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Jyoti Madhusoodanan Douglas Storace still has the dollar bill that he triumphantly taped above his laboratory bench seven years ago, a trophy from a successful wager. His postdoctoral mentor, Larry Cohen at Yale University in New Haven, Connecticut, bet that Storace couldn’t express a protein sensor of voltage changes in mice back in September 2012. Storace won. The bill is a handy reminder that the experiments he aims to try in his new lab can work. And it’s a testament to just how tricky it is to correctly express these sensors and track their signals. Storace, now an assistant professor at Florida State University in Tallahassee, plans to use these sensors, known as genetically encoded voltage indicators (GEVIs), to study how neurons in the olfactory bulb sense and react to smells. GEVIs are voltage-sensitive, fluorescent proteins that change colour when a neuron fires or receives a signal. Because GEVIs can be targeted to individual cells and directly indicate a cell’s electrical signals, researchers consider them to be the ideal probes for studying neurons. But they have proved frustratingly difficult to use. “Being able to visualize voltage changes in a cell has always been the dream,” says neuroscientist Bradley Baker at the Korea Institute of Science and Technology in Seoul. “But probes that looked great often didn’t behave in ways that were useful.” Early GEVIs disappointed on several levels. They were bright when a cell was resting and dimmed when the cell fired an action potential, producing signals that were tough to distinguish from the background. And they failed to concentrate in the nerve-cell membranes, where they function. But researchers are beginning to solve these issues. Some are turning to advanced fluorescent proteins or chemical dyes for better signals; others are using directed evolution and high-throughput screens to make GEVIs more sensitive to voltage changes. Meanwhile, biologists are putting these molecules through their paces. GEVIs, says neuroscientist Katalin Toth at Laval University in Quebec City, Canada, are not yet widely used, but they’re getting there. “They are becoming brighter and faster — and growing in popularity,” she says. “I think this is the dawn of GEVIs.” © 2019 Springer Nature Limited

Keyword: Brain imaging
Link ID: 26703 - Posted: 10.15.2019

By Amanda Chicago Lewis In June of 2018, Mark Pennington received troubling news from his ex-girlfriend, with whom he shared custody of their 2-year-old son. She had taken a hair follicle from the boy, she said, and had it analyzed at a lab. A drug test had returned positive for THC, the intoxicating compound in marijuana; evidently their son had been exposed to it, presumably in Mr. Pennington’s presence. He was told that, from then on, he would be permitted to see the child only once a week, and under supervision. “I was mortified,” Mr. Pennington recalled recently. “My jaw hit the floor. I just knew from the bottom of my heart I hadn’t gotten any THC in my son’s system.” However, Mr. Pennington had been providing his son with honey infused with cannabidiol, or CBD, a nonintoxicating compound that, like THC, is found in varying amounts in the plant known as cannabis. THC is federally illegal, and until recently so was all cannabis. But last December, the Farm Bill legalized hemp — cannabis that contains less than 0.3 percent THC. With that, CBD became legal. It can now be found at stores across the country, in everything from tinctures and massage oils to coffee and makeup. Mr. Pennington, who lives in Colorado, where growing hemp for CBD has been legal since 2014, worked for Colorado Hemp Honey, a company that sells CBD-infused raw honey across the country. Mr. Pennington was despondent about possibly losing custody of his child, until he spoke with Frank Conrad, the chief technology officer and lab director at Colorado Green Lab, a scientific consultant to the cannabis industry. Mr. Conrad directed him to a little-known study published in 2012 in the Journal of Analytical Toxicology that showed that a common forensic drug testing method could easily mistake the presence of CBD for THC. In short, the drug testing lab may have erred; it was entirely possible that the CBD Mr. Pennington had given his child had caused the drug test to produce a false positive for THC. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26702 - Posted: 10.15.2019

Dean Burnett It’s a damp, midweek afternoon. Even so, Cardiff’s walk-in stress management course has pulled in more than 50 people. There are teenagers, white-haired older people with walking aids, people from Caucasian, Asian and Middle Eastern backgrounds. There is at least one pair who look like a parent and child – I’m unsure who is there to support whom. The course instructor makes it clear that she is not going to ask people to speak out about their own stress levels in this first class: “We know speaking in public is stressful in itself.” She tells us a bit about previous attendees: a police officer whose inexplicable and constant worrying prevented him from functioning; a retired 71-year-old unable to shake the incomprehensible but constant fatigue and sadness that blighted his life; a single mother unable to attend her daughter’s school concert, despite the disappointment it would cause. What is the common theme that links these people – and the varied group sitting there this afternoon and listening? Stress may once just have been a kind of executive trophy – “I’m so stressed!” – but recent research suggests it is a key element in developing mental health problems such as depression and anxiety. The constant, stress-induced stimulation of key brain regions seems to be a major contributor to anxiety. And, in turn, vital brain regions becoming unresponsive and inflexible is believed to be a fundamental element of depressive disorders. Why do these regions become unresponsive? Possibly because they’re overworked, exhausted, by the effects of stress. This would explain why anxiety and depression regularly occur together. © 2019 Guardian News & Media Limited

Keyword: Depression; Stress
Link ID: 26701 - Posted: 10.15.2019

Madeline K. Sofia Carine Chen-McLaughlin smoked for more than 40 years. She didn't want to be a smoker. She'd tried to stop literally dozens of times over the decades. But she always came back. Smoking was "one of my oldest, dearest friends," she said of her habit. "To not have that relationship was very, very scary." Then she heard about a clinical trial to treat nicotine addiction with something a little unusual: magic mushrooms. Well, not actual magic mushrooms, but a little pill of a drug called psilocybin. It's the ingredient in mushrooms that gives people hallucinogenic visions. New research shows that psilocybin may be an effective treatment for diseases like depression and addiction. While the work is still in its early stages, there are signs that psilocybin might help addicts shake the habit by causing the brain to talk with itself in different ways. "These brain changes lead to, often times, a sense of unity," says Matthew Johnson, an experimental psychologist at Johns Hopkins University. It all may sound a little "woo-woo," he admits, but it seems to be working. Early results suggest that psilocybin, coupled with therapy, may be far more effective than other treatments for smoking, such as the nicotine patch. Magic mushrooms have been used by indigenous communities for thousands of years, and research on psilocybin isn't all that new, either. Work began in the 1950s and 1960s. But studies involving it and other psychedelics dropped off following the passage of the Controlled Substance Act in 1970, which outlawed hallucinogens and other drugs. "The medical applications became, really, a casualty of a political war," Johnson says. © 2019 npr

Keyword: Drug Abuse
Link ID: 26700 - Posted: 10.15.2019

By Katie Thomas and Sheila Kaplan In 2009, not long after Dr. Margaret Hamburg became commissioner of the Food and Drug Administration, a package arrived at her home. Inside was a clunky device called an e-cigarette. “It was my first exposure to this emerging, new technology,” Dr. Hamburg recalled. The package was sent by an antismoking activist as a warning about a product that was taking off in the United States. But over the next decade, the federal government — across the span of two presidential administrations — allowed the rise of a largely unregulated industry that may be addicting a new generation to nicotine. E-cigarettes and vaping devices, with $7 billion in annual sales, have become a part of daily life for millions of Americans. Youth use has skyrocketed with the proliferation of flavors targeting teenagers, such as Bazooka Joe Bubble Gum and Zombie Blood. And nearly 1,300 people have been sickened by mysterious vaping-related lung injuries this year. Yet the agency has not vetted the vast majority of vaping devices or flavored liquids for safety. In dozens of interviews, federal officials and public health experts described a lost decade of inaction, blaming an intense lobbying effort by the e-cigarette and tobacco industries, fears of a political backlash in tobacco-friendly states, bureaucratic delays, and a late reprieve by an F.D.A. commissioner who had previously served on the board of a chain of vaping lounges. “The minute you saw cotton candy flavors — come on,” said Dr. Thomas R. Frieden, the former director of the Centers for Disease Control and Prevention, who had warned since 2013 of the harms to adolescents. “Everything that could have been done should have been done to get them off the market.” © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26699 - Posted: 10.14.2019

Heidi Ledford Until a few months ago, pulmonologist Sean Callahan didn’t typically ask his patients if they vaped. He thought that e-cigarettes might help smokers wean themselves off cigarettes, and that the risks of vaping would probably take years to become clear. The emergence of a mysterious, sometimes lethal, lung injury associated with vaping has changed his mind. Callahan works at the University of Utah Health in Salt Lake City, which has treated about 20 victims of the outbreak. “It was surprising: the overwhelming number of them — and how young they were,” he says. Researchers and physicians alike were caught unprepared by the illness, which has now sickened about 1,300 US vapers and killed 26. Scientists are scrambling to find out why, and to save other vapers from the same fate. “Everything is rapidly evolving,” says Brandon Larsen, a pulmonary pathologist at the Mayo Clinic in Phoenix, Arizona. “I could tell you something today and next week it could be totally wrong.” A paper1 published by Larsen and his colleagues in the New England Journal of Medicine on 2 October undercut a popular theory behind the outbreak — and underscored how far researchers still have to go to pinpoint its cause. Many of those sickened in the outbreak had vaped cartridges containing tetrahydrocannabinol (THC) — the active ingredient in marijuana — that was diluted with oily chemicals. Larsen’s study is the largest analysis to date of lung tissue taken from sickened vapers. The scientists searched for evidence of lipoid pneumonia, a condition that arises when oil enters the lungs. It is marked by lipid found in lung tissue and also in cells called macrophages, which normally sweep up debris in the lungs. But Larsen and his colleagues did not find substantial lipid droplets in any of their samples from 17 patients. Instead, their findings point to general lung damage and inflammation caused by exposure to toxic chemicals. © 2019 Springer Nature Limited

Keyword: Drug Abuse
Link ID: 26698 - Posted: 10.14.2019

Sandra G. Boodman The July day wasn’t too steamy — a rarity in Madison, Ala. — and her toddler’s physical therapy session wasn’t scheduled for another hour, so Jeannette Vega thought she’d take 26-month-old Tiana outside to play in their yard. Immediately, she was struck by her younger daughter’s difficulty climbing up the sturdy low-slung plastic slide, something Tiana had been able to do with ease only a week earlier. To distract her, Jeannette opened the door of the family’s truck. “Come on, let’s get in and buckle up,” she remembers saying. Tiana took particular delight in clambering into her car seat and fastening her seat belt. Not this time. The little girl seemed rooted to the ground, impervious to her mother's encouragement. "It wasn't that she wouldn't [comply]," Jeannette recalled of the 2015 incident. "I could tell she just couldn't." Later that afternoon, she mentioned Tiana's difficulties to the physical therapist who had been working with the little girl for more than a year to try to overcome her significant, unexplained developmental delays. “This isn’t normal, to regress after so many months of therapy,” Jeannette, now 37, remembers the therapist telling her. She mentioned a disorder Jeannette had never heard of and suggested it might be the cause. Jeannette did a quick search, dismissed the possibility and said she “forgot about it.” But the first anguished words she blurted out nearly a half-year later on that shattering day in the specialist’s office when she learned what was wrong, was that the therapist had been right.

Keyword: Autism
Link ID: 26697 - Posted: 10.14.2019

By Aaron E. Carroll There’s a decent chance you’ll be reading about diet soda studies until the day you die. (The odds are exceedingly good it won’t be the soda that kills you.) The latest batch of news reports came last month, based on another study linking diet soda to an increased risk of death. As usual, the study (and some of the articles) lacked some important context and caused more worry than was warranted. There are specific reasons that this cycle is unlikely to end. 1. If it’s artificial, it must be bad. People suspect, and not always incorrectly, that putting things created in a lab into their bodies cannot be good. People worry about genetically modified organisms, and monosodium glutamate and, yes, artificial sweeteners because they sound scary. But everything is a chemical, including dihydrogen monoxide (that’s another way of saying water). These are just words we use to describe ingredients. Some ingredients occur naturally, and some are coaxed into existence. That doesn’t inherently make one better than another. In fact, I’ve argued that research supports consuming artificial sweeteners over added sugars. (The latest study concludes the opposite.) 2. Soda is an easy target In a health-conscious era, soda has become almost stigmatized in some circles (and sales have fallen as a result). It’s true that no one “needs” soda. There are a million varieties, and almost none taste like anything in nature. Some, like Dr Pepper, defy description. But there are many things we eat and drink that we don’t “need.” We don’t need ice cream or pie, but for a lot of people, life would be less enjoyable without those things. None of this should be taken as a license to drink cases of soda a week. A lack of evidence of danger at normal amounts doesn’t mean that consuming any one thing is huge amounts is a good idea. Moderation still matters. © 2019 The New York Times Company

Keyword: Obesity
Link ID: 26696 - Posted: 10.14.2019

By Emily Willingham Most of us could use more sleep. We feel it in our urge for an extra cup of coffee and in a slipping cognitive grasp as a busy day grinds on. And sleep has been strongly tied to our thinking, sharpening it when we get enough and blunting it when we get too little. What produces these effects are familiar to neuroscientists: external light and dark signals that help set our daily, or circadian, rhythms, “clock” genes that act as internal timekeepers, and neurons that signal to one another through connections called synapses. But how these factors interact to freshen a brain once we do sleep has remained enigmatic. Findings published on October 10 in two papers in Science place synapses at center stage. These nodes of neuronal communication, researchers show, are where internal preparations for sleep and the effects of our sleep-related behaviors converge. Cellular timekeepers rhythmically prep areas around the synapses in anticipation of building synaptic proteins during slumber. But the new findings indicate neurons don’t end up building these critical proteins in the absence of sleep. Advertisement The results suggest the brain is “getting prepared for an event, but it doesn’t mean you actually follow through on doing it,” says Robert Greene, a neuroscientist at the University of Texas Southwestern Medical Center, who was not involved in the study. Greene calls the studies “fascinating,” saying they confirm a “long suspected” connection between internal timekeeping and sleep behaviors. © 2019 Scientific American

Keyword: Sleep
Link ID: 26695 - Posted: 10.11.2019

By Denise Grady The outbreak of lung illnesses linked to vaping grew by more than 200 cases in a week, now totaling 1,299, the Centers for Disease Control and Prevention reported on Thursday. Twenty-nine people have died from vaping-related illnesses, health officials said. The figures mean that 219 new cases and seven new deaths were reported. Cases have occurred in 49 states, the District of Columbia and the United States Virgin Islands. A 17-year-old boy died in the Bronx last week, the youngest death so far linked to vaping. Utah and Massachusetts officials confirmed their states’ first vaping deaths this week. Indiana health officials announced late Thursday afternoon that two more people had died. The ages of those who died range from 17 years to 75 years, with a median of 49. The exact cause of the illness is still unknown. Many of those who became ill had vaped THC, some had used both THC and nicotine, and others report vaping only nicotine. Federal and state health authorities are testing vaping materials and studying tissue samples from patients in an effort to find the cause of the outbreak. They are particularly concerned about the huge amount of illicit THC products in circulation, which contain unknown mixtures of solvents, diluting agents and flavorings that may be toxic to the lungs. The United States Army said it was treating two soldiers for vaping-related illness. The Army did not say what products the two soldiers had been using, according to an earlier report in The Wall Street Journal. The military has banned e-cigarettes from the exchanges on bases. © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26694 - Posted: 10.11.2019

Allison Aubrey There's fresh evidence that eating a healthy diet, one that includes plenty of fruits and vegetables and limits highly processed foods, can help reduce symptoms of depression. A randomized controlled trial published in the journal PLOS ONE finds that symptoms of depression dropped significantly among a group of young adults after they followed a Mediterranean-style pattern of eating for three weeks. Participants saw their depression "score" fall from the "moderate" range down to the "normal" range, and they reported lower levels of anxiety and stress too. Alternatively, the depression scores among the control group of participants — who didn't change their diets — didn't budge. These participants continued to eat a diet higher in refined carbohydrates, processed foods and sugary foods and beverages. Their depression scores remained in the "moderate severity" range. "We were quite surprised by the findings," researcher Heather Francis, a lecturer in clinical neuropsychology at Macquarie University in Sydney, Australia, told NPR via email. "I think the next step is to demonstrate the physiological mechanism underlying how diet can improve depression symptoms," Francis said. In this study, participants in the "healthy eating" arm of the study ate about six more servings of fruits and vegetables per week, compared with the control group. Participants "who had a greater increase in fruit and vegetable intake showed the greatest improvement in depression symptoms," Francis said. © 2019 npr

Keyword: Depression; Obesity
Link ID: 26693 - Posted: 10.11.2019

Between 1999 and 2017, the United States experienced a 10-fold increase in the number of people who died from overdoses of Valium and other benzodiazepines. For years, scientists thought that these powerful sedatives, which are used to treat anxiety, muscle spasms, and sleeping disorders, worked alone to calm nerves. Now, in an article published in Science, researchers from the National Institutes of Health show that this view of the drugs and the neural circuits they affect may have to change. In a study of mice, scientists discovered that both may need the assistance of a ‘sticky’ gene, named after a mythological figure, called Shisa7. “We found that Shisa7 plays a critical role in the regulation of inhibitory neural circuits and the sedative effects some benzodiazepines have on circuit activity,” said Wei Lu, Ph.D., a Stadtman Investigator at NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope the results will help researchers design more effective treatments for a variety of neurological and neuropsychiatric disorders that are caused by problems with these circuits.” Dr. Lu’s lab studies the genes and molecules used to control synapses; the trillions of communications points made between neurons throughout the nervous system. In this study, his team worked with researchers led by Chris J. McBain, Ph.D., senior investigator at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), to look at synapses that rely on the neurotransmitter gamma-aminobutyric acid (GABA) to calm nerves. Communication at these synapses happens when one neuron fires off packets of GABA molecules that are then quickly detected by proteins called GABA type A (GABAA) receptors on neighboring neurons.

Keyword: Drug Abuse; Stress
Link ID: 26692 - Posted: 10.11.2019

Will Stone & Allison Aubrey There's no doubt that opioids have been massively overprescribed in U.S. In the haste to address the epidemic, there's been pressure on doctors to reduce prescriptions of these drugs — and in fact prescriptions are declining. But along the way, some chronic pain patients have been forced to rapidly taper or discontinue the drugs altogether. Now, the U.S. Department of Health and Human Services has a new message for doctors: Abrupt changes to a patient's opioid prescription could harm them. On Thursday, the agency issued new guidelines for physicians on how best to manage opioid prescriptions. They recommend a deliberate approach to lowering doses for chronic pain patients who have been on long-term opioid therapy. "It must be done slowly and carefully," says Adm. Brett P. Giroir, MD, assistant secretary for health for HHS. "If opioids are going to be reduced in a chronic patient it really needs to be done in a patient-centered, compassionate, guided way." This is a course correction of sorts. In 2016, the Centers for Disease Control and Prevention issued prescribing guidelines. Those highlighted the risks of addiction and overdose and encouraged providers to lower doses when possible. In response, many doctors began to limit their pain pill prescriptions, and in some cases cut patients off. These guidelines led to rigid rules in some cases. Giroir says it's concerning that some clinicians, policymakers, and health systems are "interpreting guidelines as mandates." © 2019 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 26691 - Posted: 10.11.2019

Jef Akst In the past few years, a number of high-profile studies have linked parental age at birth, and paternal age in particular, with a child’s autism risk. Walid Yassin, a neuropsychiatric researcher at the University of Tokyo, wanted to know if having older parents correlated with characteristics of the brain that have been linked to autism. When Yassin and his colleagues examined the brain scans of 39 adult males with high-functioning autism spectrum disorder (ASD) and of 37 typically developing males, they found that paternal age correlated with characteristics of the white matter in regions of the brain responsible for social interactions in analyses of all 76 individuals. Specifically, in the men with older fathers, these areas had higher radial diffusivity, a measure of water diffusing toward the axonal membrane instead of along the axon, suggesting damage to nerve cells’ myelin sheaths, says Yassin. “And such difference in radial diffusivity has been previously reported in ASD.” Magdalena Janecka, an epidemiologist who specializes in autism at the Icahn School of Medicine at Mount Sinai in New York, applauds the study’s focus on the brain. “We have a lot of epidemiological associations . . . but what [underlies them] is still very much underexplored,” she says. “The authors did a great job at exploring the mechanism that could connect the two.” But Janecka adds that the results can’t distinguish whether the link between age and autism is due to an accumulation of mutations in the sperm of older men, or if men who choose to have children later in life are enriched for certain traits associated with autism. “Is the effect we’re observing due to age or is it due to some underlying propensity of men who delay fatherhood?” she asks. © 1986–2019 The Scientist.

Keyword: Autism; Epigenetics
Link ID: 26690 - Posted: 10.11.2019

Bianca Nogrady As droughts go, the one plaguing the antidepressant drug development landscape for the past few decades has been noteworthy. Since the advent of serotonin and norepinephrine reuptake inhibitors in the 1980s and 1990s, there has been a dearth of new pharmacological therapies for mood disorders, says psychiatrist Samantha Meltzer-Brody, director of the University of North Carolina’s Perinatal Psychiatry Program. “The same medications largely that were there when I went to medical school a long time ago were still the ones we’ve been using.” Given this state of affairs, Meltzer-Brody says she had the “most modest” of expectations a few years ago when she got involved in the first clinical trial testing a new drug, SAGE-547, for postpartum depression. Developed by Massachusetts-based Sage Therapeutics, SAGE-547 is a solution of allopregnanolone, a neuroactive metabolite of the sex hormone progesterone, which plays key roles in the female reproductive system. Progesterone and allopregnanolone levels peak during the third trimester of pregnancy, then crash immediately after delivery. Preclinical data suggested the drop in allopregnanolone could be a trigger for postpartum depression in some women. The company-funded trial involved administering SAGE-547 to a handful of patients with postpartum depression as an intravenous infusion over 48 hours. The response in the first patient treated with SAGE-547 was dramatic. From being withdrawn and depressed with no appetite before treatment, she began smiling, talking, eating, and interacting, Meltzer-Brody says. “After that first patient, we thought either that’s one heck of a placebo or maybe there’s a signal.” Three more patients were treated, with similar results. Known by the generic name brexanolone, the drug sped through Phase 2 and Phase 3 trials before being approved by the US Food and Drug Administration (FDA) on March 19. © 1986–2019 The Scientist

Keyword: Depression
Link ID: 26689 - Posted: 10.10.2019

By Gina Kolata A new drug, created to treat just one patient, has pushed the bounds of personalized medicine and has raised unexplored regulatory and ethical questions, scientists reported on Wednesday. The drug, described in the New England Journal of Medicine, is believed to be the first “custom” treatment for a genetic disease. It is called milasen, named after the only patient who will ever take it: Mila (mee-lah) Makovec, who lives with her mother, Julia Vitarello, in Longmont, Colo. Mila, 8, has a rapidly progressing neurological disorder that is fatal. Her symptoms started at age 3. Within a few years, she had gone from an agile, talkative child to one who was blind and unable to stand or hold up her head. She needed a feeding tube and experienced up to 30 seizures a day, each lasting one or two minutes. Ms. Vitarello learned in December 2016 that Mila had Batten’s disease. But the girl’s case was puzzling, doctors said. Batten’s disease is recessive — a patient must inherit two mutated versions of a gene, MFSD8, to develop the disease. Mila had one just mutated gene, and the other copy seemed normal. That should have been sufficient to prevent the disease. In March 2017, Dr. Timothy Yu and his colleagues at Boston Children’s Hospital discovered that the problem with the intact gene lay in an extraneous bit of DNA that had scrambled the manufacturing of an important protein. That gave Dr. Yu an idea: Why not make a custom piece of RNA to block the effects of the extraneous DNA? Developing such a drug would be expensive, but there were no other options. © 2019 The New York Times Company

Keyword: Epilepsy
Link ID: 26688 - Posted: 10.10.2019

Jessica Wright Delicate lines dance across a screen mounted on the wall of the operating room. Their peaks and valleys become pronounced, suddenly flatten into a straight line—and then return, stronger than before. These digital traces represent the buzz of neurons in 12-year-old Kevin Lightner, read by two thin electrodes that surgeons have inserted deep into his brain. Kevin, who has autism and has had seizures since he was 8 years old, lies uncharacteristically still in the center of the room, draped under a blue sheet, his tiger-print pajamas neatly folded on a nearby shelf. What’s happening in this room may be the last chance to bring Kevin’s seizures under control. An hour and a half ago, neurosurgeon Saadi Ghatan removed a roughly 2-inch by 1-inch piece of the top of Kevin’s skull. He replaced it with a rectangular metal device, carefully screwed into the newly exposed edges of bone. The implant, a “responsive neurostimulation device,” is now transmitting signals from the electrodes planted in Kevin’s thalamus. The surgeons’ hope is that the device will learn to recognize what kind of brain activity precedes Kevin’s seizures and discharge electrical pulses to prevent them—like a “defibrillator for the brain,” as Ghatan puts it. If it works, it could save Kevin’s life. Ghatan projects the device’s readout to the screen by gently placing a black wand over the exposed metal in Kevin’s skull. The signal on the screen is surprisingly strong, given that it stems from the thalamus, a brain region that reveals its activity only weakly, if at all—and so is rarely the choice for monitoring seizures. © 1986–2019 The Scientist.

Keyword: Autism; Epilepsy
Link ID: 26687 - Posted: 10.10.2019

By Elizabeth Preston Heidi the octopus is sleeping. Her body is still, eight arms tucked neatly away. But her skin is restless. She turns from ghostly white to yellow, flashes deep red, then goes mottled green and bumpy like plant life. Her muscles clench and relax, sending a tendril of arm loose. From the outside, the cephalopod looks like a person twitching and muttering during a dream, or like a napping dog chasing dream-squirrels. “If she is dreaming, this is a dramatic moment,” David Scheel, an octopus researcher at Alaska Pacific University, said in the documentary. Heidi was living in a tank in his living room when her snooze was captured by the film crew, and he speculates that she is imagining catching and eating a crab. But an octopus is almost nothing like a person. So how much can anyone really say with accuracy about what Heidi was doing? When our two branches of the animal family tree diverged, backbones hadn’t been invented. Yet octopuses, cuttlefish and squid, on their own evolutionary path, developed impressive intelligence. They came up with their own way to build big brains. Much of an octopus’s brain is spread throughout its body, especially its arms. It makes sense to be cautious when we guess what’s going on in these animals’ minds. Looking at a behavior like Heidi’s is “a bit like going to a crime scene,” said Nicola Clayton, a psychologist at the University of Cambridge who studies comparative cognition. “You’ve got some evidence in front of you, but you’d need to know so much more to understand better what’s causing the behavior.” It’s only conjecture to say the octopus is dreaming without more data, she said. Does the sequence of Heidi’s color changes match an experience she had while awake? Dreaming in humans mostly happens during rapid-eye movement, or R.E.M., sleep. Could we observe something similar in octopuses? Dr. Clayton points out that a human sleeper might flush red because she’s overheated. © 2019 The New York Times Company

Keyword: Sleep; Evolution
Link ID: 26686 - Posted: 10.09.2019

Ashley Yeager In March 2018, researchers reported evidence suggesting that adult humans do not generate new neurons in the hippocampus—the brain’s epicenter of learning and memory. The result contradicted two decades of work that said human adults actually do grow new neurons there, and revealed a need for new and better tools to study neurogenesis, Salk Institute President Fred Gage, who generated foundational evidence for adult human neurogenesis, told The Scientist at the time. Since that study was published, several other teams have used similar techniques—but have come to different conclusions, publishing evidence that adult humans do indeed grow new hippocampal neurons, even at the age of 99. Despite the equivocal results, Maura Boldrini, a neuroscientist at Columbia University, and a number of other neuroscientists tell The Scientist they think neurogenesis does occur in the adult human brain, bolstering learning and memory and possibly also our stress and emotional responses. Neurogenesis is “fundamentally important for the brain to react to all sorts of different insults and prevent neurological and psychiatric problems,” Boldrini says. Because of its role in brain function, researchers want to learn how neurogenesis works to potentially use it to treat brain trauma, neurodegeneration, psychiatric disorders, such as depression, and possibly even the ill effects of aging. The growth of new neurons is well studied in newborn and adult animals, especially rodents. There’s prolific neurogenesis as the brain develops, which then drops off and plateaus in adulthood, only occurring in particular areas of the brain. Examinations of human postmortem tissue suggest that the process is similar in people, based on antibody markers that label neural progenitors and young neurons. But those signals can be hard to detect in preserved cells, and the gap in time between the death of a donor and when her tissue is fixed and analyzed can affect the reliability of the markers, scientists say, which might explain the disparities in findings between different studies. © 1986–2019 The Scientist

Keyword: Neurogenesis
Link ID: 26685 - Posted: 10.09.2019

Allison Aubrey The condition strikes young children. It can start with run-of-the-mill virus symptoms, like fever or sniffles. But, then the kids lose control of their limbs, may have trouble swallowing or breathing, or even end up paralyzed. This terrifying experience happened to more than 570 families since 2014, whose children were struck with an illness called acute flaccid myelitis, or AFM. "It was really scary," says Susan Coyne, the mother of a son, Evan Mazanec, who developed AFM back in 2014 when he was 7 years old. "When this first started, no one really knew what it was," she says. It came on quickly, starting with a fever and an ear infection. Coyne says the limb weakness and paralysis began several days later — just as Evan was getting over the fever. He lost control of his arms and legs. "He couldn't move them, he couldn't lift them, he couldn't walk," Coyne says. He spent a year and a half in intensive rehab. He had to learn to walk and move his arms again. "It set him back years," Coyne says. Scientists have struggled to understand what causes this rare childhood disease. Now, one theory is gaining ground. A paper published Monday in the journal Pediatrics finds the condition may be triggered by a virus. The disease follows a pattern: Scientists have documented outbreaks every other year, beginning in 2014, and again in 2016 and 2018. Last year, there were 233 cases in the U.S. It strikes young kids, average age of 6. And, it can lead to long-term paralysis. © 2019 npr

Keyword: Movement Disorders; Development of the Brain
Link ID: 26684 - Posted: 10.09.2019