said the project came about after she and her colleagues had brainstormed what traits and skills helped people to succeed in the modern age. “If you look at who does well in life right now, it’s geeks,” she said. Drawing on the twins’ records, the scientists found that children born to older fathers tended to score slightly higher on the geek index. For a father aged 25 or younger, the average score of the children was 39.6. That figure rose to 41 in children with fathers aged 35 to 44, and to 47 for those with fathers aged over 50. The effect was strongest in boys, where the geek index rose by about 1.5 points for every extra five years of paternal age. The age of the children’s mothers seemed to have almost no effect on the geek index. © 2017 Guardian News and Media Limited

Keyword: Epigenetics; Development of the Brain
Link ID: 23757 - Posted: 06.21.2017

By Diana Kwon Glioblastomas, highly aggressive malignant brain tumors, have a high propensity for recurrence and are associated with low survival rates. Even when surgeons remove these tumors, deeply infiltrated cancer cells often remain and contribute to relapse. By harnessing neutrophils, a critical player in the innate immune response, scientists have devised a way to deliver drugs to kill these residual cells, according to a study published today (June 19) in Nature Nanotechnology. Neutrophils, the most common type of white blood cell, home in to areas of injury and inflammation to fight infections. Prior studies in both animals and humans have reported that neutrophils can cross the blood-brain barrier, and although these cells are not typically attracted to glioblastomas, they are recruited at sites of tumor removal in response to post-operative inflammation. To take advantage of the characteristics of these innate immune cells, researchers at China Pharmaceutical University encased paclitaxel, a traditional chemotherapy drug, with lipids. These liposome capsules were loaded into neutrophils and injected in the blood of three mouse models of glioblastoma. When the treatment was applied following surgical removal of the main tumor mass, the neutrophil-carrying drugs were able to cross the blood-brain barrier, destroy residual cancer cells, and slow the growth of new tumors. Overall, mice receiving treatment lived significantly longer than controls. © 1986-2017 The Scientist

Keyword: Brain imaging; Neuroimmunology
Link ID: 23756 - Posted: 06.21.2017

By Karl Gruber Birds, fish, and even humans have shattered barriers when it comes to mating rituals, from which partner initiates the courting to which one picks up the check at a fancy restaurant. But things are a bit simpler for frogs, as males and females stick to clearly defined roles: Males serenade the females, and females pick their favorite males to mate. Now, a new study suggests that the smooth guardian frog of Borneo (Limnonectes palavanensis) is an exception to that rule. During the mating season, the female frogs sing to the males in an attempt to win them over—a reversal of the normal process. In fact, if you see a single frog surrounded by a bunch of serenading croakers, called a “lek,” it’s most likely a lucky male being courted by a chorus of females. Males occasionally belt out “advertisement calls” to let females know that they are available. After mating, it’s the males who stay behind to care for the eggs, even taking tadpoles to small ponds after they hatch. This is the first known example of role reversal in singing frogs, scientists write in a recent issue of Behavioral Ecology and Sociobiology. It may even represent the first case of full-blown sex role reversal, which would also require that males do the mate choosing. Researchers are working on that now, but they say that—judging by the high rate of female serenading—males may be the picky ones. © 2017 American Association for the Advancement of Science.

Keyword: Sexual Behavior
Link ID: 23755 - Posted: 06.21.2017

By SAM QUINONES COVINGTON, KY. — Not long ago, I visited a Narcotics Anonymous meeting where men with tattoos and short-cropped hair sat in a circle and talked out their errors. One had lived under an overpass, pimping his girlfriend’s daughter for cash to buy heroin. As the thought brought him to tears, his neighbor patted his shoulder. Others owned to stealing from grandparents, to losing jobs and children. Soon, most in the room — men with years of street addiction behind them — were wiping their eyes. What made the meeting remarkable, however, was not the stories, but where it was taking place. Unit 104 is a 70-man pod in Kenton County Detention Center in northern Kentucky, across the Ohio River from Cincinnati. The unit, and an equivalent one for women, is part of a new approach to jail made necessary by our nationwide epidemic of opiate addiction. Drug overdoses are now the leading cause of death among Americans under 50. As the country has awakened to that epidemic, a new mantra has emerged: “We can’t arrest our way out of this,” accompanied by calls for more drug-addiction treatment. Yet the opiate epidemic has swamped our treatment-center infrastructure. Only one in 10 addicts get the treatment they need, according to a 2016 surgeon general’s report. New centers are costly to build, politically difficult to find real estate for and beyond the means of most uninsured street addicts, anyway. So where can we quickly find cheap new capacity for drug treatment accessible to the street addict? Jail is one place few have thought to look. Jails typically house inmates awaiting trial or serving up to a year for a misdemeanor crime. Many inmates are drug addicts. They vegetate for months, trading crime stories in an atmosphere of boredom and brutality. Any attempt at treatment is usually limited to a weekly visit by a pastor or an Alcoholics Anonymous volunteer. When inmates are released, they’re in the clothes they came in with, regardless of the weather, and have no assistance to re-enter the real world. This kind of jail has always been accepted as an unavoidable fixed cost of government. © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 23754 - Posted: 06.20.2017

By Michael Price Whether it’s giving to charity or helping a stranger with directions, we often assist others even when there’s no benefit to us or our family members. Signs of such true altruism have been spotted in some animals, but have been difficult to pin down in our closest evolutionary relatives. Now, in a pair of studies, researchers show that chimpanzees will give up a treat in order to help out an unrelated chimp, and that chimps in the wild go out on risky patrols in order to protect even nonkin at home. The work may give clues to how such cooperation—the foundation of human civilization—evolved in humans. “Both studies provide powerful evidence for forms of cooperation in our closest relatives that have been difficult to demonstrate in other animals besides humans,” says Brian Hare, an evolutionary anthropologist at Duke University in Durham, North Carolina, who was not involved with the research. In the first study, psychologists Martin Schmelz and Sebastian Grüneisen at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, trained six chimps at the Leipzig Zoo to play a sharing game. Each chimp was paired with a partner who was given a choice of four ropes to pull, each with a different outcome: give just herself a banana pellet; give just the subject a pellet; give both of them pellets; or forgo her turn and let her partner make the decision instead. © 2017 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 23753 - Posted: 06.20.2017

By Timothy Revell Feeling sad? Soon your dolls will be able to tell. To demonstrate the power of a new chip that can run artificially intelligent algorithms, researchers have put it in a doll and programmed it to recognise emotions in facial images captured by a small camera. The doll can recognise eight emotions in total, including surprise and happiness, all while running on a small battery and without doing any processing in the cloud. The total cost of putting the new chip together is just €115 – an indicator of how easy it is becoming to give devices basic AI abilities. “In the near future, we will see a myriad of eyes everywhere that will not just be watching us, but trying to help us,” says project leader Oscar Deniz at the University of Castilla-La Mancha in Ciudad Real, Spain. Recent advances in AI mean we already have algorithms that can recognise objects, lip-read, make basic decisions and more. It’s only a matter of time before these abilities make their way on to little cheap chips like this one, and then put into consumer devices. “We will have wearable devices, toys, drones, small robots, and things we can’t even imagine yet that will all have basic artificial intelligence,” says Deniz. © Copyright New Scientist Ltd.

Keyword: Emotions
Link ID: 23752 - Posted: 06.20.2017