Allison Aubrey There are lots of reasons why many of us don't get the recommended seven hours or more of sleep each night. Travel schedules, work deadlines, TV bingeing and — a big one — having young children all take a toll. Research published recently in the journal Sleep finds that up to six years after the birth of a child, many mothers and fathers still don't sleep as much as they did before their child was born. For parents, there's just less time in the day to devote to yourself. So, can you catch up on sleep? That partly depends on how much sleep you've missed. A study in the current issue of Current Biology points to just how quickly the adverse effects of sleep deprivation can kick in. Researchers at the University of Colorado Boulder recruited a bunch of young, healthy adults who agreed to a stay in a sleep lab. Some were allowed to sleep no more than five hours per night for five consecutive days. "After five days, people [gained] as much as 5 pounds," says study author Christopher Depner, who studies the links between sleep loss and metabolic diseases. Lack of sleep can throw off the hormones that regulate appetite, he explains, so people tend to eat more. Depner and his colleagues also documented a decrease in insulin sensitivity among the sleep-deprived participants. "In some people, it decreased to a level where they'd be considered pre-diabetic," he says. Presumably, that rise in blood sugar would be only temporary in these young, healthy people. But it's a striking indicator of how much a lack of sleep can influence metabolism. © 2019 npr

Keyword: Sleep
Link ID: 26072 - Posted: 03.25.2019

David Cox Claudia Kieffer remembers the first time she encountered the drug she describes as having “saved my life”. Eight years ago, Kieffer, who had suffered from treatment-resistant depression for decades, was given ketamine as a routine anaesthetic, as part of a post-mastectomy breast reconstruction procedure. But as well as alleviating the pain, Kieffer noticed an instantaneous change in her state of mind. “My head suddenly felt different to any previous time in my entire life,” she says. “I wasn’t high. It wasn’t like I had smoked a joint or had morphine. It was like a spring breeze had blown through my head and just cleaned out all the detritus that had built up over years and years. And when you’ve suffered from depression for as long as I had, it feels like you’re drowning. So when something comes along that makes you feel so very different and healthy, you want to know what that drug is.” Get Society Weekly: our newsletter for public service professionals Read more At the time, Kieffer had tried almost every depression-related treatment available, without success. “I’d had three nervous breakdowns and been hospitalised three times,” she remembers. “I’d had 13 rounds of electric-shock therapy and it didn’t help. When I was in my 20s and 30s, I would self-medicate, just because that’s what you do when you don’t know what else to do. I was thinking about taking my life every single day. I just wanted to fall asleep and not wake up.”

Keyword: Depression; Drug Abuse
Link ID: 26071 - Posted: 03.25.2019

By Benedict Carey Whatever its other properties, memory is a reliable troublemaker, especially when navigating its stockpile of embarrassments and moral stumbles. Ten minutes into an important job interview and here come screenshots from a past disaster: the spilled latte, the painful attempt at humor. Two dates into a warming relationship and up come flashbacks of an earlier, abusive partner. The bad timing is one thing. But why can’t those events be somehow submerged amid the brain’s many other dimming bad memories? Emotions play a role. Scenes, sounds and sensations leave a deeper neural trace if they stir a strong emotional response; this helps you avoid those same experiences in the future. Memory is protective, holding on to red flags so they can be waved at you later, to guide your future behavior. But forgetting is protective too. Most people find a way to bury, or at least reshape, the vast majority of their worst moments. Could that process be harnessed or somehow optimized? Perhaps. In the past decade or so, brain scientists have begun to piece together how memory degrades and forgetting happens. A new study, published this month in the Journal of Neuroscience, suggests that some things can be intentionally relegated to oblivion, although the method for doing so is slightly counterintuitive. For the longest time, forgetting was seen as a passive process of decay and the enemy of learning. But as it turns out, forgetting is a dynamic ability, crucial to memory retrieval, mental stability and maintaining one’s sense of identity. © 2019 The New York Times Company

Keyword: Learning & Memory
Link ID: 26070 - Posted: 03.23.2019

By Jennifer Couzin-Franke Earlier this week, the Lieber Institute for Brain Development, a nonprofit housed at Johns Hopkins University School of Medicine in Baltimore, Maryland, announced a new neuroscience research initiative that aims to tackle a gaping hole in medicine: the interplay between brain diseases and their genomic drivers among African-Americans. The goal is to better understand how brain diseases play out in this population, which has been profoundly underrepresented in neuroscience research. To build trust among African-Americans in Baltimore and eventually beyond, the venture includes a partnership with the African-American Clergy Medical Research Initiative, a group of clergy leaders in the city. African-American scientists at Lieber are already involved, but project leaders hope to engage those at other institutions as the work expands. The effort builds on Lieber’s rapidly growing brain bank, which now stands at about 3000 brains, with more than 400 new brains collected each year, all donated by next of kin. Many are from young and middle-aged people who die suddenly of suicide, drug overdose, or other causes. Although most of the brains are from people of European ancestry, more than 700 are from African-Americans. Despite growing recognition that African-Americans are underrepresented in medical research—and face discrimination and other hardships that can heighten health risks—study of brain diseases in this population have lagged behind, says Daniel Weinberger, the institute’s director. ScienceInsider spoke with Weinberger, a psychiatrist and schizophrenia researcher who came to the Lieber Institute in 2011 from the National Institute of Mental Health. The conversation has been edited for brevity and clarity. © 2019 American Association for the Advancement of Science

Keyword: Alzheimers; Genes & Behavior
Link ID: 26069 - Posted: 03.23.2019

By Emilia Clarke Just when all my childhood dreams seemed to have come true, I nearly lost my mind and then my life. I’ve never told this story publicly, but now it’s time. It was the beginning of 2011. I had just finished filming the first season of “Game of Thrones,” a new HBO series based on George R. R. Martin’s “A Song of Ice and Fire” novels. With almost no professional experience behind me, I’d been given the role of Daenerys Targaryen, also known as Khaleesi of the Great Grass Sea, Lady of Dragonstone, Breaker of Chains, Mother of Dragons. As a young princess, Daenerys is sold in marriage to a musclebound Dothraki warlord named Khal Drogo. It’s a long story—eight seasons long—but suffice to say that she grows in stature and in strength. She becomes a figure of power and self-possession. Before long, young girls would dress in platinum wigs and flowing robes to be Daenerys Targaryen for Halloween. The show’s creators, David Benioff and D. B. Weiss, have said that my character is a blend of Napoleon, Joan of Arc, and Lawrence of Arabia. And yet, in the weeks after we finished shooting the first season, despite all the looming excitement of a publicity campaign and the series première, I hardly felt like a conquering spirit. I was terrified. Terrified of the attention, terrified of a business I barely understood, terrified of trying to make good on the faith that the creators of “Thrones” had put in me. I felt, in every way, exposed. In the very first episode, I appeared naked, and, from that first press junket onward, I always got the same question: some variation of “You play such a strong woman, and yet you take off your clothes. Why?” In my head, I’d respond, “How many men do I need to kill to prove myself?” © 2019 Condé Nast

Keyword: Stroke
Link ID: 26068 - Posted: 03.23.2019

By Veronique Greenwood The sun bears were making faces at each other. And that was a bit of a surprise. Comparative psychologists have been studying the facial expressions of primates like orangutans and gorillas for years. They have evolved in complex societies and thus need to be able to convey their joy, anger, and other emotions to their companions. But nobody had thought to look at creatures like sun bears, who live mostly solitary lives. Marina Davila-Ross, a primatologist at the University of Portsmouth in England, and her colleagues learned that a handful of the Southeast Asian bears, which primarily live alone in the wild, were in a rehabilitation center near the orangutan center in Malaysia where Dr. Davila-Ross was doing research. Curious about whether facial communication was more common in the animal kingdom that people thought, they deployed cameras to capture hours of footage of the bears interacting with each other. In a study published Thursday in Scientific Reports, they say that sun bears do use facial expressions to communicate, suggesting that the capacity to do so may be widespread, and that social creatures do not have a monopoly on expressing themselves this way. Sun bears are exceedingly solitary. A female’s one or two cubs will live with her for about two years, and then set off for lives on their own. Adults seem to rarely meet, except for mating. At the center, bears that cannot be released back into the wild live in enclosures in groups of five or six. For the bears, it was an unnatural setup — but it was perfect for the scientists. In their footage of 22 bears going about their daily lives, the scientists zeroed in on moments when the animals were playing, batting at each other and grappling good-humoredly. They watched for moments where the playing bears were looking into each other’s faces, and then they looked for certain facial expressions, like opening one’s mouth wide and showing teeth. © 2019 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 26067 - Posted: 03.23.2019

Katarina Zimmer It’s well established that exercise is good for the mammalian brain. As early as 1999, researchers discovered considerably more newborn neurons in the hippocampi of mice that had access to a running wheel than in animals that didn’t. But 20 years later, scientists are still trying to understand why. A team of Australian and German researchers has uncovered one mechanism that explains how exercise boosts neurogenesis in mice: the activity causes platelets circulating in the blood to release factors that boost the growth of neural precursor cells in the hippocampus, the researchers report today (March 21) in Stem Cell Reports. “We all know about the positive effect of exercise on the brain and other organ systems, but what the actual mechanism is to promote new neuron production is still a bit of a mystery,” remarks Vince Tropepe, who studies neurogenesis at the University of Toronto and who was not involved in the study. “This paper is quite interesting in that they’ve identified a player—these platelets and platelet-derived factors that are circulating in the blood after exercise—that might be a mediator of this effect.” The researchers came to this conclusion through a series of experiments comparing mice that had access to a running wheel for four days with control mice that didn’t. Lab mice voluntarily run up to 10 kilometers per night, “equivalent to us running more than a marathon a day,” explains coauthor Tara Walker, a senior research associate at the Queensland Brain Institute. © 1986 - 2019 The Scientist

Keyword: Neurogenesis; Development of the Brain
Link ID: 26066 - Posted: 03.23.2019

Laura Sanders With great fanfare, a new antidepressant entered the U.S. market in March, the first fundamentally new medicine for depression in decades. Based on the anesthetic ketamine, the drug — called Spravato — is intended to help people with severe depression quickly, taking effect within hours or days instead of the weeks that typical antidepressants take. But for all the hubbub, big questions have gone unanswered about the drug, developed by Janssen Pharmaceuticals, Inc. Some psychiatrists are concerned that the drug was approved by the U.S. Food and Drug Administration based on skimpy data, under standards that were less rigorous than those required for previous antidepressants. It remains unclear, for example, what happens as someone stops taking the drug, as well as whether it has long-term effects. The data on Spravato raise more questions than they answer, says psychiatrist Alan Schatzberg of Stanford University. “And I think that’s unfortunate.” Despite those unknowns, some psychiatrists are relieved to have another drug to try, particularly for people with depression so severe that other drugs have failed to help. Spravato “does something that very few things in psychiatry can do — it works for people who didn’t respond to other treatments, and it works fast,” says psychiatrist Dan Iosifescu of New York University’s School of Medicine. “I really welcome having another powerful tool in my toolbox.” |© Society for Science & the Public 2000 - 2019

Keyword: Depression; Hormones & Behavior
Link ID: 26065 - Posted: 03.23.2019

By Paul Raeburn When the brain remembers, proteins in two locations deep within the organ—the amygdala and hippocampus—encode the memory until it is stored, or “consolidated” in the vernacular. Neuroscientists once thought that a memory, when put in its place, became permanent and stable. That’s a problem for patients with post-traumatic stress disorder (PTSD), plagued by crippling, debilitating memories that they cannot shake. “We wish that we could somehow target unpleasant or pathological memories and reduce their emotional strength,” says Bryan A. Strange, founder of the Laboratory of Clinical Science at the Universidad Politécnica de Madrid. During the past two decades or so, it has become clear that these memories are not fixed and unshakable. They can be manipulated in ways that might ultimately ease the suffering of patients, not just ones with a PTSD diagnosis but also those afflicted by phobias, depression and other stress-related conditions. Strange is among the researchers looking for leads to tamp down toxic memories. He and his colleagues reported in a Science Advances paper on March 20 that the anesthetic propofol can be used to alter such recollections, if administered in the right circumstances. © 2019 Scientific American

Keyword: Stress; Learning & Memory
Link ID: 26064 - Posted: 03.22.2019

By Bahar Gholipour Philosophers have spent millennia debating whether we have free will, without reaching a conclusive answer. Neuroscientists optimistically entered the field in the 1980s, armed with tools they were confident could reveal the origin of actions in the brain. Three decades later, they have reached the same conclusion as the philosophers: Free will is complicated. Now, a new research program spanning 17 universities and backed by more than $7 million from two private foundations hopes to break out the impasse by bringing neuroscientists and philosophers together. The collaboration, the researchers say, can help them tackle two important questions: What does it take to have free will? And whatever that is, do we have it? Neuroscience’s first and most famous encounter with free will occurred in 1983, when physiologist Benjamin Libet made a peculiar discovery. A brain signal called the readiness potential was known to precede self-initiated actions, such as raising a hand or spontaneously tapping a finger. Libet found the readiness potential starts to rise before people report they are aware of their decision to move. Many took that as a challenge to the existence of free will. But subsequent studies argued that was a flawed interpretation, and that the results said little about free will. © 2019 American Association for the Advancement of Science

Keyword: Consciousness
Link ID: 26063 - Posted: 03.22.2019

By Richard Klasco, M.D. Q. I have completely lost my sense of smell and can taste only a few things. I have seen doctors and taken tests, but no answers. I know I’m not the only one with this problem. Any ideas? A. Humans are able to perceive an astounding one trillion odors. But our sense of smell is fragile. About a quarter of adults, and more than half of those over 80, have some degree of olfactory impairment. The sense of taste is often affected at the same time, as the neural pathways of smell and taste commingle in the brain. Having an impaired sense of smell may be more than a nuisance. Studies have linked a decreased sense of smell to a heightened risk for Parkinson’s disease, Alzheimer’s disease, multiple sclerosis and premature death. Common causes of a decreased sense of smell include nasal problems, such as deviated septum and nasal polyps; viruses, such as rhinovirus and Epstein-Barr virus; chronic sinusitis; head injury; and certain cancers. Environmental exposure to cigarette smoke, alcohol, air pollution and toxins further increase the risk. Yet, in about 16 percent of people, no cause can be identified. Eating nuts and fish has been associated with protection against smell impairment, as have exercise and use of cholesterol-lowering drugs and oral steroids. It is unknown, however, whether changing one’s dietary or exercise habits will improve the sense of smell. Medical evaluation typically begins with an otolaryngologist, an ear, nose and throat doctor who will use a standardized scratch-and-sniff test to assess any olfactory deficits. Laboratory tests of blood and nasal mucus and imaging studies, such as CT or M.R.I. scans, are often needed. In some cases, endoscopic surgery, a flexible camera inserted into the nose, may aid in diagnosis and provide therapeutic benefits. © 2019 The New York Times Company

Keyword: Chemical Senses (Smell & Taste)
Link ID: 26062 - Posted: 03.22.2019

By Kelly Servick “Futile”—that’s the devastating label now attached to two highly anticipated clinical trials of a drug that targets β-amyloid, the neuron-killing protein fragment littering the brains of people with Alzheimer’s disease. Biogen in Cambridge, Massachusetts, and Eisai in Tokyo, the pharmaceutical partners developing the drug, called aducanumab, today announced their decision to halt a pair of ongoing phase III trials after seeing the results of a “futility analysis,” in which an independent committee found that the drug was unlikely to slow cognitive decline as intended. This latest blow to the β-amyloid approach has left researchers asking: Do any of the remaining antiamyloid drug trials have a better chance, or is it time to declare the whole approach, well, futile? “Amyloid definitely has something to do with Alzheimer’s—there’s far too much evidence to dismiss,” organic chemist Derek Lowe wrote today on his drug industry blog In the Pipeline. (The blog is hosted by Science Translational Medicine, which, like ScienceInsider, is published by AAAS.) “But the situation is clearly more complicated than people have hoped, because otherwise, all the attempts to address amyloid … would have yielded some tiny bit of clinical benefit.” There were reasons to think that aducanumab might succeed where antiamyloid drugs from Merck & Co., Eli Lilly and Company, and others had failed. The drug is an antibody designed to bind to and eliminate sticky β-amyloid plaques that build up around neurons, block their communication, and, ultimately, kill them. And it was clear from a smaller clinical trial that this drug was very effective at clearing plaques—“that’s one of the reasons we were sanguine about this trial,” says neurologist Dennis Selkoe of Brigham and Women’s Hospital in Boston, who treats patients who were enrolled in one of the trials. Studies also suggest aducanumab can attack the most noxious form of amyloid—so-called oligomers—that other drugs may have left untouched. © 2019 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 26061 - Posted: 03.22.2019

Jef Akst A robot interacting with young honey bees in Graz, Austria, exchanged information with a robot swimming with zebrafish in Lausanne, Switzerland, and the robots’ communication influenced the behavior of each animal group, according to a study published in Science Robotics today (March 20). “It’s the first time that people are using this kind of technology to have two different species communicate with each other,” says Simon Garnier, a complex systems biologist at New Jersey Institute of Technology who did not participate in the study. “It’s a proof of concept that you can have robots mediate interactions between distant groups.” He adds, however, that the specific applications of such a setup remains to be seen. As robotics technology has advanced, biologists have sought to harness it, building robots that look and behave like animals. This has allowed researchers to control one side of social interactions in studies of animal behavior. Robots that successfully integrate into animal populations also provide scientists with a means to influence the groups’ behavior. “The next step, we were thinking . . . [is] adding features to the group that the animals cannot do because they don’t have the capabilities to do so,” José Halloy, a physicist at Paris Diderot University who has been working on developing robots to interact intelligently with animals for more than a decade, writes in an email. “The simple and striking thing is that robots can use telecommunication or the Internet and animals cannot do that.” © 1986 - 2019 The Scientist.

Keyword: Animal Communication; Language
Link ID: 26060 - Posted: 03.22.2019

By Adrian Cho BOSTON—MRI scanners can map a person's innards in exquisite detail, but they say little about composition. Now, physicists are pushing MRI to a new realm of sensitivity to trace specific biomolecules in tissues, a capability that could aid in diagnosing Alzheimer's and other diseases. The advance springs not from improved scanners, but from better methods to solve a notoriously difficult math problem and extract information already latent in MRI data. The new techniques, described this month at a meeting of the American Physical Society here, could soon make the jump to the clinic, says Shannon Kolind, a physicist at the University of British Columbia (UBC) in Vancouver, Canada, who is using them to study multiple sclerosis (MS). "I don't think I'm being too optimistic to say that will happen in the next 5 years," she says. Sean Deoni, a physicist at Brown University, says that "any scanner on the planet can do this." An MRI scanner uses magnetic fields and radio waves to tickle the nuclei of hydrogen atoms—protons—in molecules of water, which makes up more than half of soft tissue. The protons act like little magnets, and the scanner's strong magnetic field makes them all point in one direction. A pulse of radio waves then tips the protons away from the magnetic field, causing them to twirl en masse, like so many gyroscopes. The protons then radiate radio waves of their own. © 2019 American Association for the Advancement of Scienc

Keyword: Brain imaging; Multiple Sclerosis
Link ID: 26059 - Posted: 03.21.2019

By Heather Murphy An essential rite of passage for many an otherwise nonviolent child involves cutting an earthworm down the middle and watching as the two halves squirm. One half — the one with the brain — will typically grow into a full worm. Scientists have now identified the master control gene responsible for that regrowth in one particularly hardy type of worm. How hardy? Chop the three-banded panther worm in halves or thirds — either crosswise or diagonally — and each segment will regenerate just fine, said Mansi Srivastava, a professor of organismic and evolutionary biology at Harvard University. Within eight days, you’ll have two or three fully functioning new worms, mouth, brain and all. “It’s hard to kill them,” she said. Dr. Srivastava and her co-authors published a paper Friday outlining their genetic discovery. The process is known as “full-body regeneration,” and the term has captured the imagination of many individuals ready for a fresh start or second self. “I’ll get a new body right now!!” one person wrote in a lively Reddit thread about the finding, adding “I knew it was coming!!” Another posted: “Two of me working together and sharing our stuff? Count me in!” Headlines suggesting that the scientists have found the DNA switch that could lead to human limb regrowth have fueled hopes that the discovery will offer precisely that. Unfortunately, no one is growing a new arm or getting a second body with the help of marine worm DNA anytime soon, said Peter W. Reddien, a biologist with M.I.T.’s Whitehead Institute for Biomedical Research and another author of the paper. But he added that he didn’t totally blame people for getting carried away because his field truly is stranger than fiction. “You can damage large amounts of the heart muscle of a fish and the heart will come back,” he said. “You can remove the jaw or even the entire head and some animals will grow it back. It’s amazing.” What’s accurate in this particular case is that a master control gene known as E.G.R. — or early growth response — is present in many kinds of organisms, including humans. An injury that pierces skin often activates it, he said. But activation is just one small piece of a larger puzzle. © 2019 The New York Times Company

Keyword: Development of the Brain
Link ID: 26058 - Posted: 03.21.2019

New rules to reduce naturally high testosterone levels in female athletes have been branded "unscientific". Last year, athletics chiefs ruled women with levels of five nanomoles per litre or more must have hormone treatment before being allowed to compete. But experts, reporting in the British Medical Journal, say there is a lack of evidence about testosterone's effects and the cut-off figure is arbitrary. A decision on the legality of the rules is expected later this month. The International Association of Athletics Federations (IAAF) delayed implementing its regulations after South African runner Caster Semenya contested the legality of the new rules. She was banned from international competitions for nearly a year for having testosterone levels above the athletics body's limit for female athletes. World athletics bosses have previously said they want to protect the sanctity of fair and open competition. Writing in an editorial in the BMJ, Dr Sheree Bekker, from the University of Bath, and Prof Cara Tannenbaum, from the University of Montreal, say the IAAF's regulations risked "setting an unscientific precedent for other cases of genetic advantage". "The medical profession does not define biological sex or physical function by serum testosterone levels alone," they say. And they warned that the proposed rules could have "far reaching implications" on individuals and societies. Dr Bekker and Prof Tannenbaum argue that testosterone levels vary naturally in men and women, with higher averages among elite athletes. But there is also a big crossover between men and women, with 16% of men classified as having low testosterone and 14% of women having high, according to some definitions. They say testosterone is just one indicator of sports performance and many other factors also play a role. "If more science is needed... then call for health research organisations to deliver on this mandate," they say. © 2019 BBC

Keyword: Sexual Behavior
Link ID: 26057 - Posted: 03.21.2019

Ian Sample Science editor Scientists have developed a test for Parkinson’s disease based on its signature odour after teaming up with a woman who can smell the condition before tremors and other clinical symptoms appear. The test could help doctors diagnose patients sooner and identify those in the earliest stages of the disease, who could benefit from experimental drugs that aim to protect brain cells from being killed off. Perdita Barran, of the University of Manchester, said the test had the potential to decrease the time it took to distinguish people with normal brain ageing from those with the first signs of the disorder. “Being able to say categorically, and early on, that a person has Parkinson’s disease would be very useful,” she said. Get Society Weekly: our newsletter for public service professionals Read more Most people cannot detect the scent of Parkinson’s, but some who have a heightened sense of smell report a distinctive, musky odour on patients. One such “super smeller” is Joy Milne, a former nurse, who first noticed the smell on her husband, Les, 12 years before he was diagnosed. Milne only realised she could sniff out Parkinson’s when she attended a patient support group with her husband and found everyone in the room smelled the same. She thought little more about it until she mentioned the odour to Tilo Kunath, a neurobiologist who studies Parkinson’s at Edinburgh University. © 2019 Guardian News & Media Limited

Keyword: Parkinsons; Chemical Senses (Smell & Taste)
Link ID: 26056 - Posted: 03.20.2019

By Pam Belluck The first drug for women suffering postpartum depression received federal approval on Tuesday, a move likely to pave the way for a wave of treatments to address a debilitating condition that is the most common complication of pregnancy. The drug works very quickly, within 48 hours — a significant improvement over currently available antidepressants, which can take two to four weeks to have an effect, if they work at all. Experts say the new treatment will provide immediate relief for mothers whose depression keeps them from providing their babies with the care, bonding and nurturing that is crucial for healthy development. As many as one in seven American women experience depression during or after pregnancy. "Postpartum depression is a serious condition that, when severe, can be life-threatening,” Dr. Tiffany Farchione, acting director of the Division of Psychiatry Products at the Food and Drug Administration’s Center for Drug Evaluation and Research, said in a statement. “This approval marks the first time a drug has been specifically approved to treat postpartum depression, providing an important new treatment option.” There are limitations to the new drug, brexanolone, which will be marketed as Zulresso. It is delivered by infusion over 60 hours, during which a new mother must remain in a certified medical center, under supervision should she get dizzy or faint, as several patients did in clinical trials. The infusion will be expensive, averaging $34,000 per patient before discounts, according to Sage Therapeutics, the manufacturer. That does not include the costs of staying in a medical center for two and half days. Company officials say they expect that insurers will cover the treatment; insurers said this week that they are evaluating the drug. A pill made with a similar molecule, which would be much more accessible and easier for patients, is showing promise in its clinical trials and would be submitted for approval in a couple of years if the results are good, according to Sage. © 2019 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 26055 - Posted: 03.20.2019

Terry Gross When Frans de Waal started studying nonhuman primates, in the Netherlands more than 40 years ago, he was told not to consider the emotions of the animals he was observing. "Thoughts and feelings — the mental processes basically — were off limits," he says. "We were told not to talk about them, because they were considered by many scientists as 'inner states' and you only were allowed to talk about 'outer states.' " But over the course of his career, de Waal became convinced that primates and other animals express emotions similar to human emotions. He's now the director of the Living Links Center at the Yerkes National Primate Research Center in Atlanta, where his office window looks out on a colony of chimps. "I am now at the point that I think emotions are more like organs," he says. "All my organs are present in a rat's body, and the same way, I think, all my emotions are probably present in the rat." De Waal writes about primate empathy, rivalry, bonding, sex and murder in his new book, Mama's Last Hug. The title of the book was inspired by a tender interaction between a dying 59-year-old chimp named Mama and de Waal's mentor, Jan van Hooff, who had known Mama for more than 40 years. "People were surprised [by] how humanlike the expression of Mama was and how humanlike her gestures were," de Waal says of the interaction. "I thought, 'Well, everyone knows that chimps are our closest relative, so why wouldn't the way they express their emotions be extremely similar to ours?' But people were surprised by that." © 2019 npr

Keyword: Emotions; Evolution
Link ID: 26054 - Posted: 03.20.2019

By Michelle Roberts Health editor, BBC News online Smoking potent 'skunk-like' cannabis increases your risk of serious mental illness, say researchers. They estimate around one in 10 new cases of psychosis may be associated with strong cannabis, based on their study of European cities and towns. In London and Amsterdam, where most of the cannabis that is sold is very strong, the risk could be much more, they say in The Lancet Psychiatry. Daily use of any cannabis also makes psychosis more likely, they found. Experts say people should be aware of the potential risks to health, even though the study is not definitive proof of harm. Lead researcher and psychiatrist Dr Marta Di Forti said: "If you decide to use high potency cannabis bear in mind there is this potential risk." Dr Adrian James from the Royal College of Psychiatrists said: "This is a good quality study and the results need to be taken seriously." People experiencing psychosis lose touch with reality, and may hear voices, see things that are not actually there or have delusional, confused thoughts. It is a recognised medical condition and different to getting high on a drug. There is disagreement as to what extent cannabis might cause or worsen mental health problems and many countries have gone ahead and legalised or decriminalised cannabis use. Doctors are concerned about the growing use of high potency cannabis that contains lots of the ingredient THC - the one that gives the high. Skunk-like cannabis with a THC content of 14% now makes up 94% of the drug sold on the streets of London, according to experts. © 2019 BBC

Keyword: Drug Abuse; Schizophrenia
Link ID: 26053 - Posted: 03.20.2019