By Brian Platzer Three years ago I wrote an essay for Well about the chronic dizziness that had devastated my life. In response, I received thousands of letters, calls, tweets, emails and messages from Times readers who were grateful to see a version of their own story made public. Their symptoms varied. While some experienced a constant disequilibrium and brain fog that were similar to mine, others had become accustomed to a pattern of short periods of relative health alternating with longer periods of vertigo. Most of them, like me, felt that family and friends often didn’t understand how dizziness could be so debilitating. They told me that the combination of the loneliness and feelings of uselessness that come from an inability to work or spend time with family led to despair and depression. And, most commonly, they felt that the medical system made them feel responsible for their own suffering. “Doctors began to suggest that anxiety or depression were the cause of my symptoms,” a young woman from Connecticut wrote. “I eventually gave up on the quest for answers, as their attitudes added stress to an already stressful reality.” “Have been to so many doctors that keep saying, ‘It’s all in your head. There’s nothing wrong with you,’” wrote an older woman from Ohio. “Mostly been told there is nothing they can find,” wrote a middle-aged woman from Illinois. Her doctor told her it was probably just depression and anxiety. Dizziness is among the most common reasons people visit their doctor in the United States. When patients first experience prolonged dizziness, they may go to an emergency room or to see their primary care physician. That’s what I did. And I heard what most patients hear: “People get dizzy for all sorts of reasons, and it should resolve itself soon.” It’s true that dizziness often is a temporary symptom. The most common causes of dizziness are benign paroxysmal positional vertigo (caused by displaced pieces of small bone-like calcium in the inner ear), and vestibular neuritis (dizziness attributed to a viral infection or tiny stroke of the vestibular nerve), both of which typically last only weeks or months. © 2020 The New York Times Company

Keyword: Miscellaneous
Link ID: 27036 - Posted: 02.13.2020

By Veronique Greenwood When you look at a reconstruction of the skull and brain of Neoepiblema acreensis, an extinct rodent, it’s hard to shake the feeling that something’s not quite right. Huddled at the back of the cavernous skull, the brain of the South American giant rodent looks really, really small. By some estimates, it was around three to five times smaller than scientists would expect from the animal’s estimated body weight of about 180 pounds, and from comparisons to modern rodents. In fact, 10 million years ago the animal may have been running around with a brain weighing half as much as a mandarin orange, according to a paper published Wednesday in Biology Letters. The glory days of rodents, in terms of the animals’ size, were quite a long time ago, said Leonardo Kerber, a paleontologist at Universidade Federal de Santa Maria in Brazil and an author of the new study. Today rodents are generally dainty, with the exception of larger creatures like the capybara that can weigh as much as 150 pounds. But when it comes to relative brain size, N. acreensis, represented in this study by a fossil skull unearthed in the 1990s in the Brazilian Amazon, seems to be an extreme. The researchers used an equation that relates the body and brain weight of modern South American rodents to get a ballpark estimate for N. acreensis, then compared that with the brain weight implied by the volume of the cavity in the skull. The first method predicted a brain weighing about 4 ounces, but the volume suggested a dinky 1.7 ounces. Other calculations, used to compare the expected ratio of the rodent’s brain and body size with the actual fossil, suggested that N. acreensis’ brain was three to five times smaller than one would expect. © 2020 The New York Times Company

Keyword: Evolution; Brain imaging
Link ID: 27035 - Posted: 02.13.2020

Jon Hamilton Scientists have taken a small step toward personalizing treatment for depression. A study of more than 300 people with major depression found that brain wave patterns predicted which ones were most likely to respond to the drug sertraline (Zoloft), a team reported Monday in the journal Nature Biotechnology. If the approach pans out, it could offer better care for the millions of people in the U.S. with major depression. "This is definitely a step forward," says Michele Ferrante, who directs the computational psychiatry and computational neuroscience programs at the National Institute of Mental Health. He was not a part of the study. Right now, "one of our great frustrations is that when a patient comes in with depression we have very little idea what the right treatment for them is," says Dr. Amit Etkin, an author of the study and a professor of psychiatry at Stanford University. "Essentially, the medications are chosen by trial and error." Etkin is also the CEO of Alto Neuroscience, a Stanford-backed start-up developing computer-based approaches to diagnosing mental illness and selecting treatments. In the study, researchers used artificial intelligence to analyze the brainwave patterns in more than 300 patients who'd been diagnosed with major depression. Then they looked to see what happened when these same patients started treatment with sertraline. And one pattern of electrical activity seemed to predict how well a patient would do. "If the person scores particularly high on that, the recommendation would be to get sertraline," Etkin says. © 2020 npr

Keyword: Depression
Link ID: 27034 - Posted: 02.11.2020

Rachel Patton McCord, Rebecca A. Prosser Have you ever slipped when trying to avoid sugar, quit smoking, or break another habit or addiction? Usually that one piece of cake or one cigarette won’t ruin your whole plan, but for people struggling with cocaine addiction, one slip can undo months of hard work. Cocaine consumption is increasing, with 2.2 million people in the U.S. admitting to recent cocaine use in 2017. In 2014, the National Survey on Drug Use and Health estimated that nearly 1 million Americans were addicted to cocaine. The effect of cocaine on the brain and body is so powerful that, even after state-of-the-art treatments, many people trying to quit cocaine relapse within a year. What if cocaine could be made less euphoric, so that a single use by a recovering addict doesn’t result in a full-blown relapse? Scientists at the Mayo Clinic recently published progress toward making this idea a reality – a gene therapy that would treat cocaine addiction by making cocaine less rewarding. We are a molecular biologist and a neurobiologist who are interested in understanding and treating human disease, including neurological disorders such as cocaine addiction. As University of Tennessee faculty members leading basic biomedical research, we have worked for years on how genes are turned on and off in people and the effects of cocaine on mice, respectively. So, we were excited to see a promising convergence of novel gene therapy and cocaine addiction therapy. Beginning more than 20 years ago, scientists have worked to engineer a new version of a human protein that could break down cocaine so quickly that it doesn’t produce an addictive high. We all have the normal human protein BChE that helps regulate neurotransmitters, and which can slowly break down cocaine. Targeted mutations in BChE can turn it into a super-CocH – a protein that can quickly break down cocaine. When this CocH is injected into the bloodstream, it breaks down cocaine very fast – before the user can experience the pleasurable effects – so a dose of cocaine is less rewarding. Being less rewarding means it is easier to stop using cocaine. © 2010–2020, The Conversation US, Inc.

Keyword: Drug Abuse; Neuroimmunology
Link ID: 27033 - Posted: 02.11.2020

Catherine Offord The first time Kees van Heeringen met Valerie, the 16-year-old girl had just jumped from a bridge. It was the 1980s and van Heeringen was working as a trainee psychiatrist at the physical rehabilitation unit at Ghent University Hospital in Belgium. As he got to know Valerie, who’d lost both legs in the jump and spent several months at the hospital, he pieced together the events leading up to the moment the teenager tried to end her life, including stressful interactions with people around her and a steady accumulation of depression symptoms. Van Heeringen, who would later describe the experience in his 2018 book The Neuroscience of Suicidal Behavior, says Valerie’s story left a permanent impression on him. “I found it very difficult to understand,” he tells The Scientist. He asked himself why anyone would do “such a horrible thing,” he recalls. “It was the first stimulus for me to start studying suicidal behavior.” In 1996, van Heeringen founded the Ghent University Unit for Suicide Research. He’s been its director ever since, helping to drive scientific research into the many questions he and others have about suicide. Many of the answers remain as elusive as they seemed that day in the rehabilitation unit. Suicide rates are currently climbing in the US and many other countries, and suicide is now the second leading cause of death among young people globally, after traffic accidents. The World Health Organization recently estimated that, worldwide, one person ends their own life every 40 seconds. © 1986–2020 The Scientist.

Keyword: Depression
Link ID: 27032 - Posted: 02.11.2020

By Randi Hutter Epstein It was a staple of medical thinking dating to the 1910s that stress was the body’s alarm system, switching on only when terrible things happened, often leaving a person with an either-or choice: fight or flight. The neuroscientist Bruce S. McEwen trailblazed a new way of thinking about stress. Beginning in the 1960s, he redefined it as the body’s way of constantly monitoring daily challenges and adapting to them. Dr. McEwen, who died on Jan. 2 at 81, described three forms of stress: good stress — a response to an immediate challenge with a burst of energy that focuses the mind; transient stress — a response to daily frustrations that resolve quickly; and chronic stress — a response to a toxic, unrelenting barrage of challenges that eventually breaks down the body. It was Dr. McEwen’s research into chronic stress that proved groundbreaking. He and his research team at Rockefeller University in Manhattan discovered in 1968 that stress hormones had a profound effect on the brain. In studies using animals (five rats in the initial one), Dr. McEwen and his colleagues demonstrated that toxic stress atrophied neurons near the hippocampus, the brain’s memory and learning center, while expanding neurons near the amygdala, an area known for vigilance toward threats. Describing the burden of continuing stress, he coined the term “allostatic load” (derived from allostasis, the process by which the body seeks to regain stability, or homeostasis, in response to stressors). Their discoveries, first published in the journal Nature in 1968, ignited a new field of research, one that would reveal how stress hormones and other mediators change the brain, alter behavior and impact health, in some cases accelerating disease. At the time, only a few scientists were asserting that the brain remains malleable throughout life, challenging the dogma that the brain stops changing after adolescence. Dr. McEwen’s studies documenting how hormones alter neurons lent credence to this emerging idea. © 2020 The New York Times Company

Keyword: Stress; Hormones & Behavior
Link ID: 27031 - Posted: 02.11.2020

By Perri Klass, M.D. Whenever I write about attention deficit hyperactivity disorder — whether I’m writing generally about the struggles facing these children and their families or dealing more specifically with medications — I know that some readers will write in to say that A.D.H.D. is not a real disorder. They say that the rising numbers of children taking stimulant medication to treat attentional problems are all victims, sometimes of modern society and its unfair expectations, sometimes of doctors, and most often of the rapacious pharmaceutical industry. I do believe that A.D.H.D. is a valid diagnosis, though a diagnosis that has to be made with care, and I believe that some children struggle with it mightily. Although medication should be neither the first nor the only treatment used, some children find that the stimulants significantly change their educational experiences, and their lives, for the better. Dr. Mark Bertin, a developmental pediatrician in Pleasantville, N.Y., who is the author of “Mindful Parenting for A.D.H.D.,” said, “On a practical level, we know that correctly diagnosed A.D.H.D. is real, and we know that when they’re used properly, medications can be both safe and effective.” The choice to use medications can be a difficult one for families, he said, and is made even more difficult by “the public perception that they’re not safe, or that they fundamentally change kids.” He worries, he says, that marketing is really effective, and wants to keep it “at arm’s length,” far away from his own clinical decisions, not allowing drug reps in the office, not accepting gifts — but acknowledging, all the same, that it’s probably not possible to avoid the effects of marketing entirely. Still, he said, when it comes to stimulants, “the idea that we’re only using them because of the pharmaceutical industry is totally off base,” and can make it much harder to talk with parents about the potential benefits — and the potential problems — of treating a particular child with a particular medication. “When it comes to A.D.H.D. in particular, it’s a hard enough thing for families to be dealing with without all the fear and judgment added on.” © 2020 The New York Times Company

Keyword: ADHD; Drug Abuse
Link ID: 27030 - Posted: 02.10.2020

By Everyday Einstein Sabrina Stierwalt People from all cultures laugh, although we may laugh at different things. (I once interviewed for a job in the Netherlands and none of my jokes landed. I didn’t get that job.) Apes also laugh. We know this because there are scientists whose job it is to tickle animals. I’m not even kidding. What a life! Advertisement Humans start laughing as early as 3 months into life, even before we can speak. This is true even for babies who are deaf or blind. Peekaboo, it turns out, is particularly a global crowd-pleaser. And we know this because studying baby laughter is an actual job, too. So, the ubiquitous nature of laughter suggests that it must serve a purpose, but what? Why do we laugh? Here are a few scientific reasons Laughter clearly serves a social function. It is a way for us to signal to another person that we wish to connect with them. In fact, in a study of thousands of examples of laughter, the speakers in a conversation were found to be 46 percent more likely to laugh than the listeners. We’re also 30 times more likely to laugh in a group. Young children between the ages of 2.5 and 4 were found to be eight times more likely to laugh at a cartoon when they watched it with another child even though they were just as likely to report that the cartoon was funny whether alone or not. Evolutionarily speaking, this signal of connection likely played an important role in survival. Upon meeting a stranger, we want to know: What are your intentions with me? And who else are you aligned with? © 2020 Scientific American

Keyword: Emotions
Link ID: 27029 - Posted: 02.10.2020

By Jane E. Brody Climate change is not the only source of dire projections for the coming decade. Perhaps just as terrifying from both a health and an economic perspective is a predicted continued rise in obesity, including severe obesity, among American adults. A prestigious team of medical scientists has projected that by 2030, nearly one in two adults will be obese, and nearly one in four will be severely obese. The estimates are thought to be particularly reliable, as the team corrected for current underestimates of weight given by individuals in national surveys. In as many as 29 states, the prevalence of obesity will exceed 50 percent, with no state having less than 35 percent of residents who are obese, they predicted. Likewise, the team projected, in 25 states the prevalence of severe obesity will be higher than one adult in four, and severe obesity will become the most common weight category among women, non-Hispanic black adults and low-income adults nationally. Given the role obesity plays in fostering many chronic, disabling and often fatal diseases, these are dire predictions indeed. Yet, as with climate change, the powers that be in this country are doing very little to head off the potentially disastrous results of expanding obesity, obesity specialists say. Well-intentioned efforts like limiting access to huge portions of sugar-sweetened soda, the scientists note, are effectively thwarted by well-heeled industries able to dwarf the impact of educational efforts by health departments that have minuscule budgets by comparison. With rare exceptions, the sugar and beverage industries have blocked nearly every attempt to add an excise tax to sugar-sweetened beverages. Claims that such a tax is regressive and unfairly targets low-income people is shortsighted, according to Zachary J. Ward, public health specialist at Harvard and the lead author of the new report, published in The New England Journal of Medicine in December. © 2020 The New York Times Company

Keyword: Obesity
Link ID: 27028 - Posted: 02.10.2020

By Chris Woolston Sometimes it takes multitudes to reveal scientific truth. Researchers followed more than 7,000 subjects to show that a Mediterranean diet can lower the risk of heart disease. And the Women’s Health Initiative enlisted more than 160,000 women to show, among other findings, that postmenopausal hormone therapy put women at risk of breast cancer and stroke. But meaningful, scientifically valid insights don’t always have to come from studies of large groups. A growing number of researchers around the world are taking a singular approach to pain, nutrition, psychology and other highly personal health issues. Instead of looking for trends in many people, they’re designing studies for one person at a time. A study of one person — also called an N of 1 trial — can uncover subtle, important results that would be lost in a large-scale study, says geneticist Nicholas Schork of the Translational Genomics Research Institute in Phoenix. The results, he says, can be combined to provide insights for the population at large. But with N of 1 studies, the individual matters above all. “People differ at fundamental levels,” says Schork, who discussed the potential of N of 1 studies in a 2017 issue of the Annual Review of Nutrition. And the only way to understand individuals is to study them. Case studies of individuals in odd circumstances have a long history in medical literature. But the concept of a clinical medicine N of 1 study gathering the same level of information as a large study goes back to an article published in the New England Journal of Medicine in 1986. Hundreds of N of 1 studies have been published since then, and the approach is gaining momentum, says Suzanne McDonald, N of 1 research coordinator at the University of Queensland in Brisbane, Australia.

Keyword: Genes & Behavior; Schizophrenia
Link ID: 27027 - Posted: 02.10.2020

By Laura Sanders Immune cells in the brain chew up memories, a new study in mice shows. The finding, published in the Feb. 7 Science, points to a completely new way that the brain forgets, says neuroscientist Paul Frankland of the Hospital for Sick Children Research Institute in Toronto, who wasn’t involved in the study. That may sound like a bad thing, but forgetting is just as important as remembering. “The world constantly changes,” Frankland says, and getting rid of unimportant memories — such as a breakfast menu from two months ago — allows the brain to collect newer, more useful information. Exactly how the brain stores memories is still debated, but many scientists suspect that connections between large groups of nerve cells are important (SN: 1/24/18). Forgetting likely involves destroying or changing these large webs of precise connections, called synapses, other lines of research have suggested. The new result shows that microglia, immune cells that can clear debris from the brain, “do exactly that,” Frankland says. Microglia are master brain gardeners that trim extra synapses away early in life, says Yan Gu, a neuroscientist at Zhejiang University School of Medicine in Hangzhou, China. Because synapses have a big role in memory storage, “we started to wonder whether microglia may induce forgetting by eliminating synapses,” Gu says. Gu’s team first gave mice an unpleasant memory: mild foot shocks, delivered in a particular cage. Five days after the shocks, the mice would still freeze in fear when they were placed in the cage. But 35 days later, they had begun to forget and froze less often in the room. © Society for Science & the Public 2000–2020

Keyword: Learning & Memory; Neuroimmunology
Link ID: 27026 - Posted: 02.07.2020

Abby Olena Researchers have shown previously that excessive proliferation of the cells of the brain, which can cause macrocephaly, or large head size, is associated with autism. Now, the authors of a study published in Cell Stem Cell last week (January 30) have connected that overgrowth with replication stress, subsequent DNA damage, and dysfunction in neural progenitor cells derived from induced pluripotent stem cells from patients with autism spectrum disorder. “It is striking,” Bjoern Schwer, a molecular biologist at the University of California, San Francisco, who studies DNA repair and genomic stability in neural cells and did not participate in the study, writes in an email to The Scientist. “These are fascinating findings with many implications for autism spectrum disorder—and potentially for other neurodevelopmental disorders too.” In 2016, a group led by Schwer and Frederick Alt of Boston Children’s Hospital showed that mice have clusters of double-strand DNA breaks in the genomes of their neural progenitor cells. These hotspots are concentrated in neural-specific genes, which tend to be longer than genes expressed in other cell types and have also been associated with neurological diseases. Rusty Gage, a neuroscientist at the Salk institute, Meiyan Wang, a graduate student in the Gage lab, and their colleagues collaborated with Alt to explore whether or not these same damaged clusters would show up in the genomes of human neural progenitor cells. Wang went to the Alt lab to learn how to map genome-wide double-strand breaks. Then, she used the technique on several neural progenitor cell lines that had been previously derived in the Gage lab: three from patients with macrocephalic autism spectrum disorder and three from neurotypical controls. © 1986–2020 The Scientist

Keyword: Autism; Genes & Behavior
Link ID: 27025 - Posted: 02.07.2020

By Bernardo Kastrup At least since the Enlightenment, in the 18th century, one of the most central questions of human existence has been whether we have free will. In the late 20th century, some thought neuroscience had settled the question. However, as it has recently become clear, such was not the case. The elusive answer is nonetheless foundational to our moral codes, criminal justice system, religions and even to the very meaning of life itself—for if every event of life is merely the predictable outcome of mechanical laws, one may question the point of it all. But before we ask ourselves whether we have free will, we must understand what exactly we mean by it. A common and straightforward view is that, if our choices are predetermined, then we don’t have free will; otherwise we do. Yet, upon more careful reflection, this view proves surprisingly inappropriate. To see why, notice first that the prefix “pre” in “predetermined choice” is entirely redundant. Not only are all predetermined choices determined by definition, all determined choices can be regarded as predetermined as well: they always result from dispositions or necessities that precede them. Therefore, what we are really asking is simply whether our choices are determined. In this context, a free-willed choice would be an undetermined one. But what is an undetermined choice? It can only be a random one, for anything that isn’t fundamentally random reflects some underlying disposition or necessity that determines it. There is no semantic space between determinism and randomness that could accommodate choices that are neither. This is a simple but important point, for we often think—incoherently—of free-willed choices as neither determined nor random. © 2020 Scientific American

Keyword: Consciousness
Link ID: 27024 - Posted: 02.07.2020

Sarah O’Meara Xiaoming Zhou is a neurobiologist at East China Normal University in Shanghai. Here he speaks to Nature about his research into age-related hearing loss, and explains why he hopes that brain training could help to lessen declines in sensory perception generally, and so ward off neurodegenerative diseases. What is your current research focus? We want to better understand the neural basis for why a person’s hearing function declines as they grow older. For example, we have performed research to see whether we can reverse age-related changes to the auditory systems of rodents. We gave the animals a set of tasks, such as learning to discriminate between sounds of different frequencies or intensities. These exercises caused the rodents’ hearing to improve, and also promoted changes to the hippocampus, a part of the brain structure closely associated with learning and memory. The relationship with the hippocampus suggests that new kinds of brain training might help to attenuate our declines in perception and other brain functions, such as learning and memory, as we grow older — and so have the potential to stave off neurodegenerative diseases. How is ageing-related science developing in China? As has happened in the rest of the world, a rapidly ageing population has brought significant concern to policymakers. However, as far as I know, only a few neuroscience laboratories in China are specifically focused on learning more about the underlying mechanisms that cause changes in brain function as we age. This is despite the fact that such research could have a considerable impact on the welfare of older people in the future. © 2020 Springer Nature Limited

Keyword: Alzheimers
Link ID: 27023 - Posted: 02.07.2020

By Laura Sanders Injecting a swarm of nanoparticles into the blood of someone who has suffered a brain injury may one day help to limit the damage — if experimental results in mice can be translated to humans. In mice, these nanoparticles seemed to reduce dangerous swelling by distracting immune cells from rushing to an injured brain. The results, described online January 10 in the Annals of Neurology, hint that the inflammation-fighting nanoparticles might someday make powerful medicine, says John Kessler, a neurologist at Northwestern Medicine in Chicago. “All the data we have now suggest that they’re going to be safe, and they’re likely to work” for people, Kessler says. “But we don’t know that yet.” After an injury, tissue often swells as immune cells flock to the damage. Swelling of the brain can be dangerous because the brain is contained within the skull and “there’s no place to go,” Kessler says. The resulting pressure can be deadly. But nanoparticles might serve as an immune-cell distraction, the results in mice suggest. Two to three hours after a head injury, mice received injections of tiny biodegradable particles made of an FDA-approved polymer — the same sort that’s used in some dissolving sutures. Instead of rushing toward the brain, a certain type of immune cell called monocytes began turning their sights on these invaders. These monocytes engulfed the nanoparticles, and the cells and their cargo got packed off to the spleen for elimination, the researchers found. Because these nanoparticles are quickly taken out of circulation, the researchers injected the mice again one and two days later, in an effort to ease inflammation that might crop back up in the days after the injury. © Society for Science & the Public 2000–2020

Keyword: Brain Injury/Concussion
Link ID: 27022 - Posted: 02.05.2020

By Charles Zanor We all know people who say they have “no sense of direction,” and our tendency is almost always to minimize such claims rather than take them at full force. Yet for some people that description is literally true, and true in all circumstances: If they take a single wrong turn on an established route they often become totally lost. This happens even when they are just a few miles from where they live. Ellen Rose had been a patient of mine for years before I realized that she had this life-long learning disability. Advertisement I was made aware of it not long after I moved my psychology office from Agawam, Massachusetts to Suffield, Connecticut, just five miles away. I gave Ellen a fresh set of directions from the Springfield, Massachusetts area that took her south on Interstate 91 to Exit 47W, then across the Connecticut River to Rte 159 in Suffield. I thought it would pose no problem at all for her. A few minutes past her scheduled appointment time she called to say that she was lost. She had come south on Route 91 and had taken the correct exit, but she got confused and almost immediately hooked a right onto a road going directly north, bringing her back over the Massachusetts line to the town of Longmeadow. She knew this was wrong but did not know how to correct it, so I repeated the directions to get on 91 South and so on. Minutes passed, and then more minutes passed, and she called again to say that somehow she had driven by the exit she was supposed to take and was in Windsor, Connecticut. I kept her on the phone and guided her turn by turn to my office. Advertisement When I asked her why she hadn’t taken Exit 47W, she said that she saw it but it came up sooner than she expected so she kept going. This condition—developmental topographic disorientation—didn’t even have a formal name until 2009, when Giuseppe Iaria reported his first case in the journal Neuropsychologia. To understand DTD it is best to begin by saying that there are two main ways that successful travelers use to navigate their environment. © 2020 Scientific American,

Keyword: Learning & Memory; Development of the Brain
Link ID: 27021 - Posted: 02.05.2020

By Kelly Servick Since its launch in 2013, the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative has doled out about $1.3 billion in grants to develop tools that map and manipulate the brain. Until now, it has operated with no formal director. But last week, the National Institutes of Health (NIH), which manages the initiative and is a key funder, announced that neurobiologist John Ngai would take the helm starting in March. Ngai, whose lab at the University of California, Berkeley, focuses on the neural underpinnings of the sense of smell, has helped lead BRAIN-funded efforts to classify the brain’s dizzying array of cell types with RNA sequencing. Ngai told ScienceInsider about how the initiative is evolving and how he hopes to influence it. The interview has been edited for clarity and brevity. Q: Why is the BRAIN Initiative getting a director now? A: The initiative has been run day to day by a terrific team of senior program directors and staff with oversight from the 10 NIH institutes and centers that are involved in BRAIN. Walter Koroshetz [director of the National Institute of Neurological Disorders and Stroke] and Josh Gordon [director of the National Institute of Mental Health] have been overseeing the activities of BRAIN … kind of in addition to their “day jobs.” I think as enterprises emerge from their startup phase, which is typically the first 5 years, the question is how do you translate this into a sustainable enterprise, and yet maintain this cutting-edge innovation? … How do we leverage all the accomplishments that have been made, not just within BRAIN, but in molecular biology, in engineering, in chemistry and computer science, in data science. The initiative really will benefit from somebody thinking about this 24/7. © 2019 American Association for the Advancement of Science.

Keyword: Brain imaging; Chemical Senses (Smell & Taste)
Link ID: 27020 - Posted: 02.05.2020

Jon Hamilton Scientists have found a clue to how autism spectrum disorder disrupts the brain's information highways. The problem involves cells that help keep the traffic of signals moving smoothly through brain circuits, a team reported Monday in the journal Nature Neuroscience. The team found that in both mouse and human brains affected by autism, there's an abnormality in cells that produce a substance called myelin. That's a problem because myelin provides the "insulation" for brain circuits, allowing them to quickly and reliably carry electrical signals from one area to another. And having either too little or too much of this myelin coating can result in a wide range of neurological problems. For example, multiple sclerosis occurs when the myelin around nerve fibers is damaged. The results, which vary from person to person, can affect not only the signals that control muscles, but also the ones involved in learning and thinking. The finding could help explain why autism spectrum disorders include such a wide range of social and behavioral features, says Brady Maher, a lead investigator at the Lieber Institute for Brain Development and an associate professor in the psychiatry department at Johns Hopkins School of Medicine. "Myelination could be a problem that ties all of these autism spectrum disorders together," Maher says. And if that's true, he says, it might be possible to prevent or even reverse the symptoms using drugs that affect myelination. © 2020 npr

Keyword: Autism; Glia
Link ID: 27019 - Posted: 02.04.2020

By Shola Lawal These are tough times for fireflies. Like a lot of other insects, they face increasing threats from habitat loss, pesticides and pollution. But they also have a problem that’s unique to luminous bugs: It’s getting harder for them to reproduce because light pollution is outshining their mating signals. Fireflies, it turns out, use their special glowing powers in courtship: Males light up to signal availability and females respond with patterned flashes to show that they’re in the mood. But bright light from billboards, streetlights and houses is interfering and blocking potential firefly couples from pairing up. The problem can reach far from big cities: Bright light gets diffused in the atmosphere and can be reflected into the wilderness. In addition to messing with mating signals, it also disrupts the feeding patterns of the females of some species that glow to attract and eat males. The finding was part of a study published Monday in the journal BioScience. The study, by researchers at Tufts University and the International Union for Conservation of Nature, warned that fireflies could eventually face extinction globally because of multiple threats, including light pollution and habitat loss and habitat degradation from insecticides and chemical pollution. Many insects are affected by habitat loss, but fireflies have it particularly bad, said Sara M. Lewis, a biology professor at Tufts and the lead researcher on the study. “Some fireflies get hit especially hard when their habitat disappears because they need special conditions to complete their life cycle,” she said. Fireflies are a type of beetle. There are more than 2,000 species of them, found mainly in wetlands. But mangrove forests and marshes around the world are increasingly vanishing to make way for cash crops like palm oil, according to the new study. © 2020 The New York Times Company

Keyword: Sexual Behavior; Biological Rhythms
Link ID: 27018 - Posted: 02.04.2020

By Sue Halpern During the 2016 Presidential primary, SPARK Neuro, a company that uses brain waves and other physiological signals to delve into the subliminal mind, decided to assess people’s reactions to the Democratic candidates. The company had not yet launched, but its C.E.O., Spencer Gerrol, was eager to refine its technology. In a test designed to uncover how people are actually feeling, as opposed to how they say they are feeling, SPARK Neuro observed, among other things, that the cadence of Bernie Sanders’s voice grabbed people’s attention, while Hillary Clinton’s measured tones were a bore. A few months later, Katz Media Group, a radio-and-television-ad representative firm, hired Gerrol’s group to study a cohort of undecided voters in Florida and Pennsylvania. The company’s chief marketing officer, Stacey Schulman, picked SPARK Neuro because its algorithm took into account an array of neurological and physiological signals. “Subconscious emotion underlies conscious decision-making, which is interesting for the marketing world but critically important in the political realm,” Schulman told me. “This measures how the body is responding, and it happens before you articulate it.” Neuromarketing—gauging consumers’ feelings and beliefs by observing and measuring spontaneous, unmediated physiological responses to an ad or a sales pitch—is not new. “For a while, using neuroscience to do marketing was something of a fad, but it has been applied to commerce for a good ten years now,” Schulman said. Nielsen, the storied media-insight company, has a neuromarketing division. Google has been promoting what it calls “emotion analytics” to advertisers. A company called Realeyes claims to have trained artificial intelligence to “read emotions” through Webcams; another called Affectiva says that it “provides deep insight into unfiltered and unbiased consumer emotional response to brand content” through what it calls “facial coding.” Similarly, ZimGo Polling, a South Korean company that operates in the United States, has paired facial-recognition technology with “automated emotion understanding” and natural language processing to give “insights into how people feel about real-time issues,” and “thereby enables a virtual 24/7 town hall meeting with citizens.” This is crucial, according to the C.E.O. of ZimGo’s parent company, because “people vote on emotion.” © 2020 Condé Nast

Keyword: Attention; Emotions
Link ID: 27017 - Posted: 02.04.2020