By Nathaniel Scharping | Don’t get a big head, your mother may have told you. That’s good advice, but it comes too late for most of us. Humans have had big heads, relatively speaking, for hundreds of thousands of years, much to our mothers’ dismay. Our oversize noggins are a literal pain during childbirth. Babies have to twist and turn as they exit the birth canal, sometimes leading to complications that necessitate surgery. And while big heads can be painful for the mother, they can downright transformative for babies: A fetus’ pliable skull deforms during birth like putty squeezed through a tube to allow it to pass into the world. This cranial deformation has been known about for a long time, but in a new study, scientists from France and the U.S. actually watched it happen using an MRI machine during labor. The images, published in a study in PLOS One, show how the skulls (and brains) of seven infants squished and warped during birth to pass through the birth canal. They also shine new light on how much our skulls change shape as we’re born. The researchers recruited pregnant women in France to undergo an MRI a few weeks before pregnancy and another in the minutes before they began to actually give birth. In total, seven women were scanned in the second stage of labor, when the baby begins to make its way out of the uterus. They were then rushed to the maternity ward to actually complete giving birth.

Keyword: Development of the Brain; Brain imaging
Link ID: 26252 - Posted: 05.20.2019

Before he was born, his parents knew their boy was in trouble. That was clear from what their doctors' saw in their baby's ultrasound. And tragically, the boy died when he was only ten months old. But in his short life, he left behind a valuable legacy by helping scientists understand a crucial type of brain cell. That's because — as it turned out — the child had none. "One of the things about being a pediatric geneticist is on any given day you can see a patient you could spend the rest of your life or your career thinking about," Dr. James Bennett told Quirks & Quarks host Bob McDonald. Dr. Bennett is a physician and researcher from Seattle Children's Hospital and assistant professor of pediatric genetics at the University of Washington. Devastating problems with brain development On the first day he met the child — the boy's very first day of life — Dr. Bennett said he could tell this baby needed a lot of support. The baby was having difficulty breathing, had an enlarged head as well as some very significant abnormalities of his brain. "Every single part of his brain was affected. There was no connection between the left side and the right side of his brain. And there was too much fluid on the brain — that the spaces that hold fluid around the brain were enlarged. And the white matter, which is the part of the brain that sort of connects the neurons — you can think of it as sort of the wires connecting things in the brain — was decreased and abnormal," said Dr. Bennett. Scientists had never seen a medical mystery like this before, so Dr. Bennett was determined to figure out what was wrong with the infant. He he undertook a "diagnostic odyssey" to identify the cause of this extremely rare condition. ©2019 CBC/Radio-Canada

Keyword: Development of the Brain; Glia
Link ID: 26251 - Posted: 05.20.2019

By John Horgan In a previous post I summarized my remarks at “Souls or Selfish Genes,” a conversation at Stevens Institute of Technology about religious versus scientific views of humanity. I represented the agnostic position and David Lahti, a biologist and philosopher at the City University of New York, a position more friendly to theism. Below is Lahti’s summary of his opening comments. –John Horgan I’ve been asked to deal with the question of “Souls vs. Selfish Genes”. And whereas I am sure this is a false dichotomy, I’m not quite sure how exactly to fit the two parts of the truth together. But I’ll give you a few thoughts I’ve had about it, which can at least start us off. First, selfish genes. This of course is a reference to Richard Dawkins’ 1976 book of the same name, which is a popular and sensational description of a revolution in our understanding of the way evolution by natural selection operates. Briefly, we discovered in the 1960s-70s that the organismic individual was generally the most important level at which natural selection operates, meaning that evolution by natural selection proceeds primarily via certain individuals in a population reproducing more successfully than others. In fact, this is too simplistic. Hamilton’s theory of kin selection showed that it’s actually below the level of the individual where we really have to concentrate in order to explain certain traits, such as the self-sacrificial stinging of bees and the fact that some young male birds help their mother raise her next brood instead of looking for a mate. Those individuals are not being as selfish as we might predict. © 2019 Scientific American

Keyword: Consciousness; Genes & Behavior
Link ID: 26250 - Posted: 05.20.2019

Jon Hamilton When Sterling Witt was a teenager in Missouri, he was diagnosed with scoliosis. Before long, the curvature of his spine started causing chronic pain. It was "this low-grade kind of menacing pain that ran through my spine and mostly my lower back and my upper right shoulder blade and then even into my neck a little bit," Witt says. The pain was bad. But the feeling of helplessness it produced in him was even worse. "I felt like I was being attacked by this invisible enemy," Witt says. "It was nothing that I asked for, and I didn't even know how to battle it." So he channeled his frustration into music and art that depicted his pain. It was "a way I could express myself," he says. "It was liberating." Witt's experience is typical of how an unpleasant sensation can become something much more complicated, scientists say. "At its core, pain is just something that hurts or makes you say ouch," says Karen Davis, a senior scientist at the Krembil Brain Institute in Toronto. "Everything else is the outcome of the pain, how it then impacts your emotions, your feelings, your behaviors." The ouch part of pain begins when something — heat, certain chemicals or a mechanical force — activates special nerve endings called nociceptors. © 2019 npr

Keyword: Pain & Touch
Link ID: 26249 - Posted: 05.20.2019

By Neuroskeptic | A paper in PNAS got some attention on Twitter recently. It’s called Childhood trauma history is linked to abnormal brain connectivity in major depression and in it, the authors Yu et al. report finding (as per the Significance Statement) A dramatic primary association of brain resting-state network (RSN) connectivity abnormalities with a history of childhood trauma in major depressive disorder (MDD). The authors go on to note that even though “the brain imaging took place decades after trauma occurrence, the scar of prior trauma was evident in functional dysconnectivity.” Now, I think that this talk of dramatic scarring is overblown, but in this case there’s also a wider issue with the use of a statistical method which easily lends itself to misleading interpretations – canonical correlation analysis (CCA). First, we’ll look at what Yu et al. did. In a sample of 189 unmedicated patients with depression, Yu et al. measured the resting-state functional connectivity of the brain using fMRI. They then analyzed this to give a total of 55 connection strengths for each individual. Each of these 55 measures reflects the functional coupling between two brain networks. For each patient, Yu et al. also administered questionnaires measuring personality, depression and anxiety symptoms, and history of trauma. These measures were then compressed into 4 clinical clusters, (i) anxious misery (ii) positive traits (iii) physical and emotional neglect or abuse, and (iv) sexual abuse.

Keyword: Depression; Development of the Brain
Link ID: 26248 - Posted: 05.20.2019

Hannah Devlin Science correspondent A mind-controlled hearing aid that allows the wearer to focus on particular voices has been created by scientists, who say it could transform the ability of those with hearing impairments to cope with noisy environments. The device mimics the brain’s natural ability to single out and amplify one voice against background conversation. Until now, even the most advanced hearing aids work by boosting all voices at once, which can be experienced as a cacophony of sound for the wearer, especially in crowded environments. Nima Mesgarani, who led the latest advance at Columbia University in New York, said: “The brain area that processes sound is extraordinarily sensitive and powerful. It can amplify one voice over others, seemingly effortlessly, while today’s hearing aids still pale in comparison.” This can severely hinder a wearer’s ability to join in conversations, making busy social occasions particularly challenging. Scientists have been working for years to resolve this problem, known as the cocktail party effect. The brain-controlled hearing aid appears to have cracked the problem using a combination of artificial intelligence and sensors designed to monitor the listener’s brain activity. The hearing aid first uses an algorithm to automatically separate the voices of multiple speakers. It then compares these audio tracks to the brain activity of the listener. Previous work by Mesgarani’s lab found that it is possible to identify which person someone is paying attention to, as their brain activity tracks the sound waves of that voice most closely. © 2019 Guardian News & Media Limited

Keyword: Hearing
Link ID: 26247 - Posted: 05.18.2019

By Dhruti Shah BBC News When Dani Donovan wanted to show her colleagues what life was like for her as someone diagnosed with Attention Deficit Hyperactivity Disorder (ADHD), she never thought her sketches would lead to a series of web comics with a celebrity fan base. The 28-year-old, who lives in Omaha, Nebraska, was diagnosed about a decade ago with ADHD and now hopes her comics will help others to understand the challenges for those with the condition. She told the BBC: "I'd just started a new job working in data visualisation, and it was the first time I was able to be really open about having ADHD and talk to my colleagues about what it's like. "We were telling stories and joking about how I always get off track while I'm telling stories, and I said that it's very much like having a sleepy train conductor running my train of thought. I had the idea for a flowchart, I posted it on Twitter and it took off immediately." Her graphic shows that when she hears non-ADHD storytelling, it involves a straight move from the start of a story to the end. Her storytelling, however, involves a pre-story prologue before moving to the start of the story, and then wandering through 'too many details', a side-story and losing her train of thought before reaching the end of the tale - and then apologising. However, as with all things that hit the internet - once it's let loose, be careful of memes and amendments. Dani's diagram was re-versioned by an unknown person who split the flowcharts and created a meme with 'How a normal person tells a story' taking the place of the 'Non-ADHD Storytelling' heading Dani had given her first flowchart, and 'How I tell a story' replacing the 'ADHD Storytelling' heading for the meandering flowchart. © 2019 BBC

Keyword: ADHD
Link ID: 26246 - Posted: 05.18.2019

Ruth Williams Sequencing the nuclear RNA of more than 100,000 individual postmortem brain cells from people with and without autism spectrum disorder indicates the types of genes dysregulated in the condition and the types of cells in which such dysregulation occurs. The results, reported in Science today (May 16), help narrow the focus of future ASD studies to the most likely molecular and cellular anomalies, say researchers. “It’s using the latest technology, it’s looking at the single cell level, and it validates and extends previous observations,” says autism researcher Daniel Geschwind of the University of California, Los Angeles, who was not involved in the research. “It takes the previous work and brings it to a level of resolution that we didn’t have before.” “This was an experiment that needed to be done,” adds geneticist Stephan Sanders of the University of California, San Francisco, writing in an email to The Scientist. “At the tissue level, it broadly replicates previous data in autism. Then, [it] provides a first look at which cell types are responsible for the differences.” ASD, which currently affects somewhere around 1 in 60 children in the United States, includes a broad range of conditions that are characterized by an impaired ability to communicate and interact socially. The heterogeneous nature of ASD has made studies of its molecular pathology difficult. Nevertheless, gene expression studies carried out on postmortem brain tissue from ASD patients have pointed to commonly affected pathways, including synapse function, says Dmitry Velmeshev, an author of the study and postdoc in the lab of neurologist Arnold Kriegstein, also an author. © 1986–2019 The Scientist

Keyword: Autism
Link ID: 26245 - Posted: 05.18.2019

By DAN HURLEY MAY 15, 2019 The piercing, high-pitched noises were first heard by a couple of recently arrived United States Embassy officials in Havana in late 2016, soon after Donald Trump was elected president. They heard the noises in their homes, in the city’s leafy western suburbs. If they moved to a different room, or walked outside, the noise stopped. The two officials said they believed that the sound was man-made, a form of harassment. Around the same time, they began to develop a variety of symptoms: headaches, fatigue, dizziness, mental fog, hearing loss, nausea. On Dec. 30, 2016, the Embassy’s chargé d’affaires, Jeffrey DeLaurentis, and his security chief, Anthony Spotti, were told what the men were experiencing. By then, a third Embassy worker who lived nearby also heard the sounds and began developing symptoms. DeLaurentis eventually sent the three for evaluation by an otolaryngologist at the University of Miami, who told them they had damage to their inner ears’ vestibular organs. Similar reports of sickness after hearing noises began trickling in from other diplomats in Havana. One of them, a foreign-service officer, told me he was awakened one morning in March by a screeching noise. “It paralyzed me,” he said. “When the sound occurred, I could not move. I couldn’t get up until it stopped.” In the days that followed, he felt extreme fatigue, heard a ringing in his ears, found himself making many mistakes at work and became sensitive to loud sounds and bright light. That month, DeLaurentis called a meeting of his senior staff to tell them what was going on. He insisted that they tell no one else — not even their families — which had the perverse effect of heightening the staff members’ anxiety rather than calming it. Within days, DeLaurentis felt compelled to call an open meeting of the American staff. More than 60 people crammed into the Embassy’s Sensitive Compartmented Information Facility — an inner sanctum for confidential communications. They were told about the noises and the symptoms and were offered the opportunity to be tested if they had concerns. Nearly all of those present, as well as some family members, soon asked to be evaluated.

Keyword: Emotions
Link ID: 26244 - Posted: 05.17.2019

By Jessica Wright, Clinicians can reliably diagnose autism in some toddlers roughly two years earlier than the typical age of diagnosis, a new study suggests. The researchers assessed more than 1,200 toddlers for autism at least twice using standard diagnostic tools. They diagnosed roughly one in three with the condition by age 2; 84 percent of these toddlers retained the label at their last visit, which was at age 3 on average. The finding suggests clinicians should take autism traits in toddlers seriously, says co-lead researcher Karen Pierce, professor of neurosciences at the University of California, San Diego. “If children meet criteria and they do show signs and symptoms, don’t wait; let’s get them the help and the treatment that they need,” Pierce says. Experts are divided on whether autism can reliably be diagnosed before age 3. The American Academy of Pediatrics recommends screening for autism starting at 18 months. However, the U.S. Preventive Services Task Force—a government panel that makes recommendations about preventive medicine—has said there is insufficient evidence to recommend universal screening before 3. The new study suggests that early screening and diagnosis may benefit some proportion of children: It indicates that some toddlers are likely to have clear enough signs of autism to warrant a diagnosis before 2 years of age, says Zachary Warren, associate professor of pediatrics, psychiatry and behavioral sciences at Vanderbilt University in Nashville, Tennessee. “The study shows that well-trained, expert teams evaluating young kids with autism are able to pick up concerns at fairly young ages for some kids,” says Warren, who was not involved in the work. “It’s an interesting and creative approach to understanding screening and diagnosis.” © 2019 Scientific American

Keyword: Autism
Link ID: 26243 - Posted: 05.17.2019

By Gina Kolata At least six million obese teenagers in the United States are candidates for weight-loss surgery, experts estimate. Fewer than 1,000 of them get it each year. Many of these adolescents already have complications of obesity, like diabetes or high blood pressure. But doctors have been uncertain just how well surgery works for young patients, and whether they can handle the consequences, including a severely restricted diet. A new study provides some hopeful answers. Researchers followed 161 teenagers aged 13 to 19, and 396 adults aged 25 to 50, for five years after weight-loss surgery. The teenagers actually fared better than the adults. The adolescents lost at least as much weight, and were more likely to see high blood pressure and diabetes ease or go away, the investigators reported on Wednesday in the New England Journal of Medicine. “This really changes the game,” said Dr. Amir Ghaferi, a bariatric surgeon at the University of Michigan, who was not involved in the research. The paper, he said, added to evidence that obesity, like cancer, is best treated early, before long-term damage from related conditions, such as high blood pressure and diabetes, sets in. To have the surgery, teenagers in the study had to meet the same criteria as adults: a body mass index of at least 35 — for instance, a person who is 5 feet 2 inches tall and weighs 192 pounds or more — and obesity-related health problems. Alternately, the adolescents could have a B.M.I. of at least 40 — such as a person who is 5 feet 2 inches tall and weighs at least 220 pounds — without other conditions linked to obesity. There is no exact data on the number of teenagers who meet those criteria in the United States, said Dr. Thomas Inge, chief of pediatric surgery at Children’s Hospital Colorado and lead author of the new study. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26242 - Posted: 05.17.2019

Aimee Cunningham Nutrition advice can be confusing. Studies that bolster the health benefits of a food or nutrient seem inevitably to be followed by other work undercutting the good news. One reason for the muddle is that nutrition studies sometimes depend on people’s self-reporting of past meals. And because people may forget or even lie about what they’ve been consuming, that data can be flawed, creating conflicting reports about what’s healthy and what’s not, research has shown. But even if people had a photographic memory of all of their meals, that alone wouldn’t provide enough information. How bodies react to and process food can vary widely from person to person and be dependent on genes, the microbes that live inside the gut, a person’s current health, what the food contains or even how it was made (SN: 1/9/16, p. 8). “The problem is that nutrition research is rocket science,” says David Ludwig, a pediatric endocrinologist at Boston Children’s Hospital. “There are potentially thousands of different nutrients and factors in food that could influence our biology or our senses as we eat. Those can interact in unpredictable and complicated ways.” Given the complexity that comes with researching diet, one approach is to study people in a controlled environment, so that researchers know exactly what the participants are eating. A study that tied eating highly processed foods to weight gain, published online May 16 in Cell Metabolism, did just that. Here’s what the researchers learned — and what they still can’t answer. © Society for Science & the Public 2000 - 2019

Keyword: Obesity
Link ID: 26241 - Posted: 05.17.2019

By Kim Tingley Humans have been drinking fermented concoctions since the beginning of recorded time. But despite that long relationship with alcohol, we still don’t know what exactly the molecule does to our brains to create a feeling of intoxication. Likewise, though the health harms of heavy drinking are fairly obvious, scientists have struggled to identify what negative impacts lesser volumes may lead to. Last September, the prestigious peer-reviewed British medical journal The Lancet published a study that is thought to be the most comprehensive global analysis of the risks of alcohol consumption. Its conclusion, which the media widely reported, sounded unequivocal: “The safest level of drinking is none.” Sorting through the latest research on how to optimize your well-being is a constant and confounding feature of modern life. A scientific study becomes a press release becomes a news alert, shedding context at each stage. Often, it’s a steady stream of resulting headlines that seem to contradict one another, which makes it easy to justify ignoring them. “There’s so much information on chocolate, coffee, alcohol,” says Nicholas Steneck, a former consultant to the Office of Research Integrity for the U.S. Department of Health and Human Services. “You basically believe what you want to believe unless people are dropping dead all over the place.” Scientific studies are written primarily for other scientists. But to make informed decisions, members of the general public have to engage with them, too. Does our current method of doing so — study by study, conclusion by conclusion — make us more informed as readers or simply more mistrustful? As Steneck asks: “If we turn our back on all research results, how do we make decisions? How do you know what research to trust?” It’s a question this new monthly column aims to explore: What can, and can’t, studies tell us when it comes to our health? © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26240 - Posted: 05.17.2019

Bruce Bower People and Neandertals separated from a common ancestor more than 800,000 years ago — much earlier than many researchers had thought. That conclusion, published online May 15 in Science Advances, stems from an analysis of early fossilized Neandertal teeth found at a Spanish site called Sima de los Huesos. During hominid evolution, tooth crowns changed in size and shape at a steady rate, says Aida Gómez-Robles, a paleoanthropologist at University College London. The Neandertal teeth, which date to around 430,000 years ago, could have evolved their distinctive shapes at a pace typical of other hominids only if Neandertals originated between 800,000 and 1.2 million years ago, she finds. Gómez-Robles’ study indicates that, if a common ancestor of present-day humans and Neandertals existed after around 1 million years ago, “there wasn’t enough time for Neandertal teeth to change at the rate [teeth] do in other parts of the human family tree” in order to end up looking like the Spanish finds, says palaeoanthropologist Bernard Wood of George Washington University in Washington, D.C. Many researchers have presumed that a species dubbed Homo heidelbergensis, thought to have inhabited Africa and Europe, originated around 700,000 years ago and gave rise to an ancestor of both Neandertals and Homo sapiens by roughly 400,000 years ago. Genetic evidence that Sima de los Huesos fossils came from Neandertals raised suspicions that a common ancestor with H. sapiens existed well before that (SN Online: 3/14/16). Recent Neandertal DNA studies place that common ancestor at between 550,000 and 765,000 years old. But those results rest on contested estimates of how fast and how consistently genetic changes accumulated over time. |© Society for Science & the Public 2000 - 2019.

Keyword: Evolution
Link ID: 26239 - Posted: 05.17.2019

By LUKE DITTRICH On Valentine’s Day, 2018, five months after Hurricane Maria made landfall, Daniel Phillips stood at the edge of a denuded forest on the eastern half of a 38-acre island known as Cayo Santiago, a clipboard in his hand, his eyes on the monkeys. The island sits about a half-mile off the southeast coast of Puerto Rico, near a village called Punta Santiago. Phillips and his co-workers left the mainland shortly after dawn, and the monkeys had already begun to gather by the time they arrived, their screams and oddly birdlike chirps louder than the low rumble of the motorboat that ferried the humans. The monkeys were everywhere. Some were drinking from a large pool of stagnant rainwater; some were grooming each other, nit-picking; some were still gnawing on the plum-size pellets of chow that Phillips hurled into the crowd a half-hour before. Two sat on the naked branch of a tree, sporadically mating. They were all rhesus macaques, a species that grows to a maximum height of about two and a half feet and a weight of about 30 pounds. They have long, flexible tails; dark, expressive eyes; and fur ranging from blond to dark brown. Phillips’s notebook was full of empty tables. There were places for the monkeys’ ID numbers, which were tattooed on their chests and inner thighs, places for a description of their behavior, places for the time of day. There was a place for his own name, too, and he wrote it at the top of each page. Daniel Phillips is not a Puerto Rican name, whatever that means, but he was born here, in a big hospital in Fajardo. He arrived more than a month early and spent his first weeks in an incubator, but grew up to be a high school and college wrestler; as a biology major, he became interested in monkeys, and was invited by a primatologist from Duke University to take a job as a research assistant here on Cayo Santiago.

Keyword: Stress
Link ID: 26238 - Posted: 05.15.2019

By Simon Makin Something in elderly blood is bad for brains. Plasma from old mice or humans worsens cognition and biological indicators of brain health, when infused into young mice. Conversely, plasma from young mice (or humans) rejuvenates old brains. Much of this research has come from neurobiologist Tony Wyss-Coray’s group at Stanford University, which is pursuing what constituents of blood might be responsible. One previous study identified a protein, which declines with age, that has powerful beneficial effects. That protein can cross from the blood into the brain, but Wyss-Coray wondered how certain molecules contained in blood typically “talk” to the brain. Must they interact with brain cells directly, or can they communicate indirectly, through the gateway to the brain, the blood-brain barrier? To investigate, Wyss-Coray’s team tried a new approach in their latest study, published May 13 in Nature Medicine. “We reasoned that the most obvious way plasma would interact with the brain is through blood vessels,” Wyss-Coray says. “So, we looked at proteins that change with age and had something to do with the vasculature.” One protein that becomes more abundant with age, VCAM1, stood out, and the team showed that it appears to play a pivotal role in the effects of aged blood on the brain. Biological and cognitive measures alike indicated that blocking VCAM1 not only prevents old plasma from damaging young mouse brains but can even reverse deficits in old mice. The work has important implications for age-related cognitive decline and brain diseases. “Cognitive dysfunction in aging is one of our biggest biomedical challenges, and we have no effective medical therapies. None,” says neuroscientist Dena Dubal, of the University of California, San Francisco, who was not involved in the study. “It’s such an important line of investigation; it has tremendous implications.” © 2019 Scientific American

Keyword: Alzheimers
Link ID: 26237 - Posted: 05.15.2019

By MOISES VELASQUEZ-MANOFF When Catherine Jacobson first heard about the promise of cannabis, she was at wits’ end. Her 3-year-old son, Ben, had suffered from epileptic seizures since he was 3 months old, a result of a brain malformation called polymicrogyria. Over the years, Jacobson and her husband, Aaron, have tried giving him at least 16 different drugs, but none provided lasting relief. They lived with the grim prognosis that their son — whose cognitive abilities never advanced beyond those of a 1-year-old — would likely continue to endure seizures until the cumulative brain injuries led to his death. In early 2012, when Jacobson learned about cannabis at a conference organized by the Epilepsy Therapy Project, she felt a flicker of hope. The meeting, in downtown San Francisco, was unlike others she had attended, which were usually geared toward lab scientists and not directly focused on helping patients. This gathering aimed to get new treatments into patients’ hands as quickly as possible. Attendees weren’t just scientists and people from the pharmaceutical industry. They also included, on one day of the event, families of patients with epilepsy. The tip came from a father named Jason David, with whom Jacobson began talking by chance outside a presentation hall. He wasn’t a presenter or even very interested in the goings-on at the conference. He had mostly lost faith in conventional medicine during his own family’s ordeal. But he claimed to have successfully treated his son’s seizures with a cannabis extract, and now he was trying to spread the word to anyone who would listen. The idea to try cannabis extract came to David after he found out that the federal government held a patent on cannabidiol, a molecule derived from the cannabis plant that is commonly referred to as CBD. Unlike the better-known marijuana molecule delta-9-tetrahydrocannabinol, or THC, CBD isn’t psychoactive; it doesn’t get users high. But in the late 1990s, scientists at the National Institutes of Health discovered that it could produce remarkable medicinal effects. In test tubes, the molecule shielded neurons from oxidative stress, a damaging process common in many neurological disorders, including epilepsy.

Keyword: Drug Abuse; Epilepsy
Link ID: 26236 - Posted: 05.15.2019

Sarah Boseley Health editor A drug that could prolong the lives of children with a rare muscle-wasting disease has been approved by the NHS in England after lengthy negotiations with the manufacturer over the high price. Spinraza could help between 600 and 1,200 children and adults in England and Wales who have the genetic condition spinal muscular atrophy (SMA). It affects the nerves in the spinal cord, making muscles weaker and causing problems with movement, breathing and swallowing. It can shorten the life expectancy of babies and toddlers. The drug can slow the progress of the disease but the company making the drug, Biogen, was asking for a high price, that effectively amounted to more than £400,000 for a year of good quality life, according to the National Institute for Health and Care Excellence (Nice), which assesses value for money. Nice said there was limited data on its long-term effectiveness and turned it down last August, to the distress of affected families. Simon Stevens, the NHS England chief executive, said agreement had been reached and children would shortly get Spinraza, the market name of the drug nusinursen. “This promising treatment has the potential to be life changing for children and their families,” said Stevens. “The NHS has now reached one of the most comprehensive deals in the world, which allows us to assess real-world evidence of its long-term benefits. © 2019 Guardian News & Media Limited

Keyword: Movement Disorders; Muscles
Link ID: 26235 - Posted: 05.15.2019

By Gretchen Reynolds A need and desire to be in motion may have been bred into our DNA before we even became humans and could have helped to guide the evolution of our species, according to a fascinating new study of the genetics of physical activity. The study uses big data and sophisticated genetic analyses to determine that some of the gene variants associated with how much and whether people move seem to have joined our ancestors’ genome hundreds of thousands of years ago, making them integral to human existence and well-being and raising interesting questions about what that means today, when most humans are sedentary. There has been evidence for some time that whether and how much people and other animals move depends to some extent on family history and genetics. Past twin studies and genome-wide association studies — which scan genomes looking for snippets of DNA shared by individuals who also share certain traits — suggest that about 50 percent of physical activity behavior in people may depend on genes. Our tendency to move or not is different from our innate aerobic fitness. Someone could be born with a large inherited endurance capacity and no interest at all in leaving the couch, or vice versa. Little has been known, though, about when any of the gene variants associated with moving became integrated into the human genome, and that question matters. Many of the most common chronic illnesses and conditions in people today, including Type 2 diabetes, obesity, heart disease, osteoarthritis and others, are associated with being inactive. But some other species, including chimps, which share much of our DNA, retain robust good health even when they move relatively little. © 2019 The New York Times Company

Keyword: Genes & Behavior
Link ID: 26234 - Posted: 05.15.2019

Mitchel Daniel If you’re looking for love, it pays to stand out from the crowd. Or at least that’s how it works in some parts of the animal kingdom. Scientists have found that in several species – green swordtail fish, Trinidadian guppies, fruit flies, Poecilia parae fish – ladies overwhelmingly go for the guy that looks different from the rest. But the reason for this attraction to novelty has remained a mystery. So my colleagues and I used the Trinidadian guppy to investigate the psychology behind why many females have an affinity for the unusual. Male features that attract females The guppy has long been a workhorse for biologists like me who are interested in understanding the mating decisions that animals make and the evolutionary forces behind those decisions. Male guppies attempt to woo females using courtship dances that show off the elaborate color patterns adorning their bodies. The females of the species are color pattern connoisseurs, carefully choosing among their suitors based, in large part, on their visual appeal. This tendency has made the guppy an excellent model for studying mate choice. Male guppies showcase their colors during their courtship dances. Many types of animals exhibit what evolutionary biologists call directional preferences, an attraction to more of a certain thing – think bigger antlers, a longer tail or brighter color spots. And there are evolutionary theories that help make sense of these preferences. If a male can grow more extreme features, that can be a sign that he is in good physical condition, has good genes, or would make a good parent. What’s less clear, though, is why females should value unusualness in a mate. © 2010–2019,

Keyword: Sexual Behavior; Evolution
Link ID: 26233 - Posted: 05.15.2019