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By CLYDE HABERMAN Scrambling for ways to contain America’s out-of-control opioid crisis, some experts in the field are convinced that one bit of good advice is to just say no to the enduring “just say no” antidrug message. Addiction, they say, is not a question of free will or a correctable character flaw, as a lot of people would like to believe. Rather, it is an affliction of the brain that needs to be treated as one would any chronic illness. One possible approach, an experimental vaccine, draws attention in this offering from Retro Report, a series of short video documentaries exploring major news stories of the past and their lasting impact. This vaccine would be intended principally for men and women already hooked on heroin or related opioids like Oxycodone and fentanyl — people who would be at risk of death should they detoxify and then relapse, as all too many do. If it works, the vaccine would stop opioids by effectively blocking them from reaching the brain by way of the circulatory system. At the same time, it would not interfere with other treatments for addicts, like methadone and buprenorphine, or with a compound like naloxone that reverses overdoses. The vaccine is designed to create high levels of antibodies, said Dr. Gary Matyas, an immunologist who has been developing it at the Walter Reed Army Institute of Research, in Silver Springs, Md. “You inject heroin, the antibodies basically grab all the heroin, bind it all up, and the heroin can’t cross the blood-brain barrier,” he told Retro Report. “And so there’s no high.” Presumably, in time, the heroin would be expelled from the body like any waste product. “It would be part of their therapy for recovering,” Dr. Matyas said of addicts. “If they mess up and take a dose of heroin, the heroin won’t work.” But will the vaccine itself work? It still must be tested on humans, and that is not a speedy process; it could take a decade or more, Dr. Matyas said, for there to be “a licensed product.” Among the questions are how large the dosages would have to be and how often they would need to be administered. Nonetheless, he is encouraged by the success he has had with lab mice and rats. © 2018 The New York Times Company
Keyword: Drug Abuse
Link ID: 24869 - Posted: 04.16.2018
Omega-3 fatty acid supplements taken orally proved no better than placebo at relieving symptoms or signs of dry eye, according to the findings of a well-controlled trial funded by the National Eye Institute (NEI), part of the National Institutes of Health. Dry eye disease occurs when the film that coats the eye no longer maintains a healthy ocular surface, which can lead to discomfort and visual impairment. The condition affects an estimated 14 percent of adults in the United States. The paper was published online April 13 in the New England Journal of Medicine. Annual sales of fish- and animal-derived supplements amount to more than a $1-billion market in the United States, according to the Nutrition Business Journal. Many formulations are sold over-the-counter, while others require a prescription or are available for purchase from a health care provider. “The trial provides the most reliable and generalizable evidence thus far on omega-3 supplementation for dry eye disease,” said Maryann Redford, D.D.S., M.P.H., program officer for clinical research at NEI. Despite insufficient evidence establishing the effectiveness of omega-3s, clinicians and their patients have been inclined to try the supplements for a variety of conditions with inflammatory components, including dry eye. “This well-controlled investigation conducted by the independently-led Dry Eye Assessment and Management (DREAM) Research Group shows that omega-3 supplements are no better than placebo for typical patients who suffer from dry eye.” The 27-center trial enrolled 535 participants with at least a six-month history of moderate to severe dry eye. Among them, 349 people were randomly assigned to receive 3 grams daily of fish-derived omega-3 fatty acids in five capsules.
Keyword: Vision
Link ID: 24868 - Posted: 04.16.2018
Merrit Kennedy What makes a group of animals genetically similar to each other? Traditionally, scientists have thought that animals living near each other are more likely to have things in common genetically. Another explanation is that animals living in similar environments — like high altitudes or hot temperatures — might evolve in similar ways. But loggerhead sea turtles appear to have broken that common wisdom. Their genetic similarities are closely linked to the magnetic field of the nesting area where they were born, according to new research from scientists at the University of North Carolina, Chapel Hill, published in Current Biology. And that magnetic imprinting is a better indicator of genetic similarity than that of groups of turtles that live near each other or in similar environments, says J. Roger Brothers, the lead author of the study. "A lot of different animals including sea turtles detect Earth's magnetic field and then derive navigational information from it and use it to find their way across or throughout long-distance migrations," Brothers says. Turtles likely "imprint" to the magnetic field of their nesting area at a very young age or even before they hatch. This acts like a kind of compass for them, he says, even as they leave the East Coast of the U.S. and travel hugely long distances, in some cases all the way to Africa. © 2018 npr
Keyword: Animal Migration
Link ID: 24867 - Posted: 04.14.2018
Jason Bittel In most North American hummingbirds, males court females by diving at them head on — but Costa’s hummingbirds (Calypte costae) perform their courtship dives off to the side. Researchers now find that this strategy allows the males to aim sounds at potential mates as if they were using a megaphone. During high-speed courtship dives, males fan their tails at the last second to create a high-pitched chirp. The faster the dive, the more those tail feathers vibrate and the higher the pitch created by the would-be Romeos. Researchers suspect that females prefer higher-pitched dives, which results in various strategies to boost the frequency of the noise a male makes. A study1 published on 12 April in Current Biology finds that male Costa’s hummingbirds can twist half of their tail feathers in the direction of the female, manipulating the volume and pitch of their chirps (see video). The researchers suspect that the targeted noise also masks audio cues that the females can use to judge how fast the males are diving. “You can think of the feather as being like a flashlight,” says Chris Clark, an ornithologist at the University of California, Riverside. “If you point the flashlight straight at something, the light is much brighter. And if you look at it from the side, at a 90-degree angle, there’s still some light but not nearly as much.” © 2018 Macmillan Publishers Limited
Keyword: Sexual Behavior; Evolution
Link ID: 24866 - Posted: 04.14.2018
By Robert F. Service Powerful chemical countermeasures could one day enter the battle against opioid addiction, which killed more than 42,000 people in the United States in 2016. Doctors and first responders already use medications to combat the effects of opioids, including the high and the slowed breathing of an overdose. But the new candidate drugs target the neural circuitry of addiction itself. A compound known as OV329 is the latest addition. In animal studies it quiets the brain's reward system, sharply reducing cravings and halting addicted animals' tendency to self-administer cocaine and other habit-forming drugs. Other drugs in the pipeline also target the reward system, albeit through a different mechanism. All raise hopes that doctors could soon have a new way to treat addiction, and not just to drugs and alcohol. The medicines could potentially also be used to fight food and gambling addictions. "It's a great unmet medical need," says Richard Silverman, a chemist at Northwestern University in Evanston, Illinois, who developed OV329. OV329 has now been picked up by Ovid Therapeutics in New York City, which is continuing animal studies and hopes to launch human trials of the would-be drug. "It's a very interesting compound and clearly very promising," says Andrea Hohmann, a neuroscientist at Indiana University in Bloomington who is not involved in the work. © 2018 American Association for the Advancement of Science.
Keyword: Drug Abuse
Link ID: 24865 - Posted: 04.13.2018
By Simon Makin Everyone has unwelcome thoughts from time to time. But such intrusions can signal serious psychiatric conditions—from “flashbacks” in post-traumatic stress disorder (PTSD) to obsessive negative thinking in depression to hallucinations in schizophrenia. “These are some of the most debilitating symptoms,” says neuroscientist Michael Anderson of the University of Cambridge. New research led by Anderson and neuroscientist Taylor Schmitz, now at McGill University, suggests these symptoms may all stem from a faulty brain mechanism responsible for blocking thoughts. Researchers studying this faculty usually focus on the prefrontal cortex (PFC), a control center that directs the activity of other brain regions. But Anderson and his colleagues noticed that conditions featuring intrusive thoughts—such as schizophrenia—often involve increased activity in the hippocampus, an important memory region. The severity of symptoms such as hallucinations also increases with this elevated activity. In the new study, Anderson and his team had healthy participants learn a series of word pairs. The subjects were presented with one word and had to either recall or suppress the associated one. When participants suppressed thoughts, brain scans detected increased activity in part of the PFC and reduced activity in the hippocampus. The findings, which were published last November in Nature Communications, are consistent with a brain circuit in which a “stop” command from the PFC suppresses hippocampus activity. © 2018 Scientific American
Keyword: Attention
Link ID: 24864 - Posted: 04.13.2018
By CEYLAN YEGINSU LONDON — Two decades after creating the clone Dolly the sheep and paving the way for new research into Parkinson’s, Dr. Ian Wilmut revealed on Wednesday that he has the disease himself. The 73-year-old professor, who lives in Scotland, announced on World Parkinson’s Day that he learned four months ago that he had the disease, and that he would participate in a major research program to test new types of treatments intended to slow the disease’s progression. “Initiatives of this kind are very effective not only because they bring more people together, but because they will include people with different experience and expertise,” Dr. Wilmut said in a statement. He was referring to the new Dundee-Edinburgh Parkinson’s Research Initiative, which aims to investigate the causes of the disease and to translate scientific discoveries into new therapies. “It was from such a rich seedbed that Dolly developed, and we can hope for similar benefits in this project,” he added. In 1996, Dr. Wilmut and a team of scientists at the Roslin Institute in Edinburgh cloned an adult sheep, resulting in the birth of Dolly. The achievement shocked researchers who had said it could not be done. But Dolly’s birth proved that cells from anywhere in the body could behave like a newly fertilized egg, an idea that transformed scientific thinking and encouraged researchers to find techniques to reprogram adult cells. The new research led to the discovery of induced pluripotent stem cells, or iPSCs, which hold great promise as a therapy for Parkinson’s because of their potential to repair damaged tissues, according to the Dundee-Edinburgh Parkinson’s Research Initiative. © 2018 The New York Times Company
Keyword: Parkinsons
Link ID: 24863 - Posted: 04.13.2018
In 2007, I spent the summer before my junior year of college removing little bits of brain from rats, growing them in tiny plastic dishes, and poring over the neurons in each one. For three months, I spent three or four hours a day, five or six days a week, in a small room, peering through a microscope and snapping photos of the brain cells. The room was pitch black, save for the green glow emitted by the neurons. I was looking to see whether a certain growth factor could protect the neurons from degenerating the way they do in patients with Parkinson's disease. This kind of work, which is common in neuroscience research, requires time and a borderline pathological attention to detail. Which is precisely why my PI trained me, a lowly undergrad, to do it—just as, decades earlier, someone had trained him. Now, researchers think they can train machines to do that grunt work. In a study described in the latest issue of the journal Cell, scientists led by Gladstone Institutes and UC San Francisco neuroscientist Steven Finkbeiner collaborated with researchers at Google to train a machine learning algorithm to analyze neuronal cells in culture. The researchers used a method called deep learning, the machine learning technique driving advancements not just at Google, but Amazon, Facebook, Microsoft. You know, the usual suspects. It relies on pattern recognition: Feed the system enough training data—whether it's pictures of animals, moves from expert players of the board game Go, or photographs of cultured brain cells—and it can learn to identify cats, trounce the world's best board-game players, or suss out the morphological features of neurons.
Keyword: Brain imaging; Learning & Memory
Link ID: 24862 - Posted: 04.13.2018
Sarah Boseley Health editor Drinking will shorten your life, according to a study that suggests every glass of wine or pint of beer over the daily recommended limit will cut half an hour from the expected lifespan of a 40-year-old. Those who think a glass of red wine every evening will help keep the heart healthy will be dismayed. The paper, published in the Lancet medical journal, says five standard 175ml glasses of wine or five pints a week is the upper safe limit – about 100g of alcohol, or 12.5 units in total. More than that raises the risk of stroke, fatal aneurysm (a ruptured artery in the chest), heart failure and death. The risks for a 40-year-old of drinking over the recommended daily limit were comparable to smoking, said one leading scientist. “Above two units a day, the death rates steadily climb,” said David Spiegelhalter, Winton professor for the public understanding of risk at the University of Cambridge. “The paper estimates a 40-year-old drinking four units a day above the guidelines [the equivalent of drinking three glasses of wine in a night] has roughly two years’ lower life expectancy, which is around a 20th of their remaining life. This works out at about an hour per day. So it’s as if each unit above guidelines is taking, on average, about 15 minutes of life, about the same as a cigarette. “Of course, it’s up to individuals whether they think this is worthwhile.” There is still a small benefit to drinking, which has been much flagged in the past. It does reduce the chance of a non-fatal heart attack. But, said Dr Angela Wood, from the University of Cambridge, lead author of the study, “this must be balanced against the higher risk associated with other serious – and potentially fatal – cardiovascular diseases.” © 2018 Guardian News and Media Limited
Keyword: Drug Abuse
Link ID: 24861 - Posted: 04.13.2018
By Alex Beard Deb Roy and Rupal Patel pulled into their driveway on a fine July day in 2005 with the beaming smiles and sleep-deprived glow common to all first-time parents. Pausing in the hallway of their Boston home for Grandpa to snap a photo, they chattered happily over the precious newborn son swaddled between them. This normal-looking suburban couple weren’t exactly like other parents. Roy was an AI and robotics expert at MIT, Patel an eminent speech and language specialist at nearby Northeastern University. For years, they had been planning to amass the most extensive home-video collection ever. From the ceiling in the hallway blinked two discreet black dots, each the size of a coin. Further dots were located over the open-plan living area and the dining room. There were 25 in total throughout the house – 14 microphones and 11 fish-eye cameras, part of a system primed to launch on their return from hospital, intended to record the newborn’s every move. It had begun a decade earlier in Canada – but in fact Roy had built his first robots when he was just was six years old, back in Winnipeg in the 1970s, and he’d never really stopped. As his interest turned into a career, he wondered about android brains. What would it take for the machines he made to think and talk? “I thought I could just read the literature on how kids do it, and that would give me a blueprint for building my language and learning robots,” Roy told me. Over dinner one night, he boasted to Patel, who was then completing her PhD in human speech pathology, that he had already created a robot that was learning the same way kids learn. He was convinced that if it got the sort of input children get, the robot could learn from it. © 2018 Guardian News and Media Limited
Keyword: Development of the Brain; Learning & Memory
Link ID: 24860 - Posted: 04.12.2018
By Lydia Denworth The demands of parenthood are so considerable that it’s fair to wonder why any adult takes on the challenge. Mammalian babies are especially helpless—and among mammals, only humans can see beyond individual sacrifice to understand a species’s survival depends on caring for its young. Yet there is remarkable consistency in the way all mammals change their behavior upon becoming parents. Suddenly they are motivated to care for their young, and know how to feed and shelter, nurture and protect new babies. Parents also give up a lot of adult social interaction, whether it is mating with other mice or going barhopping with friends. “What this means is that there is this instinctive or genetically programmed aspect to the drive to take care of offspring,” says neuroscientist Catherine Dulac of Harvard University. But if a complicated and variable behavior like parenting is hardwired, how would that work? Reporting in Nature this week, Dulac, also a Howard Hughes Medical Institute investigator, and her colleagues have provided a wiring diagram of the brain-wide circuit that coordinates parenting behavior in mice. The study marks the first deconstruction of the architecture of a brain circuit underlying a complex social behavior. The circuit they describe resembles the hub-and-spoke flight-routing system used by airlines and relies on a type of neuron that expresses the signaling molecule galanin. A relatively small number of these galanin neurons form a parenting command center—the medial preoptic area (MPOA)—in the hypothalamus, a brain structure responsible for controlling everything from appetite to sex drive. Responding to sensory input received from all over the brain, the neurons at the hub send distinct messages to at least 20 downstream subsets of galanin neurons. Like an airport terminal serving passengers according to their destinations, these subsets of cells, which the researchers dub “pools,” handle different facets of parenting behavior such as motor control of grooming or the motivation to parent at all. © 2018 Scientific American
Keyword: Sexual Behavior
Link ID: 24859 - Posted: 04.12.2018
By Anna Azvolinsky In recent years, scientists have accomplished what previously was saved for miracle workers: they have given blind patients the ability to see better. In 2017, the vision field saw an enormous advance with the approval Luxturna, the first gene therapy to correct vision loss in certain patients with childhood onset blindness. And just last week, researchers reported that a retinal implant allowed a 69-year-old woman with macular degeneration to more than double the number of letters she could identify on a vision chart. “It’s early data but very promising, including one patient with impressive vision gains, for a disease where we don’t have any treatment options,” says Thomas Albini of the University of Miami’s Bascom Palmer Eye Institute who was not involved in the study. The implant, given to five patients with dry age-related macular degeneration (AMD), is a single sheet of retinal pigment epithelial (RPE) cells derived from human embryonic stem cells. Other teams across the globe are inventing their own form of RPE implants, and this type of approach is just one of a plethora of modalities being tested to either slow down or reverse various forms of blindness. © 1986-2018 The Scientist
Keyword: Vision
Link ID: 24858 - Posted: 04.12.2018
Phil Plait I've said this before and I will no doubt say it many times hence: I love optical illusions. For one thing, they're just fun. They warp our sense of reality, and it's really pretty cool to see how easy it is to fool our senses. Some illusions do this in complicated ways that make it hard to understand where our perception goes wrong (and yes, there are entire fields of psychology devoted to figuring out how our brain and eyes physically react to illusions). But others are surprisingly simple, yet are deeply difficult to not see. One of the best is the Müller-Lyer illusion, and the easiest way to describe it is to just show it to you: The two horizontal lines are the same length, but the lower one looks longer thanks to the Müller-Lyer illusion. The two horizontal lines are the same length, but the lower one looks longer thanks to the Müller-Lyer illusion. Despite what your eyes are telling you, those two horizontal lines are the same size! Measure them if you don't believe me. It's an utterly convincing illusion, but an illusion all the same. But still, it's simple, right? Well, visual artist Gianni Sarcone decided to play with this illusion, and created an animated version of it that is simply stunning.
Keyword: Vision
Link ID: 24857 - Posted: 04.12.2018
by Robby Berman She was wide awake and it was nearly two in the morning. When asked if everything was alright, she said, “Yes.” Asked why she couldn’t get to sleep she said, “I don’t know.” Neuroscientist Russell Foster of Oxford might suggest she was exhibiting “a throwback to the bi-modal sleep pattern." Research suggests we used to sleep in two segments with a period of wakefulness in-between. A. Roger Ekirch, historian at Virginia Tech, uncovered our segmented sleep history in his 2005 book At Day’s Close: A Night in Time’s Past. There’s very little direct scientific research on sleep done before the 20th century, so Ekirch spent years going through early literature, court records, diaries, and medical records to find out how we slumbered. He found over 500 references to first and second sleep going all the way back to Homer’s Odyssey. “It’s not just the number of references—it is the way they refer to it as if it was common knowledge,” Ekirch tells BBC. "He knew this, even in the horror with which he started from his first sleep, and threw up the window to dispel it by the presence of some object, beyond the room, which had not been, as it were, the witness of his dream." — Charles Dickens, Barnaby Rudge (1840) Here’s a suggestion for dealing with depression from English ballad 'Old Robin of Portingale': "And at the wakening of your first sleepe/You shall have a hott drinke made/And at the wakening of your next sleepe/Your sorrowes will have a slake." Two-part sleep was practiced into the 20th century by people in Central America and Brazil and is still practiced in areas of Nigeria. © Copyright 2007-2018 & BIG THINK
Keyword: Sleep
Link ID: 24856 - Posted: 04.12.2018
By Kerry Grens A variant in the gene for a certain hormone is tied to people eating more carbs. Yet a new study of 451,000 people finds that the allele doesn’t universally mean poorer health. Researchers reported yesterday (April 10) in Cell Reports that those with the sweet-tooth variant actually have lower body fat than others, and no higher risk for type 2 diabetes. They did, however, find a link between the allele and high blood pressure and a thicker waistline. “This goes against the current perception that eating sugar is bad for health. It may reduce body fat because the same allele also results in a lower consumption of protein and fat in the diet,” study coauthor Timothy Frayling, a molecular geneticist at the University of Exeter Medical School in the U.K., says in a press release. “But whilst this version of the gene lowers body fat, it also redistributes fat to the upper body, where it’s more likely to cause harm, including higher blood pressure.” The gene of interest here is FGF21, which encodes fibroblast growth factor 21, a hormone involved in alcohol and sugar consumption and insulin sensitization. The authors note that it’s a target of weight loss interventions. People with a particular allele of FGF21—20 percent of Europeans are homozygous for the variant—tend to consume relatively more sugar and alcohol than those without the allele. To see what consequences this might have on people’s health, Frayling and his colleagues collected data on 451,000 people whose genetic and health information is part of the UK Biobank. © 1986-2018 The Scientist
Keyword: Obesity; Genes & Behavior
Link ID: 24855 - Posted: 04.12.2018
By NICHOLAS BAKALAR Morning people may live longer than night owls, a new study suggests. Researchers studied 433,268 people, aged 38 to 73, who defined themselves as either “definite morning” types, “moderate morning” types, “moderate evening” types or “definite evening” types. They followed their health for an average of six-and-a-half years, tracking cause of death with death certificates. The study is in Chronobiology International. After controlling for age and sex, smoking, body mass index, sleep duration and other variables, they found that compared with “definite morning” types, “definite evening” types had a 10 percent increased risk of dying from any cause. Each increase from “morningness” to “eveningness” was associated with an increased risk for disease. Night owls were nearly twice as likely as early risers to have a psychological disorder and 30 percent more likely to have diabetes. Their risk for respiratory disease was 23 percent higher and for gastrointestinal disease 22 percent higher. The lead author, Kristen L. Knutson, an associate professor of neurology at Northwestern University, said that while being a night owl is partly genetic, people can make adjustments — gradually making bedtime earlier, avoiding using smartphones before bed, and eventually moving themselves out of the “night owl zone.” Although the reasons for their increased mortality remain unclear, she said, “Night owls should know that there may be some health consequences.” © 2018 The New York Times Company
Keyword: Biological Rhythms
Link ID: 24854 - Posted: 04.12.2018
By HEATHER MURPHY A battle over pleasure has broken out. On Twitter and in the pages of scientific journals, psychologists, neurologists and neuroscientists are forging alliances over the question of whether pleasure we get from art is somehow different from the pleasure we get from candy, sex or drugs. The debate was ignited by an opinion piece titled “Pleasure Junkies All Around!” published last year in the journal Proceedings of the Royal Society B. In it, Julia F. Christensen, a neuroscientist at the The Warburg Institute at the University of London who studies people’s responses to dance choreography, argued that many of us have been turned into “mindless pleasure junkies, handing over our free will for the next dopamine shoot” provided by social media, pornography and sugar. She offered up an unconventional solution: art, which she says engages us in ways these other pleasures do not and can “help overwrite the detrimental effects of dysfunctional urges and craving.” The paper struck a nerve with some of her fellow art and pleasure researchers, who published a rebuttal last month in the same journal. The idea that the way that art engages the brain is somehow special has been around for far too long and it is time to kill it off once and for all, they insist. “Christensen has recently argued that the pleasure induced by art is different to the pleasure induced by food, sex, sports, or drugs. Her argument, however, is contradicted by plenty of evidence showing that the pleasure from art is no different in genesis and function to the pleasure induced by food, drugs, and sex,” wrote Marcos Nadal, a psychologist at the University of the Balearic Islands who studies people’s responses to curvilinear lines in architecture and art, and Martin Skov, a neuroscientist at the Danish Research Centre for Magnetic Resonance, who studies decision-making. Their comment spurred others to rally to Dr. Christensen’s defense. The arguments over Dr. Christensen’s paper pointed to disputes within the emerging field of neuroaesthetics, or the study of the neural processes underlying our appreciation and the production of beautiful objects and artworks: © 2018 The New York Times Company
Keyword: Drug Abuse; Attention
Link ID: 24853 - Posted: 04.11.2018
Jason Murugesu We all daydream, whether about marrying Rihanna, discovering a sudden ability to sing opera or never having to answer another email again. Yet it is only in the last few decades that the science behind daydreaming, or mind-wandering as it is termed in most academic literature, has transitioned from the realms of pseudoscience to the cutting edge of cognitive neuroscience. At its most basic, daydreaming is your mind wandering from the here and now. Traditionally, daydreaming was considered to be a single psychological state of mind. This, however, caused conflict in academic literature, and the resulting confusion is the reason why you might read that daydreaming is linked to happiness in one paper, but to depression in the next. Different types of mind-wandering have been conflated. Using neuroimaging techniques, a study conducted last year by the University of York found that different types of daydreams – for example, those which are fantastical, autobiographical, future orientated or past oriented – were built up of different neuronal activation patterns, and by virtue could not be considered a single psychological construct. Nevertheless, if we consider all these types of mind-wandering together, you would be surprised about how much of our waking time we spend daydreaming. In 2008, Professor Matthew Killingsworth, then at Harvard University, used an app that contacted a large group of people at random points of the day to find out how often they were daydreaming. The app would ask its users what they were doing, and whether they were thinking about something else entirely. They found that 46.9 per cent of the time, the user was mind-wandering.
Keyword: Attention
Link ID: 24852 - Posted: 04.11.2018
By Gary Stix Self-help books often extoll the value of resilience. Last year one such primer—Bounce: Overcoming Adversity, Building Resilience and Finding Joy—proclaimed: “By strengthening your inner power, your ability to handle stressful situations and your skill in persevering after setbacks threaten to fell you, you’ll develop real resilience—you’ll develop grit.” This implies weathering adverse life events is a character trait to be cultivated. Exercising, eating right and giving yourself mental pep talks certainly may help. But neuroscientists are learning the story is not quite so simple, and that some people are likely better equipped from birth to deal with adversity. During the last 15 years discoveries about why some brains excel at resisting stress have initiated a search for new drugs to treat depression and post-traumatic stress disorder by enhancing psychological resilience. One of these compounds has now entered early-stage clinical trials. If the drug is safe and works, it will undoubtedly encounter strong demand; depression—the world’s leading cause of mental disability—never enters full remission in more than half the patients treated with psychotherapies and existing antidepressants. But depression does not affect everyone, and the molecular biology of resilience for psychiatric disorders can be clearly seen by inspecting the brains of lab animals. About a third of mice exposed to severe stress (in the form of aggressive attacks by other rodents) seem to breeze through these assaults without developing the social withdrawal, listlessness or other depression and traumalike symptoms displayed by most of their rodent lab-mates. © 2018 Scientific America
Keyword: Depression
Link ID: 24851 - Posted: 04.11.2018
By Ashley Yeager Mothers who take selective serotonin reuptake inhibitors (SSRIs), a class of commonly used antidepressants, while pregnant have babies with distinct structural changes to their brains, researchers report today (April 9) in JAMA Pediatrics. MRI scans of the babies’ brains revealed exposure to the drugs in the womb increased the volumes of the babies’ amygdalae and insular cortices—regions that play a role in processing emotions. “Hopefully these results highlight the fact that something could be going on here,” study coauthor Claudia Lugo-Candelas, a postdoctoral research fellow at Columbia University tells Time. “They point to the fact that there is a signal—we don’t know what it means, or don’t know how long it might last. But we know it’s worth studying.” The number of women using SSRIs while pregnant is increasing, but not much is known about how the medication might affect the brains of developing babies. Studies in animals suggest exposure to SSRIs can change the offspring’s brain circuitry and lead to depressive-like behaviors and anxiety later in life. In the new study, Lugo-Candelas and her colleagues studied the brains of 98 human infants, 16 babies whose mothers were treated for depression with SSRIs during pregnancy, 21 mothers with depression but not treated, and 61 mothers with no history of depression. © 1986-2018 The Scientist
Keyword: Depression; Development of the Brain
Link ID: 24850 - Posted: 04.11.2018


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