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By Benedict Carey Nothing humbles history’s great thinkers more quickly than reading their declarations on the causes of madness. Over the centuries, mental illness has been attributed to everything from a “badness of spirit” (Aristotle) and a “humoral imbalance” (Galen) to autoerotic fixation (Freud) and the weakness of the hierarchical state of the ego (Jung). The arrival of biological psychiatry, in the past few decades, was expected to clarify matters, by detailing how abnormalities in the brain gave rise to all variety of mental distress. But that goal hasn’t been achieved — nor is it likely to be, in this lifetime. Still, the futility of the effort promises to inspire a change in the culture of behavioral science in the coming decades. The way forward will require a closer collaboration between scientists and the individuals they’re trying to understand, a mutual endeavor based on a shared appreciation of where the science stands, and why it hasn’t progressed further. “There has to be far more give and take between researchers and the people suffering with these disorders,” said Dr. Steven Hyman, director of the Stanley Center for Psychiatric Research at the Broad Institute of M.I.T. and Harvard. “The research cannot happen without them, and they need to be convinced it’s promising.” The course of Science Times coincides almost exactly with the tear-down and rebuilding of psychiatry. Over the past 40 years, the field remade itself from the inside out, radically altering how researchers and the public talked about the root causes of persistent mental distress. The blueprint for reassembly was the revision in 1980 of psychiatry’s field guide, the Diagnostic and Statistical Manual of Mental Disorders, which effectively excluded psychological explanations. Gone was the rich Freudian language about hidden conflicts, along with the empty theories about incorrect or insufficient “mothering.” Depression became a cluster of symptoms and behaviors; so did obsessive-compulsive disorder, bipolar disorder, schizophrenia, autism and the rest. © 2018 The New York Times Company
Keyword: Schizophrenia; Depression
Link ID: 25703 - Posted: 11.20.2018
A countrywide shortage of a common antidepressant medication has caused alarm among doctors, pharmacists and patients with mental illnesses. Nearly a dozen pharmacies in Saskatoon and Regina have told CBC News that they have run out of bupropion— both the brand-name product Wellbutrin and its generic counterparts — and can't get more from their suppliers. More than 12,000 patients in Saskatchewan take bupropion, according to the Ministry of Health. National figures are not readily available. The prescription antidepressant is used to treat major depressive disorder and seasonal affective disorder. "This might have been the drug that gave you the energy to live your life, do the things you needed to do, get on with your job, do your studies," said Dr. Sara Dungavell, a Saskatoon psychiatrist. She said she fielded anxious phone calls from patients about the shortage. Two pharmaceutical companies that produce generic bupropion are reporting a shortage or anticipated shortage on the Health Canada website. The company that manufactures Wellbutrin, Bausch Health, reported its shortage to Health Canada six weeks ago. On Thursday, it told CBC News it had resolved its shortage, and Canadian pharmacies would receive the drug "imminently," depending on delivery schedules. By Saturday afternoon, pharmacies in Calgary, Saskatoon, Regina and Winnipeg said they had yet to receive a shipment, and their pharmacists said it was still listed as unavailable in their system. ©2018 CBC/Radio-Canada
Keyword: Depression
Link ID: 25702 - Posted: 11.20.2018
By Scott Barry Kaufman "We experience ourselves, our thoughts and feelings as something separate from the rest. A kind of optical delusion of consciousness." -- Albert Einstein "In our quest for happiness and the avoidance of suffering, we are all fundamentally the same, and therefore equal. Despite the characteristics that differentiate us - race, language, religion, gender, wealth and many others - we are all equal in terms of our basic humanity." -- Dalai Lama (on twitter) The belief that everything in the universe is part of the same fundamental whole exists throughout many cultures and philosophical, religious, spiritual, and scientific traditions, as captured by the phrase 'all that is.' The Nobel winner Erwin Schrodinger once observed that quantum physics is compatible with the notion that there is indeed a basic oneness of the universe. Therefore, despite it seeming as though the world is full of many divisions, many people throughout the course of human history and even today truly believe that individual things are part of some fundamental entity. Despite the prevalence of this belief, there has been a lack of a well validated measure in psychology that captures this belief. While certain measures of spirituality do exist, the belief in oneness questions are typically combined with other questions that assess other aspects of spirituality, such as meaning, purpose, sacredness, or having a relationship with God. What happens when we secularize the belief in oneness? © 2018 Scientific American
Keyword: Consciousness
Link ID: 25701 - Posted: 11.19.2018
By John Horgan Don't Make Me One with Everything The mystical doctrine of oneness is metaphysically disturbing, and it can foster authoritarian behavior and encourage an unhealthy detachment. Credit: Mark D Callanan Getty Images A recurring claim of sages east and west is that reality, which seems to consist of many things that keep changing, is actually one thing that never changes. This is the mystical doctrine of oneness. Enlightenment supposedly consists of realizing your oneness with reality, hence the old joke: What did the Buddhist say to the hotdog vendor? Make me one with everything. A column by my fellow Scientific American blogger, psychologist Scott Barry Kaufman, touts the oneness doctrine. “The belief that everything in the universe is part of the same fundamental whole exists throughout many cultures and philosophical, religious, spiritual, and scientific traditions,” Kaufman writes. His column considers, as his headline puts it, “What Would Happen If Everyone Truly Believed Everything Is One?" Kaufman notes that psychologists Kate Diebels and Mark Leary have explored this question. They define oneness, among other ways, as the idea that “beneath surface appearances, everything is one,” and “the separation among individual things is an illusion.” Diebels and Leary found that 20 percent of their respondents have thought about oneness “often or many times,” and many report having spiritual experiences related to oneness. Diebels and Leary state that “a belief in oneness was related to values indicating a universal concern for the welfare of other people, as well as greater compassion for other people.” Believers “have a more inclusive identity that reflects their sense of connection with other people, nonhuman animals, and aspects of nature.” © 2018 Scientific American
Keyword: Consciousness
Link ID: 25700 - Posted: 11.19.2018
Andrew Anthony Of all the mysteries of the mind, perhaps none is greater than memory. Why do we remember some things and forget others? What is memory’s relationship to consciousness and our identities? Where and how is memory stored? How reliable are our memories? And why did our memory evolve to be so rich and detailed? In a sense there are two ways of looking at memory: the literary and the scientific. There is the Proustian model in which memory is about meaning, an exploration of the self, a subjective journey into the past. And then there is the analytical model, where memory is subjected to neurological study, psychological experiments and magnetic resonance imaging. A new book – or rather a recent translation of a two-year-old book – by a pair of Norwegian sisters seeks to marry the two approaches. The co-authors of Adventures in Memory: The Science and Secrets of Remembering and Forgetting are Ylva Østby, a clinical neuropsychologist, and Hilda Østby, an editor and novelist. Their book begins in 1564, with Julius Caesar Arantius performing a dissection of a human brain. Cutting deep into the temporal lobe, where it meets the brain stem, he encounters a small, wormlike ridge of tissue that resembles a sea horse. He calls it hippocampus – or “horse sea monster” in Latin. The significance of this discovery would take almost 400 years to come to light. As with so much to do with our understanding of the brain, the breakthrough came through a malfunction. An American named Henry Molaison suffered from acute epilepsy, and in 1953 he underwent an operation in which the hippocampi from both sides of his brain were removed. The surgery succeeded in controlling his epilepsy but at the cost of putting an end to his memory. © 2018 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 25699 - Posted: 11.19.2018
By Perri Klass, M.D. More than 30 years ago, I went to a parent meeting at my oldest child’s day care center, when he was in the 2-year-old room, and it turned out that many of the children in the room were not reliably sleeping through the night. It felt like a revelation, discovering that mine was not the only child who occasionally — or regularly — woke in the night and needed some attention. In our family, we had come to terms with this, and we had managed to make — and generally keep — some rules: no food, no drink, no coming out of the crib, but yes, once a night one of your parents is willing to stagger down the hall, look in on you, rub your back and say something like, “We haven’t moved away and left you, now go back to sleep.” (Or maybe sometimes it was, “Go back to sleep or we will move away and leave you,” but that is lost in the mists of history.) It wasn’t ideal, but we were managing. In the current issue of the journal Pediatrics, researchers describe a study of almost 400 mothers in Canada who were asked to report: “During the night, how many consecutive hours does your child sleep without waking up?” The researchers took six or eight hours of uninterrupted sleep as definitions of “sleeping through the night.” They found that at 6 months of age, 62.4 percent of mothers reported that their infants slept for 6 hours or more at a stretch, and only 43 percent of the mothers reported eight-hour blocks of consecutive sleep. At 12 months, 72.1 percent of the mothers reported six hours of consecutive sleep, and 56.6 percent reported eight hours; since all infants wake several times a night, those who were reported as sleeping consecutively presumably awoke and went back to sleep by themselves without the mothers knowing it. So by these criteria, a significant number of the babies were not “sleeping through the night” at 6 months, and even at 12 months. At some time points, girls were more likely to sleep for longer periods than boys, but at other times there was no significant difference. © 2018 The New York Times Company
Keyword: Sleep; Development of the Brain
Link ID: 25698 - Posted: 11.19.2018
By Michael Price Patient BAA, who is 35, lost her sight when she was 27. She can still detect light and dark, but for all intents and purposes, she is blind. Now, she—and other formerly sighted people—may one day regain a limited form of vision using electrodes implanted in the brain. In a new study, such electrodes caused parts of BAA’s and other people’s visual cortexes to light up in specific patterns, allowing them to see shapes of letters in their mind’s eyes. The work is a step forward in a field that emerged more than 40 years ago but has made relatively little progress. The findings suggest technical ways to stimulate images in the brain “are now within reach,” says Pieter Roelfsema, a neuroscientist who directs the Netherlands Institute for Neuroscience in Amsterdam and wasn’t involved in the work. Research to electrically spur blind people’s brains to see shapes began in the 1970s, when biomedical researcher William Dobelle, then at The University of Utah in Salt Lake City, first implanted electrodes in the brain to stimulate the visual cortex. Typically, the rods and cones in retinas translate light waves into neural impulses that travel to the brain. Specialized layers of cells there, known as the visual cortex, process that information for the rest of the brain to use. Dobelle’s implants took advantage of a phenomenon known as retinal mapping. The visual field—the plane of space you see when you look out into the world—roughly maps onto a segment of the visual cortex. By electrically stimulating parts of this brain map, Dobelle could cause flashes of light called phosphenes to appear in the minds of people who were blind, but who had experienced at least a few years of vision. By stimulating different electrodes, he could get phosphenes to flash in different parts of a person’s visual field. © 2018 American Association for the Advancement of Science
Keyword: Vision; Robotics
Link ID: 25697 - Posted: 11.17.2018
Exposure to uncomfortable sensations elicits a wide range of appropriate and quick reactions, from reflexive withdrawal to more complex feelings and behaviors. To better understand the body’s innate response to harmful activity, researchers at the National Center for Complementary and Integrative Health (NCCIH), part of the National Institutes of Health, have identified activity in the brain that governs these reactions. Using heat as the source of discomfort, experiments conducted by the center’s intramural program showed that bodily responses to pain are controlled by a neural pathway involving heightened activity in the spinal cord and two parts of the brainstem. Results of the study were published in the journal Neuron. “Much is known about local spinal cord circuits for simple reflexive responses, but the mechanisms underlying more complex behaviors remain poorly understood,” said Alexander T. Chesler, Ph.D., a Stadtman Investigator at NCCIH and senior author of the study. “We set out to describe the brain pathway that controls motor responses and involuntary behaviors when the body is faced with painful experiences.” Just as people respond to increasingly uncomfortable surfaces like a sandy beach on a hot day by lifting their feet, hopping, and eventually running to a water source, so, too, do laboratory models show a predictable sequence of behaviors. Experiments showed that the parts of a brainstem involved in this circuit are the parabrachial nucleus (PBNI) and the dorsal reticular formation in the medulla (MdD). A specific group of nerve cells in the PBNI is activated by standing on a hot surface, triggering escape responses through connections to the MdD. These PBNI cells express a gene called Tac1, which codes for substances called tachykinins that participate in many functions in the body and contribute to multiple disease processes. The MdD cells involved in this circuit also express Tac1. A different group of cells in the PBNI participates in the aspects of the response to noxious heat that involve the forebrain.
Keyword: Pain & Touch
Link ID: 25696 - Posted: 11.17.2018
By Donald G. McNeil Jr. The first treatment for sleeping sickness that relies on pills alone was approved on Friday by Europe’s drug regulatory agency, paving the way for use in Africa, the last bastion of the horrific disease. With treatment radically simplified, sleeping sickness could become a candidate for elimination, experts said, because there are usually fewer than 2,000 cases in the world each year. The disease, also called human African trypanosomiasis, is transmitted by tsetse flies. The protozoan parasites, injected as the flies suck blood, burrow into the brain. Before they kill, drive their victims mad in ways that resemble the last stages of rabies. The personalities of the infected change. They have terrifying hallucinations and fly into rages; they have been known to beat their children and even attack family members with machetes. They may become ravenous and scream with pain if water touches their skin. Only in the end, do they lapse into a long coma and die. The new drug, fexinidazole, cures all stages of the disease within 10 days. Previously, everyone with the parasites found in a blood test also had to undergo a spinal tap to see if the parasites had reached their brains. If so, patients had to suffer through a complex and sometimes dangerous intravenous regimen requiring hospitalization. An oral treatment that can safely be taken at home “is a completely new paradigm — it could let us bring treatment down to the village level,” said Dr. Bernard Pecoul, founder and executive director of the Drugs for Neglected Diseases Initiative, which was started in 2005 by the medical charity Doctors Without Borders to find new cures for tropical diseases. © 2018 The New York Times Company
Keyword: Neurotoxins
Link ID: 25695 - Posted: 11.17.2018
Sara Reardon ‘Mini brains’ grown in a dish have spontaneously produced human-like brain waves for the first time — and the electrical patterns look similar to those seen in premature babies. The advancement could help scientists to study early brain development. Research in this area has been slow, partly because it is difficult to obtain fetal-tissue samples for analysis and nearly impossible to examine a fetus in utero. Many researchers are excited about the promise of these ‘organoids’, which, when grown as 3D cultures, can develop some of the complex structures seen in brains. But the technology also raises questions about the ethics of creating miniature organs that could develop consciousness. A team of researchers led by neuroscientist Alysson Muotri of the University of California, San Diego, coaxed human stem cells to form tissue from the cortex — a brain region that controls cognition and interprets sensory information. They grew hundreds of brain organoids in culture for 10 months, and tested individual cells to confirm that they expressed the same collection of genes seen in typical developing human brains1. The group presented the work at the Society for Neuroscience meeting in San Diego this month. Muotri and his colleagues continuously recorded electrical patterns, or electroencephalogram (EEG) activity, across the surface of the mini brains. By six months, the organoids were firing at a higher rate than other brain organoids previously created, which surprised the team. © 2018 Springer Nature Limited.
Keyword: Development of the Brain; Epilepsy
Link ID: 25694 - Posted: 11.16.2018
Tina Hesman Saey Whether people prefer coffee or tea may boil down to a matter of taste genetics. People with a version of a gene that increases sensitivity to the bitter flavor of caffeine tend to be coffee drinkers, researchers report online November 15 in Scientific Reports. Tea drinkers tended to be less sensitive to caffeine’s bitter taste, but have versions of genes that increase sensitivity to the bitterness of other chemicals, the researchers found. It’s long been thought that people avoid eating bitter foods because bitterness is an indicator of poison, says John Hayes, a taste researcher at Penn State who was not involved in the study. The coffee and tea findings help challenge that “overly simplistic ‘bitter is always bad, let’s avoid it’” view, he says. In the new study, researchers examined DNA variants of genes involved in detecting the bitter taste of the chemicals, caffeine, quinine — that bitter taste in tonic water — and propylthiouracil (PROP), a synthetic chemical not naturally found in food or drink. Other bitter components naturally in coffee and tea may trigger the same taste responses as quinine and PROP do, Hayes says. Researchers in Australia, the United States and England examined DNA from more than 400,000 participants in the UK Biobank, a repository of genetic data for medical research. Participants also reported other information about their health and lifestyle, including how much tea or coffee they drink each day. |© Society for Science & the Public 2000 - 2018
Keyword: Chemical Senses (Smell & Taste); Genes & Behavior
Link ID: 25693 - Posted: 11.16.2018
By Jan Hoffman READING, Mass. — He was supposed to inhale on something that looked like a flash drive and threw off just a wisp of a cloud? What was the point? A skeptical Matt Murphy saw his first Juul at a high school party in the summer of 2016, in a suburban basement crowded with kids shouting over hip-hop and swigging from Poland Spring water bottles filled with bottom-shelf vodka, followed by Diet Coke chasers. Everyone knew better than to smoke cigarettes. But a few were amusing themselves by blowing voluptuous clouds with clunky vapes that had been around since middle school. This Juul looked puny in comparison. Just try it, his friend urged. It’s awesome. Matt, 17, drew a pleasing, minty moistness into his mouth. Then he held it, kicked it to the back of his throat and let it balloon his lungs. Blinking in astonishment at the euphoric power-punch of the nicotine, he felt it — what he would later refer to as “the head rush.” “It was love at first puff,” said Matt, now 19. The next day, he asked to hit his friend’s Juul again. And the next and the next. He began seeking it out wherever he could, that irresistible feeling — three, sometimes four hits a day. So began a toxic relationship with an e-cigarette that would, over the next two years, develop into a painful nicotine addiction that drained his savings, left him feeling winded when he played hockey and tennis, put him at snappish odds with friends who always wanted to mooch off his Juul and culminated in a shouting, tearful confrontation with his parents. © 2018 The New York Times Company
Keyword: Drug Abuse
Link ID: 25692 - Posted: 11.16.2018
By Jan Hoffman Try as she might, Brittany Kligman couldn’t free herself of a pack-a-day cigarette habit, eight years in duration. And she ached to. She was mortified the time that a taxi driver sniffed as she entered his cab and remarked, “You’re a smoker, huh?” (And she had just showered!) She was getting more sinus infections. Because her chest felt uncomfortably tight when she exercised, she stopped high intensity interval training. Then SoulCycle classes. Finally, she quit working out. Then Ms. Kligman, 33, tried Juul, the sleek vaping device she credits for her liberation. Since last January, it’s been hello nicotine salts, goodbye tar. Juul gave her everything she enjoyed about cigarettes — the nicotine jolt as well as something ritualized to do with her hands — but without the stink, the stigma and the carcinogens. “The last cigarette I smoked was on July 5 when I ran out of pods,” Ms. Kligman said, referring to cartridges of mango-flavored liquid, as she took discreet hits while chatting at a downtown Manhattan cafe. “I couldn’t finish it — it made me sick. And I thought, ‘How did I used to do this?’ ” But this week, under pressure to keep its products away from teenagers, Juul announced it was suspending sales of many of its flavors (including Ms. Kligman’s beloved mango) at retail stores. The next day, the Food and Drug Administration issued new requirements that stores can only sell flavored e-cigarettes from closed-off spaces that are inaccessible to minors, a stipulation that could force many outlets to stop carrying the products. The new restrictions make smokers-turned-vapers like Ms. Kligman uneasy. “If you’re going to sell an adult product, you have to be prepared to secure it,” she said. “But it also seems like they’re making a lot of steps and loops for people like me. They’re taking away a flavor I used for smoking cessation. ” She not only intends to stock up on mango at her corner smoke shop, but is working up a Plan B: “I’ll switch to Juul’s tobacco flavor. I can get around this. Just like the kids will — they can always find a way.” © 2018 The New York Times Company
Keyword: Drug Abuse
Link ID: 25691 - Posted: 11.16.2018
By Jan Hoffman The term “electronic cigarette” refers to a battery-powered device that heats a tank or cartridge of liquid usually containing nicotine, flavorings and other chemicals, but not the cancer-causing tar found in tobacco cigarettes. Users inhale and exhale the vapor. The devices come in numerous shapes, including ones that look like pens, flash drives and hookahs. Many consumers are confused about the health implications of e-cigarettes. This is a primer about what research so far shows about these devices. Are they safer than traditional cigarettes? Yes. But that does not mean they are safe. E-cigarettes contain far fewer dangerous chemicals than those released in burning tobacco. Tobacco cigarettes typically contain 7,000 chemicals, including nearly 70 known to be carcinogenic. E-cigarettes also don’t release tar, the tobacco residue that damages lungs but also contributes to the flavor of tobacco products. In the United States, cigarettes are associated with 480,000 deaths a year from coronary heart disease, stroke and numerous cancers, among other illnesses. The research on e-cigarettes is young because the products have only been around for a little over a decade. Exacerbated by the voltage of a given device, certain e-cigarette flavors can irritate the airways, researchers say: benzaldehyde (added to cherry flavored liquids), cinnamaldehyde (gives cinnamon flavor), and diacetyl (a buttery flavor that can cause lung tissue damage called “popcorn lung.”) Some flavors become irritants when added to vaping liquids. The process of turning liquid chemicals into vapor releases harmful particulates deep into the lungs and atmosphere, including heavy metals. © 2018 The New York Times Company
Keyword: Drug Abuse
Link ID: 25690 - Posted: 11.16.2018
Ned Rozell Alaska chickadees have proven themselves brainier than Colorado chickadees. A researcher at the University of California Davis once compared black-capped chickadees from Anchorage to chickadees from Windsor, Colorado, and found that the Alaska birds cached more sunflower seeds and found the seeds quicker when they later searched for them. The Alaska chickadees also had brains that contained more neurons than those of Colorado chickadees. Vladimir Pravosudov of the UC Davis psychology department performed the study to test the notion that northern birds would be better at hiding and finding seeds than birds in a more moderate climate. He chose to capture birds in Anchorage, which has a day length of about 5 hours, 30 minutes on Dec. 22, and compare them to birds he captured near Windsor, about 50 miles north of Denver, where the Dec. 22 day length is about 9 hours, 15 minutes. With the help of biologist Colleen Handel of the U.S. Geological Survey in Anchorage, Pravosudov captured 15 black-capped chickadees using a mist net at bird feeders around Anchorage in fall 2000. He later captured 12 black-capped chickadees near Windsor. All the birds went to his lab in Davis, where he gave them the same food and amount of daylight for 45 days. After 45 days he tested eight birds from Alaska and eight from Colorado in a room with 70 caching holes drilled in wooden blocks and trees. In late summer through fall, black-capped chickadees gather and hide seeds, insects and other foods to retrieve later, when they have fewer hours of daylight to feed and less food is available. Though black-capped chickadees live their entire lives within a few square acres, the species ranges from as far north as Anaktuvuk Pass in Alaska to as far south as New Mexico. © 2018 Anchorage Daily News
Keyword: Learning & Memory; Evolution
Link ID: 25689 - Posted: 11.16.2018
By Sam Roberts Herbert Fingarette, a contrarian philosopher who, while plumbing the perplexities of personal responsibility, defined heavy drinking as willful behavior rather than as a potential disease, died on Nov. 2 at his home in Berkeley, Calif. He was 97. His daughter, Ann Fingarette Hasse, said the cause was heart failure. Professor Fingarette challenged the theory that alcoholism is a progressive disease that can be dealt with only by abstinence, and he concluded that treatment could include moderated drinking. Many academics and medical professionals denounced those views as heresy. But they were invoked by the United States Supreme Court in the 1988 decision Traynor v. Turnage. In that ruling, the court affirmed the government’s denial of education benefits to two veterans who had argued that they missed filing deadlines for those benefits because of their addiction as recovering alcoholics. Their claim that alcoholism is a disease beyond a drinker’s control was endorsed by the American Medical Association and the American Psychiatric Association. But it was rejected by the court, which ruled that certain types of alcohol abuse resulted from deliberate misconduct. Much of Professor Fingarette’s research and writing concerned accountability. That included what he called the self-deception, validated by science, that alcoholics cannot help themselves. In “Heavy Drinking: The Myth of Alcoholism as a Disease” (1988), Professor Fingarette all but accused the treatment industry of conspiring to profit from the conventional theory that alcoholism is a disease. He maintained that heavy use of alcohol is a “way of life,” that many heavy drinkers can choose to reduce their drinking to moderate levels, and that most definitions of the word “alcoholic” are phony. © 2018 The New York Times Company
Keyword: Drug Abuse; Attention
Link ID: 25688 - Posted: 11.16.2018
By Kelly Servick SAN DIEGO, CALIFORNIA—If a diseased or injured brain has lost neurons, why not ask other cells to change jobs and pick up the slack? Several research teams have taken a first step by "reprogramming" abundant nonneuronal cells called astrocytes into neurons in the brains of living mice. "Everybody is astonished, at the moment, that it works," says Nicola Mattugini, a neurobiologist at Ludwig Maximilian University in Munich, Germany, who presented the results of one such experiment here at the annual meeting of the Society for Neuroscience last week. Now, labs are turning to the next questions: Do these neurons function like the lost ones, and does creating neurons at the expense of astrocytes do brain-damaged animals any good? Many researchers remain skeptical on both counts. But Mattugini's team, led by neuroscientist Magdalena Götz, and two other groups presented evidence at the meeting that reprogrammed astrocytes do, at least in some respects, impersonate the neurons they're meant to replace. The two other groups also shared evidence that reprogrammed astrocytes help mice recover movement lost after a stroke. Some see the approach as a potential alternative to transplanting stem cells (or stem cell–derived neurons) into the damaged brain or spinal cord. Clinical trials of that strategy are already underway for conditions including Parkinson's disease and spinal cord injury. But Gong Chen, a neuroscientist at Pennsylvania State University in State College, says he got disillusioned with the idea after finding in his rodent experiments that transplanted cells produced relatively few neurons, and those few weren't fully functional. The recent discovery that mature cells can be nudged toward new fates pointed to a better approach, he says. His group and others took aim at the brain's most abundant cell, the star-shaped astrocyte. © 2018 American Association for the Advancement of Science
Keyword: Stem Cells; Glia
Link ID: 25687 - Posted: 11.15.2018
Bruce Bower Neandertals are shaking off their reputation as head bangers. Our close evolutionary cousins experienced plenty of head injuries, but no more so than late Stone Age humans did, a study suggests. Rates of fractures and other bone damage in a large sample of Neandertal and ancient Homo sapiens skulls roughly match rates previously reported for human foragers and farmers who have lived within the past 10,000 years, concludes a team led by paleoanthropologist Katerina Harvati of the University of Tübingen in Germany. Males suffered the bulk of harmful head knocks, whether they were Neandertals or ancient humans, the scientists report online November 14 in Nature. “Our results suggest that Neandertal lifestyles were not more dangerous than those of early modern Europeans,” Harvati says. Until recently, researchers depicted Neandertals, who inhabited Europe and Asia between around 400,000 and 40,000 years ago, as especially prone to head injuries. Serious damage to small numbers of Neandertal skulls fueled a view that these hominids led dangerous lives. Proposed causes of Neandertal noggin wounds have included fighting, attacks by cave bears and other carnivores and close-range hunting of large prey animals. Paleoanthropologist Erik Trinkaus of Washington University in St. Louis coauthored an influential 1995 paper arguing that Neandertals incurred an unusually large number of head and upper-body injuries. Trinkaus recanted that conclusion in 2012, though. All sorts of causes, including accidents and fossilization, could have resulted in Neandertal skull damage observed in relatively small fossil samples, he contended (SN: 5/27/17, p. 13). |© Society for Science & the Public 2000 - 2018.
Keyword: Evolution; Aggression
Link ID: 25686 - Posted: 11.15.2018
By Virginia Morell When wild orangutans spot a predator, they let out a loud “kiss-squeak,” a call that sounds like a human smooching. That noise tells tigers and other enemies, “I’ve seen you,” scientists believe, and it also lets other orangutans know danger is near. Now, researchers report having heard orangutans making this call long after predators have passed—the first evidence that primates other than humans can “talk” about the past. “The results are quite surprising,” says Carel van Schaik, a primatologist at the University of Zurich in Switzerland who was not involved in the work. The ability to talk about the past or the future “is one of the things that makes language so effective,” he says. That suggests, he adds, that the new findings could provide clues to the evolution of language itself. Many mammals and birds have alarm calls, some of which include information on the type and size of a predator, its location and distance, and what level of danger it poses. But until now, researchers have never heard wild animals announcing danger after the fact. Adriano Reis e Lameira, a postdoctoral student at the University of St. Andrews in the United Kingdom, was examining alarm calls in orangutans in Sumatra’s dense Ketambe forest, where the primates have been observed for nearly 40 years. He set up a simple experiment to investigate their alarm calls: A scientist draped in a tiger-striped, spotted, or plain sheet walked on all fours along the forest floor, right underneath lone female orangutans sitting in trees at heights of 5 to 20 meters above the ground. © 2018 American Association for the Advancement of Science
Keyword: Evolution; Language
Link ID: 25685 - Posted: 11.15.2018
Anna Azvolinsky In 1976, Huda Zoghbi (then Huda El-Hibri) was an eager first-year medical student at the American University of Beirut, Lebanon, her hometown. Halfway through that year, a civil war broke out. “Bombs were falling all around the medical campus,” the neuroscientist recalls. “I couldn’t commute 500 feet, let alone the two miles it took me to get home every day.” She and the other 62 students in her class decided that they, along with their professors, would live on campus—mostly underground, in double-walled rooms—to finish the school year. Although the medical school was considered a safe zone, as both warring factions would send their wounded there for care, an occasional bullet or piece of shrapnel still pierced the campus. One afternoon, Huda had ventured out for a walk on campus with her boyfriend, William Zoghbi, a fellow medical student. They were holding hands and for no particular reason let go. In those few seconds, a bullet flew between them. Neither was hurt, but the young couple realized in an instant how close and serious the war really was. Later, shrapnel wounded Huda’s younger brother while he was walking home from high school, so their parents decided to send them and another sibling to Texas, where their oldest sister was a professor of philosophy. The move was supposed to be temporary. But when the 1977 school year was to start in Lebanon, the civil war was still raging, and neither Huda nor her siblings could return home. © 1986 - 2018 The Scientist
Keyword: Movement Disorders; Genes & Behavior
Link ID: 25684 - Posted: 11.15.2018


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