Sarah Boseley Health editor The use of cannabis medicines to treat people with depression, anxiety, psychosis or other mental health issues cannot be justified because there is little evidence that they work or are safe, according to a major new study. A review of evidence from trials conducted over nearly 40 years, published in the journal Lancet Psychiatry, concludes that the risks outweigh the benefits. And yet, say the authors, they are being given to people with mental health problems in Australia, the US and Canada, and demand is likely to grow. Prof Louisa Degenhardt of the National Drug and Alcohol Research Centre at UNSW Sydney, Australia, lead author of the study, said the findings had important implications in countries where medical use was allowed. “There is a notable absence of high-quality evidence to properly assess the effectiveness and safety of medicinal cannabinoids compared with placebo, and until evidence from randomised controlled trials is available, clinical guidelines cannot be drawn up around their use in mental health disorders,” she said. “In countries where medicinal cannabinoids are already legal, doctors and patients must be aware of the limitations of existing evidence and the risks of cannabinoids. These must be weighed when considering use to treat symptoms of common mental health disorders. Those who decide to proceed should be carefully monitored for positive and negative mental health effects of using medicinal cannabinoids.” © 2019 Guardian News & Media Limited

Keyword: Drug Abuse; Schizophrenia
Link ID: 26769 - Posted: 10.30.2019

By Zeynep Tufekci More than a billion people around the world have smartphones, almost all of which come with some kind of navigation app such as Google or Apple Maps or Waze. This raises the age-old question we encounter with any technology: What skills are we losing? But also, crucially: What capabilities are we gaining? Talking with people who are good at finding their way around or adept at using paper maps, I often hear a lot of frustration with digital maps. North/south orientation gets messed up, and you can see only a small section at a time. And unlike with paper maps, one loses a lot of detail after zooming out. I can see all that and sympathize that it may be quite frustrating for the already skilled to be confined to a small phone screen. (Although map apps aren’t really meant to be replacements for paper maps, which appeal to our eyes, but are actually designed to be heard: “Turn left in 200 feet. Your destination will be on the right.”) But consider what digital navigation aids have meant for someone like me. Despite being a frequent traveler, I’m so terrible at finding my way that I still use Google Maps almost every day in the small town where I have lived for many years. What looks like an inferior product to some has been a significant expansion of my own capabilities. I’d even call it life-changing. Part of the problem is that reading paper maps requires a specific skill set. There is nothing natural about them. In many developed nations, including the U.S., one expects street names and house numbers to be meaningful referents, and instructions such as “go north for three blocks and then west” make sense to those familiar with these conventions. In Istanbul, in contrast, where I grew up, none of those hold true. For one thing, the locals rarely use street names. Why bother when a government or a military coup might change them—again. House and apartment numbers often aren’t sequential either because after buildings 1, 2 and 3 were built, someone squeezed in another house between 1 and 2, and now that’s 4. But then 5 will maybe get built after 3, and 6 will be between 2 and 3. Good luck with 1, 4, 2, 6, 5, and so on, sometimes into the hundreds, in jumbled order. Besides, the city is full of winding, ancient alleys that intersect with newer avenues at many angles. © 2019 Scientific American

Keyword: Attention; Learning & Memory
Link ID: 26768 - Posted: 10.30.2019

By Lisa Sanders, M.D. “Please find something wrong with me,” the 28-year-old woman pleaded. For nearly a year, she’d been looking for a reason for the strange symptoms that now dominated her life. Dr. Raphael Sung, a cardiologist specializing in finding and fixing abnormal heart rhythms at National Jewish Health hospital in Denver, was surprised by her reaction to the news that her heart was normal. Most patients are happy to get that report. For this patient, it seemed like just one more dead end. The patient’s symptoms started right after her baby was born 10 months earlier. Out of nowhere, her heart would start beating like crazy. At first, she assumed that these were anxiety attacks, triggered by the stress of bringing her premature daughter home. Her baby spent her first week of life in the newborn intensive care unit. When she was big enough to come home, she still weighed only four pounds, nine ounces. The new mother worried that without the doctors and nurses and equipment that had kept her alive, her tiny baby might die. But she didn’t. She seemed to thrive at home. Despite that, her mother’s heart continued to take off like a spooked horse several times a day. After a couple of weeks, her symptoms worsened. Sometimes her racing heart would set off terrible headaches, the worst she’d ever had. It was as if someone had thrust a sharp stick deep into her brain. The knife of pain quickly turned into a sense of pressure so intense it felt as if the back of her skull would blow off. Minutes later, she would feel the blood drain from her face; she’d be suddenly drenched in sweat. Her hands would curl into tight fists, and vomit would shoot out of her mouth like a geyser. Her husband joked (though only once) that she looked like the girl in “The Exorcist.” © 2019 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 26767 - Posted: 10.30.2019

By Gary Stix Sigmund Freud never uttered the word neuroscience. Neither did Santiago Ramón y Cajal. It was biophysicist Francis Schmitt who grafted “neuro” with “science” in 1962 when he established the Neurosciences Research Program at MIT. The new moniker was intended to encompass a merging of relevant neuro disciplines, ranging as far afield as physiology, psychology, immunology, physics and chemistry. Brains and behaviors have been scrutinized for millennia. But as psychology blogger Vaughn Bell has pointed out, the 1960s marked a shift in perspective. Neuroscience was the formal name given by Schmitt. But the period represented the beginnings of a “neuroculture,” that put brain science on a pedestal —even leading to the familiar meme proclaiming “my brain made me do it.” One example was rooted in pharmaceutical companies’ development of psychiatric drugs that resulted in their investing “millions both into divining the neurochemistry of experience and into massive marketing campaigns that linked brain functions to the psyche,” Bell notes. The field received an adrenaline boost precisely 50 years ago with the founding of the Society for Neuroscience, allowing Schmitt’s collaborative vision to be globally shared. SFN’s first annual meeting in 1971 drew 1,395 attendees to Washington, D.C. This year’s wrapped up on October 23, bringing more than 27,500 to Chicago—and the annual numbers have occasionally topped 30,000. SFN now boasts 37,000 members from more than 95 countries. © 2019 Scientific American

Keyword: Miscellaneous
Link ID: 26766 - Posted: 10.30.2019

By Perri Klass, M.D. Sleeping through the night is a hot topic in pediatrics, so it was no surprise that there was a standing-room-only crowd for a lecture on it at the national conference of the American Academy of Pediatrics in New Orleans over the weekend. The speaker, Dr. Adiaha I.A. Spinks-Franklin, a developmental behavioral pediatrician, did her training at Children’s Hospital, Boston, where her teachers included the pediatric sleep expert, Dr. Richard Ferber, whose name has become a verb: “we Ferberized our baby.” But Dr. Spinks-Franklin, an associate professor of pediatrics at Baylor College of Medicine, wasn’t talking about the burning question of whether to let babies cry. In her presentation, “Strategies to Help Sleepless Teens,” she started by reviewing the factors that can contribute to inadequate sleep in adolescents: social media and electronic devices in the bedroom. Intensely caffeinated drinks. The pressures of heavily overloaded schedules, including academic demands, extracurricular activities, travel sports teams, jobs and social lives. The biology of adolescent sleep reflects a natural and normal delay in melatonin secretion that leads to a later sleep onset time, which unfortunately coincides with early high school start times, creating a high-stress set up. Pediatricians often see adolescents with insomnia, who have trouble falling asleep or staying asleep, waking up too early or finding sleep not restful or refreshing. Evaluating insomnia in an adolescents means looking at the predisposing factors, she said, including how that adolescent responds to stress, and possible genetic influences, and the precipitating factors — the specific triggers for insomnia — and finally, the perpetuating factors, which can keep the pattern going. All these adolescents should be screened for depression and anxiety, Dr. Spinks-Franklin said; both can affect sleep onset or sleep maintenance. And both are alarmingly common in adolescents. © 2019 The New York Times Company

Keyword: Sleep; Development of the Brain
Link ID: 26765 - Posted: 10.29.2019

Patti Neighmond More Americans have been getting less than seven hours of sleep a night in the past several years, especially in professions such as health care. ER Productions Limited/Getty Images If you often hit that midafternoon slump and feel drowsy at your desk, you're not alone. The number of working Americans who get less than seven hours of sleep a night is on the rise. And the people hardest hit when it comes to sleep deprivation are those we depend on the most for our health and safety: police and health care workers, along with those in the transportation field, such as truck drivers. In a recent study, researchers from Ball State University in Muncie, Ind., analyzed data from the National Health Interview Survey. They looked at self-reports of sleep duration among 150,000 adults working in different occupations from 2010 to 2018. Researchers found the prevalence of inadequate sleep, defined as seven hours or less, increased from 30.9% in 2010 to 35.6% in 2018. But it was worse for police officers and health care workers. Around half of respondents in these professions reported not getting seven hours a night. For many, the norm was six or even just five hours. The researchers didn't examine why sleep time is dwindling. But Jagdish Khubchandani — professor of health science at Ball State University who headed the study — speculates one of the biggest reasons has to do with stress, which is on the rise among Americans. © 2019 npr

Keyword: Sleep
Link ID: 26764 - Posted: 10.29.2019

By Anahad O’Connor In recent years, hospitals and medical centers across the country have stopped selling sugar-sweetened beverages in an effort to reduce obesity and diabetes. Now a new study carried out at the University of California, San Francisco, has documented the health impact of a soda sales ban on its employees. Ten months after a sales ban went into effect, U.C.S.F. workers who tended to drink a lot of sugary beverages had cut their daily intake by about half. By the end of the study period, the group had, on average, reduced their waist sizes and belly fat, though they did not see any changes in their body mass index. Those who cut back on sugary beverages also tended to see improvements in insulin resistance, a risk factor for Type 2 diabetes. The new research, published on Monday in JAMA Internal Medicine, is the first peer-reviewed study to examine whether a workplace sales ban on sugary drinks could lead to reduced consumption of the beverages and improve employee health. At least nine other University of California campuses have said they are going to adopt similar initiatives to reduce sugary beverage sales and promote water consumption. “This was an intervention that was easy to implement,” said Elissa Epel, an author of the study and director of the Aging, Metabolism, and Emotions Center at U.C.S.F. “It’s promising because it shows that an environmental change can help people over the long run, particularly those who are consuming large-amounts of sugary beverages, and possibly even lead to a reduction in their risk of cardiometabolic disease.” In recent years, the link between sugar and obesity has drawn increasing scientific attention. Health authorities say that Americans have gotten fatter because they are consuming too many calories of all kinds. But some experts have singled out the role of added sugar consumption, which increased more than 30 percent between 1977 and 2010. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26763 - Posted: 10.29.2019

Pien Huang Alexandra Chen was a trauma specialist working in Lebanon and Jordan when she noticed that a specific group of kids were struggling in schools. Chen kept getting referrals for refugee students who had fled the war in Syria. They were having trouble focusing and finishing schoolwork. Some had even dropped out of school. She wondered to what extent the different stressors they faced — exposure to violence in Syria, lack of resources or concerns for the future — affected how they navigate their daily lives. Specifically, she wondered, which had a bigger impact: past trauma or the poverty they now lived in? Experts she wrote to said they didn't know and advised her to investigate the question herself. Chen, who's now getting her Ph.D. at Harvard, worked with a team to devise a study that aimed to untangle the threads of poverty, trauma and other adversities. They studied 240 teen Syrian refugees, comparing them with a group of 210 Jordanian youth who were also considered at-risk but didn't have a background of war. The researchers gave the teenagers surveys to gauge trauma and insecurity. To determine poverty, they asked the teens whether their families had items such as bedframes, cars, TVs, smartphones, refrigerators and water heaters. © 2019 npr

Keyword: Learning & Memory; Stress
Link ID: 26762 - Posted: 10.29.2019

By Maya Vijayaraghavan On Jan. 1, my husband asked me whether he would die that year. I said no. It happened to be my birthday, and I wanted to feel jubilant despite the tragic turn of events in our life. I thought Rahul might have another year, that he might beat the odds of dying this year. In other words, his hazard ratio was favorable compared with someone else in his situation. He liked talking about something related, hazard scores — a composite score of one’s genetic risk for a particular outcome such as diagnosis of a disease. It was his thing as a neuroscientist-physician. He developed one for Alzheimer’s disease, and was on his way to developing one for amyotrophic lateral sclerosis (ALS), the disease he had been studying even before he got sick with it. In reality, he had declined significantly since his diagnosis of ALS two years prior. First, he lost his speech, then his mobility, and very quickly breathing became a struggle. But any talk of decline came with an acceptance that his life was imminently finite, and neither of us were willing to accept that outcome. But Rahul did die, six months after that conversation. I remember some of our last conversations, when things were very difficult. His forewarning that this existence with him teetering at the brink of life and death was much easier than the life I would lead as a widow, raising two young children. I think neither of us really understood that the emptiness I’d feel would be soul-crushing. That I would cry all the time. That I would miss him so much. That I would become a ghost of my former self. That this thing they call complicated grief, in which healing doesn’t occur as it’s supposed to, and which supposedly happens only after a year, is something that I feel now. That I would think constantly about the time when my husband was first diagnosed and he got into a fight with our then-3-year-old (now 5) about how he could not carry him because he did not have the strength to and not because he did not want to.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26761 - Posted: 10.28.2019

By Stephen L. Macknik Most of us look at a bird and see its avian shape in perfect alignment with the colors of its beautiful plumage. How could it be any other way? The shape and color are derived from the same object and so the brain must process shape and color together as a unified percept. Right? Wrong. The brain processes forms and color in separate neural circuits, but because these brain regions communicate with each other, our perception appears unified. To understand how this all works, let’s do an experiment on ourselves to separate (and then recombine in our brains) the colors and shapes from an image. We will use an illusion called the Color Assimilation Grid, developed by Øyvind Kolås, a digital media artist and software developer. First, let’s apply a screen to the birds (above) so that we can sample their colors but get rid of most of their shape information. We simply take the original image and blur it (to break down the shape information, not shown) and then multiply the resultant pixels in a step-by-step, pixel-by-pixel fashion with a grid screen of the same size as the original image. In the screen, white pixels equal 1 and the gray regions equal zero, so the result is a blurry colored plaid sample of the birds’ colors. Now that we have diminished the shape information and sampled the colors, we need to do the opposite: sample the shapes after diminishing the color information, so that we can later mix the two to see how shape and color assimilate in the brain. To create the shape-only image we first turn the original image to grayscale (above) and then we apply the inverse of the screen we used in the color sampling. The result is a grayscale image of the birds with the shape information preserved, superimposed with a tiny grid of empty spaces where we can later add color information without altering the rest of the image. © 2019 Scientific American

Keyword: Vision
Link ID: 26760 - Posted: 10.28.2019

By Owain Clarke BBC Wales health correspondent World-leading research is helping scientists find new ways of trying to help younger people who have had a stroke get back to work. The study led by Manchester Metropolitan University found the speed a patient can walk is a major factor in determining how likely they are able to return to the workplace. Researchers have been working with physiotherapists and patients in Wales. It includes moving rehabilitation outdoors, including the Brecon Beacons. It is hoped it could lead to new rehabilitation methods being developed to target younger stroke patients. The average age to have a stroke in the UK is 72 for men and 78 for women. But there has been a 40% worldwide rise in people under 65 who have strokes in the last decade, according to the researchers. Image copyright Manchester Metropolitan University Image caption Researchers are studying the skeletons of stroke patients to see how joints perform when they walk What does the science say? It looked at 46 patients across Wales who had a stroke when younger than 65 years old and only 23% were able to return to work It found walking speed was a key predictor of whether a younger adult who has had a stroke could return to work They calculated a walking speed threshold of 0.93m/s (3ft a second) was a good benchmark for the likelihood of returning to work - and as a result this could be a goal set during rehabilitation As well as looking at the best environment for younger patients to recover in, it is now looking at using CGI technology to study joints to find out how stroke patients walk Nikki Tomkinson had a stroke at 53. "The world started shifting" while she was out driving in Cardiff. © 2019 BBC

Keyword: Stroke
Link ID: 26759 - Posted: 10.28.2019

By Tanya Lewis The lenses in human eyes lose some ability to focus as they age. Monovision—a popular fix for this issue—involves prescription contacts (or glasses) that focus one eye for near-vision tasks such as reading and the other for far-vision tasks such as driving. About 10 million people in the U.S. currently use this form of correction, but a new study finds it may cause a potentially dangerous optical illusion. Nearly a century ago German physicist Carl Pulfrich described a visual phenomenon now known as the Pulfrich effect: When one eye sees either a darker or a lower-contrast image than the other, an object moving side to side (such as a pendulum) appears to travel in a three-dimensional arc. This is because the brain processes the darker or lower-contrast image more slowly than the lighter or higher-contrast one, creating a lag the brain perceives as 3-D motion. Johannes Burge, a psychologist at the University of Pennsylvania, and his colleagues recently found that monovision can cause a reverse Pulfrich effect. They had participants look through a device showing a different image to each eye—one blurry and one in focus—of an object moving side to side. The researchers found that viewers processed the blurrier image a couple of milliseconds faster than the sharper one, making the object seem to arc in front of the display screen. It appeared closer to the viewer as it moved to the right (if the left eye saw the blurry image) or to the left (if the right eye did). “That does not sound like a very big deal,” Burge says, but it is enough for a driver at an intersection to misjudge the location of a moving cyclist by about the width of a narrow street lane (graphic). © 2019 Scientific American

Keyword: Vision
Link ID: 26758 - Posted: 10.28.2019

Marisa Iati Police and doctors didn’t believe the 46-year-old man when he swore that he hadn’t had alcohol before he was arrested on suspicion of drunken driving. His blood alcohol level was 0.2, more than twice the legal limit for operating a car. He refused a breathalyzer test, was hospitalized and later released. But the facts remained in contention. Then researchers discovered the unusual truth: Fungi in the man’s digestive system were turning carbohydrates into alcohol — a rarely diagnosed condition known as “auto-brewery syndrome.” In people with the syndrome, fermenting fungi or bacteria in the gut produce ethanol and can cause the patients to show signs of drunkenness. The condition, also known as gut fermentation syndrome, can occur in otherwise healthy people but is more common in patients with diabetes, obesity or Crohn’s disease. “A person is intoxicated from this fermenting yeast, and it’s a horrible illness,” said Barbara Cordell, a researcher of auto-brewery syndrome and the author of “My Gut Makes Alcohol.” The condition has rarely been studied and is diagnosed infrequently. Researchers at Richmond University Medical Center in New York, however, wrote in the journal BMJ Open Gastroenterology that they believe the syndrome is underdiagnosed. The condition made news in 2014, when the driver of a truck that spilled 11,000 salmon onto a highway claimed to have auto-brewery syndrome. The next year, a New York woman was charged with driving under the influence after she registered a blood alcohol level that was more than four times the legal limit, CNN reported. A judge dismissed the charges after being shown evidence that she had auto-brewery syndrome.

Keyword: Drug Abuse
Link ID: 26757 - Posted: 10.26.2019

By Jocelyn Kaiser HOUSTON, TEXAS—Schizophrenia tends to run in families, which suggests it’s largely inherited. But a long-running search for genes underlying this severe psychiatric condition has yielded only indirect clues. Now, by scouring the DNA of tens of thousands of people, gene hunters have for the first time nabbed a handful of rare genes that, when mutated, appear to be direct contributors to the disease—and may shed light on what goes awry in a schizophrenia patient’s brain. “These are concrete genes with mutations with a clear molecular mechanism,” says Mark Daly of the Broad Institute in Cambridge, Massachusetts, and the University of Helsinki, who is principal investigator for a consortium that presented the work last week at the annual meeting of the American Society of Human Genetics (ASHG) here. “It was a fabulous talk,” says Jennifer Mulle of Emory University in Atlanta, who studies the genetics of psychiatric disorders. “We don’t understand anything about the biological pathways [in schizophrenia]. Now, these genes give us an avenue.” People with schizophrenia, which afflicts about 0.7% of the U.S. population, have a distorted sense of reality and confused thinking; they may have hallucinations and delusions. Some patients share similar genetic abnormalities, such as missing specific chunks of DNA, but how those gaps may contribute to disease isn’t known. © 2019 American Association for the Advancement of Science

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26756 - Posted: 10.26.2019

Lena H. Sun Most people who died from vaping-related injuries used products containing THC, the psychoactive ingredient in marijuana, federal health officials said Friday, offering another data point tying the outbreak of lung illnesses to products made with that compound. Based on data available from 860 of the 1,604 patients who have fallen ill with the disease, about 85 percent reported using THC-containing products, compared to about 10 percent who reported exclusively vaping nicotine-containing products, officials said. Many sick patients said they bought THC vape products on the black market, and those have come under increased scrutiny. “The data do continue to point towards THC-containing products as the source of individuals’ injury,” said Anne Schuchat, principal deputy director at the Centers for Disease Control and Prevention, which is leading the investigation. Officials don’t know what about the products are harmful, “but we’re seeing THC as a marker for products that are risky,” she said. It is also becoming clearer that the surge in cases in recent months is not the result of better recognition of an existing disease, but “something riskier that is in much more frequent use,” she said. Schuchat cited the use of cutting agents that are added to THC-containing products to increase profit, and the increased availability of online videos that may have “skyrocketed” do-it-yourself instructions. One substance that has turned up in many product samples is vitamin E oil, known as vitamin E acetate. Experts in the legal marijuana industry have said it has been added to THC oil used to fill vape cartridges.

Keyword: Drug Abuse
Link ID: 26755 - Posted: 10.26.2019

By Carl Zimmer Evolutionary biologists retrace the history of life in all its wondrous forms. Some search for the origin of our species. Others hunt for the origin of birds. On Thursday, a team of researchers reported an important new insight into the origin of zombies — in this case, ants zombified by a fungus. Here’s how it works: Sometimes an ant, marching about its business outdoors, will step on a fungal spore. It sticks to the ant’s body and slips a fungal cell inside. The fungus, called Ophiocordyceps, feeds on the ant from within and multiplies into new cells. But you wouldn’t know it, because the ant goes on with its life, foraging for food to bring back to the nest. All the while, the fungus keeps growing until it makes up nearly half of the ant’s body mass. When Ophiocordyceps is finished feeding on its host, the fungal cells gather inside the ant’s body. They form a mat and push needlelike projections into the ant’s muscle cells. The fungal cells also send chemical signals to the ant’s brain, causing the host to do something strange. The ant departs its nest and climbs a nearby plant. In the tropics, where many species of Ophiocordyceps live, the fungus drives ants upward, to a leaf above the ground. The ant bites down, its jaws locking as it dies. The fungus sends out sticky threads that glue the corpse to the leaf. And now it is ready to take the next step in its life cycle: Out of the ant’s head bursts a giant stalk, which showers spores onto the ant trails below. “The ants are walking over a minefield,” said David Hughes, an expert on Ophiocordyceps at Pennsylvania State University. © 2019 The New York Times Company

Keyword: Evolution
Link ID: 26754 - Posted: 10.25.2019

By Jocelyn Kaiser HOUSTON, TEXAS—Two years ago, news headlines began to appear about a development that made many human geneticists uneasy. A U.S. company planned to offer a test for embryos created through in vitro fertilization (IVF) that screened the entire genome for DNA variants linked to cognitive ability, in order to help couples avoid having children with intellectual impairment. Many ethicists fear such multigene analyses could one day be used to screen embryos for desirable traits as well, such as tall stature or high IQ. For those disturbed by the prospect, a study reported here last week at the annual meeting of the American Society of Human Genetics (ASHG) may come as a relief: For now, the strategy would not work very well. Researchers, led by statistical geneticist Shai Carmi of the Hebrew University of Jerusalem, calculated exactly how much of a boost in IQ or height could be expected by scanning for relevant DNA markers in a batch of embryos and choosing those with the highest scores. The result: The gains would be slight, and prospective parents might even end up discarding their tallest or smartest potential offspring. The work "is the first to empirically test the viability of screening embryos" for traits that are influenced by many genes, says sociologist and demographer Melinda Mills of the University of Oxford in the United Kingdom. Such embryo screening goes beyond today's testing for single-gene disorders and currently "isn't plausible," she concludes. © 2019 American Association for the Advancement of Science.

Keyword: Intelligence; Genes & Behavior
Link ID: 26753 - Posted: 10.25.2019

By Laura Sanders CHICAGO — Brain cells grown into clumps in flasks are totally stressed-out and confused. Cells in these clumps have ambiguous identities and make more stress molecules than cells taken directly from human brains, researchers reported October 22 at the annual meeting of the Society for Neuroscience. These cellular clumps are grown using stem cells made from skin or blood, which under the right conditions can be coaxed into forming three-dimensional clusters of brain cells. These clusters, a type of organoid, are thought to re-create some aspects of early human brain development, a period that is otherwise difficult to study (SN: 2/20/18). The new results highlight underappreciated differences between these organoids and the human brains they are designed to mimic. “Most of the papers out there are extolling the virtues of these things,” says study coauthor Arnold Kriegstein, a developmental neurobiologist at the University of California, San Francisco. But the new study reveals “significant issues that nobody has addressed yet.” Kriegstein and colleagues compared genetic activity in human cells from brain tissue in early development with human cells grown in an organoid. Cells in the organoids had more active genes involved in stress responses. What’s more, these organoid cells didn’t fit into the neat categories of cells in actual brain tissue. Instead, some of the organoid cells showed features of two distinct categories simultaneously. “They are not normal,” Kriegstein says. © Society for Science & the Public 2000–2019.

Keyword: Development of the Brain
Link ID: 26752 - Posted: 10.25.2019

By Veronique Greenwood To the rippling sound of an aquarium pump, a small crab comes around the corner. It moves sideways, sticking close to the walls. But when it catches sight of a mussel — laid as a reward at the end of the maze it has just walked — the crab breaks into a skipping run, throwing itself on the treat with abandon. This crustacean, one of many shore crabs scooped by researchers from under a pier in Swansea, Wales, had just completed an intriguing feat: Without any guidance from researchers, it found its way to the end of a small maze. According to a paper in Biology Letters on Wednesday, shore crabs can learn to navigate a lab-rat-style maze and remember it weeks later. While crabs that have never seen the maze before bump around aimlessly, experienced crabs race to the finish line with no wrong turns. The study, one of the few to look at whether crustaceans can perform such feats, suggests that crabs are quite capable of remembering routes. Maze running could also be a way to measure the effects of changes in the sea, like ocean acidification and warming, on crabs’ cognitive abilities. Crabs often clamber through complex landscapes in their daily lives, says Edward Pope, a marine biologist at Swansea University who is an author of the new study. So, it is not particularly surprising that crabs would be able to find their way through a maze and even be able to remember it later. What was surprising, however, was just how clear the results of the study were. During the first week of the experiment, no crabs got to the end of the maze without taking wrong turns, some of them detouring six or seven times. By week four, some could race to the end flawlessly. Even the worst-performing crab took no more than three wrong turns. To see how the crabs would perform when there was no food in the maze, and thus no trace in the water of a snack to guide them, the researchers waited a couple of weeks and put the crabs back in the maze. They also tested crabs that had never seen the maze. “The conditioned animals all ran to the end of the maze expecting there to be food,” Dr. Pope said. © 2019 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 26751 - Posted: 10.25.2019

Researchers have discovered in mice how one of the few genes definitively linked to schizophrenia, called SETD1A, likely confers risk for the illness. Mice genetically engineered to lack a functioning version of the enzyme-coding gene showed abnormalities in working memory, mimicking those commonly seen in schizophrenia patients. Restoring the gene’s function corrected the working memory deficit. Counteracting the gene’s deficiencies also repaired neuronal circuit deficits in adult mice – suggesting clues for potential treatment strategies. A team of scientists led by Joseph Gogos, M.D., Ph.D., of Columbia University, New York City, reported on their research – supported by the National Institutes of Health – in Neuron. “You could call SETD1A a master regulator,” explained David Panchision Ph.D., of the NIH’s National Institute of Mental Health (NIMH), which co-funded the study. “This schizophrenia risk gene codes for an enzyme that influences the expression of many other genes. In mice, a hobbled version of SETD1A disrupted gene expression in a network harboring other genomic suspects in schizophrenia. Remarkably, the resulting abnormalities were reversible.” Researchers have identified both common and rare genetic variations that contribute to risk for schizophrenia. Mutant SETD1A is one of just a few rare genes known to unequivocally confer risk for schizophrenia. While common genetic variations linked to schizophrenia individually exert only tiny effects on risk, having just one mutant copy of SETD1A is sufficient to confer a large increase in disease risk. SETD1A plays a key role in epigenomic regulation – the switching on-and-off of genes in response to experience – a molecular process widespread in the brain. Mutations in SETD1A have primarily been found in people with schizophrenia, suggesting that this rare gene variation might hold important clues to the underlying disease process.

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26750 - Posted: 10.25.2019