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By THERESE HUSTON “Does being over 40 make you feel like half the man you used to be?” Ads like that have led to a surge in the number of men seeking to boost their testosterone. The Food and Drug Administration reports that prescriptions for testosterone supplements have risen to 2.3 million from 1.3 million in just four years. There is such a condition as “low-T,” or hypogonadism, which can cause fatigue and diminished sex drive, and it becomes more common as men age. But according to a study published in JAMA Internal Medicine, half of the men taking prescription testosterone don’t have a deficiency. Many are just tired and want a lift. But they may not be doing themselves any favors. It turns out that the supplement isn’t entirely harmless: Neuroscientists are uncovering evidence suggesting that when men take testosterone, they make more impulsive — and often faulty — decisions. Researchers have shown for years that men tend to be more confident about their intelligence and judgments than women, believing that solutions they’ve generated are better than they actually are. This hubris could be tied to testosterone levels, and new research by Gideon Nave, a cognitive neuroscientist at the University of Pennsylvania, along with Amos Nadler at Western University in Ontario, reveals that high testosterone can make it harder to see the flaws in one’s reasoning. How might heightened testosterone lead to overconfidence? One possible explanation lies in the orbitofrontal cortex, a region just behind the eyes that’s essential for self-evaluation, decision making and impulse control. The neuroscientists Pranjal Mehta at the University of Oregon and Jennifer Beer at the University of Texas, Austin, have found that people with higher levels of testosterone have less activity in their orbitofrontal cortex. Studies show that when that part of the brain is less active, people tend to be overconfident in their reasoning abilities. It’s as though the orbitofrontal cortex is your internal editor, speaking up when there’s a potential problem with your work. Boost your testosterone and your editor goes reassuringly (but misleadingly) silent. © 2017 The New York Times Company

Keyword: Hormones & Behavior; Attention
Link ID: 23776 - Posted: 06.26.2017

By Diana Kwon Across the animal kingdom, nearly all creatures sleep or display sleep-like states. The roundworm, Caenorhabditis elegans, does not sleep in a typical day-night cycle like humans and many other animals. Instead, these worms catch most of their z’s while transitioning from one larval stage to another, during a period called lethargus. When these creatures fall asleep, most of their neurons become inactive spontaneously, suggesting that sleep—at least in worms—is a passive state of the brain, according to a study published today (June 22) in Science. “The condition between sleep to wakefulness is probably one of the most drastic changes that our brains undergo,” says Manuel Zimmer, a neuroscientist at the Research Institute of Molecular Pathology at the Vienna Biocenter in Austria. “How a brain can switch between such drastically different states is not really understood.” To investigate this process, Zimmer and colleagues examined the brains of C. elegans. These worms do indeed have primitive brains, yet their nervous system comprises only 302 neurons, making it much easier to tackle than, say, the human brain, with billions of neurons, or even the fly brain, which has around 100,000 nerve cells. Using transgenic worms engineered with a fluorescent indicator that becomes active in response to high calcium levels in neurons (a proxy for neural activity), the researchers imaged the C. elegans brain during the transitions between sleep and wake states by adjusting oxygen levels. Because these soil-dwelling creatures live among low levels of oxygen (10 percent), atmospheric oxygen concentrations (21 percent) induce hyperactivity and wakefulness. © 1986-2017 The Scientist

Keyword: Sleep
Link ID: 23775 - Posted: 06.26.2017

By Natalie Grover (Reuters) - A handful of drugmakers are taking their first steps toward developing marijuana-based painkillers, alternatives to opioids that have led to widespread abuse and caused the U.S. health regulator to ask for a withdrawal of a popular drug this month. The cannabis plant has been used for decades to manage pain and there are increasingly sophisticated marijuana products available across 29 U.S. states, as well as in the District of Columbia, where medical marijuana is legal. There are no U.S. Food and Drug Administration (FDA)-approved painkillers derived from marijuana, but companies such as Axim Biotechnologies Inc, Nemus Bioscience Inc and Intec Pharma Ltd have drugs in various stages of development. The companies are targeting the more than 100 million Americans who suffer from chronic pain, and are dependent on opioid painkillers such as Vicodin, or addicted to street opiates including heroin. Opioid overdose, which claimed celebrities including Prince and Heath Ledger as victims, contributed to more than 33,000 deaths in 2015, according to the Centers for Disease Control and Prevention. Earlier this month, the FDA asked Endo International Plc to withdraw its Opana ER painkiller from the market, the first time the agency has called for the removal of an opioid painkiller for public health reasons. The FDA concluded that the drug's benefits no longer outweighed its risks. Multiple studies have shown that pro-medical marijuana states have reported fewer opiate deaths and there are no deaths related to marijuana overdose on record.(http://reut.rs/2r74Sbe) © 2017 Scientific American

Keyword: Pain & Touch; Drug Abuse
Link ID: 23774 - Posted: 06.26.2017

By JANE E. BRODY It’s perfectly normal for someone to feel anxious or depressed after receiving a diagnosis of a serious illness. But what if the reverse occurs and symptoms of anxiety or depression masquerade as an as-yet undiagnosed physical disorder? Or what if someone’s physical symptoms stem from a psychological problem? How long might it take before the true cause of the symptoms is uncovered and proper treatment begun? Psychiatric Times, a medical publication seen by some 50,000 psychiatrists each month, recently published a “partial listing” of 47 medical illnesses, ranging from cardiac arrhythmias to pancreatic cancer, that may first present as anxiety. Added to that was another “partial listing” of 30 categories of medications that may cause anxiety, including, ironically, popular antidepressants like selective serotonin reuptake inhibitors, or S.S.R.I.s. These lists were included in an article called “Managing Anxiety in the Medically Ill” meant to alert mental health practitioners to the possibility that some patients seeking treatment for anxiety or depression may have an underlying medical condition that must be addressed before any emotional symptoms are likely to resolve. Doctors who treat ailments like cardiac, endocrine or intestinal disorders would do well to read this article as well lest they do patients a serious disservice by not recognizing an emotional cause of physical symptoms or addressing the emotional components of a physical disease. © 2017 The New York Times Company

Keyword: Depression; Stress
Link ID: 23773 - Posted: 06.26.2017

Rebecca Hersher The first problem with the airplane bathroom was its location. It was March. Greg O'Brien and his wife, Mary Catherine, were flying back to Boston from Los Angeles, sitting in economy seats in the middle of the plane. "We're halfway, probably over Chicago," Greg remembers, "and Mary Catherine said, 'Go to the bathroom.' " "It just sounded like my mother," Greg says. So I said 'no.' " Mary Catherine persisted, urging her husband of 40 years to use the restroom. People started looking at them. "It was kind of funny," says Greg. Mary Catherine was more alarmed than amused. Greg has early-onset Alzheimer's, which makes it increasingly hard for him to keep track of thoughts and feelings over the course of minutes or even seconds. It's easy to get into a situation where you feel like you need to use the bathroom, but then forget. And they had already been on the plane for hours. Finally, Greg started toward the restroom at the back of the plane, only to find the aisle was blocked by an attendant serving drinks. Mary Catherine gestured to him. "Use the one in first class!" At that point, on top of the mild anxiety most people feel when they slip into first class to use the restroom, Greg was feeling overwhelmed by the geography of the plane. He pulled back the curtain dividing the seating sections. "This flight attendant looks at me like she has no use for me. I just said 'Look, I really have to go the bathroom,' and she says 'OK, just go.' " © 2017 npr

Keyword: Alzheimers; Learning & Memory
Link ID: 23772 - Posted: 06.26.2017

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