By Gina Kolata Biogen, the drug company, said on Tuesday that it would ask the Food and Drug Administration to approve an experimental drug, aducanumab, to treat people with mild cognitive impairment and the earliest signs of Alzheimer’s disease. About 10 million Americans might qualify for treatment if the drug were approved, according to Michel Vounatsos, the company’s chief executive. Even so, it is not quite time for these patients to celebrate. The company has not published the most recent analyses, and experts are mostly in the dark as to how well the drug works. It neither prevents nor cures Alzheimer’s; the company claims only that aducanumab may slow cognitive decline in some patients. In fact, Biogen announced in March that it was halting two large studies of aducanumab for treatment of Alzheimer’s disease because data showed the effort was likely to be futile. The company resurrected the drug after additional analyses suggested it might have some effect at higher doses. (“Just in time for Halloween, aducanumab has risen from the dead,” one drug industry analyst said in an email.) Here are some takeaways from Tuesday’s announcement. What is this drug? Drug companies have spent billions of dollars on failed trials for Alzheimer’s drugs. So frustrating have the findings been that some have decided to abandon the search altogether. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26742 - Posted: 10.23.2019

Ian Sample Science editor Doctors in the US have launched a clinical trial to see whether exposure to flickering lights and low frequency sounds can slow the progression of Alzheimer’s disease. A dozen patients enrolled in the trial will have daily one-hour sessions of the radical therapy which researchers hope will induce brain activity that protects against the disorder. Animal tests have shown that exposure to light and sound waves at 40Hz reinforces so-called gamma waves in the brain, with knock-on effects across the organ. In mice used to model the disease, the therapy appears to boost the activity of the brain’s immune cells, making them clear the aberrant proteins that build up in Alzheimer’s. Li-Huei Tsai, a neuroscientist who is leading the trial at MIT, told the Society for Neuroscience meeting in Chicago on Tuesday that the therapy improved the survival and health of the animals’ neurons, boosted their connectivity, and dilated blood vessels, all of which may benefit patients. “We would like to see if our approach slows Alzheimer’s disease,” Tsai told the Guardian. The patients enrolled on the trial will have cognitive tests every three months to assess their brain function and regular scans to measure their brain activity and the connectivity of neurons across the organ. © 2019 Guardian News & Media Limited

Keyword: Alzheimers; Brain imaging
Link ID: 26741 - Posted: 10.23.2019

By Laura Sanders CHICAGO — Wide swings in blood sugar can mess with sleep. Food’s relationship with sleep gets even more muddled when signs of Alzheimer’s disease are present, a study of mice suggests. The results, presented in a news briefing October 20 at the annual meeting of the Society for Neuroscience, show that Alzheimer’s disease is not confined to the brain. “Your head is attached to your body,” says neuroscientist Shannon Macauley of Wake Forest School of Medicine in Winston-Salem, N.C. Metabolism, sleep and brain health “don’t happen in isolation,” she says. Along with Caitlin Carroll, also of Wake Forest, Macauley and coauthors rigged up a way to simultaneously measure how much sugar the brain consumes, the rate of nerve cell activity and how much time mice spend asleep. Injections of glucose into the blood led to changes in the brain: a burst of metabolism, a bump in nerve cell activity and more time spent awake. “It’s like giving a kid a lollipop,” Macauley says. “They’re going to run around in a circle.” But a dip in blood sugar, caused by insulin injections, also led to more nerve cell action and more wakefulness. “You can have it go up high or go down low, and it was just really bad either way,” Macauley says. Researchers did similar analyses in mice genetically engineered to have one of two key signs of Alzheimer’s. Some of these mice had clumps of amyloid-beta protein between nerve cells, while others had tangles of a protein called tau inside nerve cells. © Society for Science & the Public 2000–2019.

Keyword: Alzheimers; Sleep
Link ID: 26740 - Posted: 10.23.2019

Tara Boyle Some of Laurie Santos's most insightful research was sparked by an embarrassing incident. One day, monkeys — her research subjects — stole all the fruit she needed to run a study. She left the research site early for the day. On the boat ride home from Cayo Santiago, the island where the monkeys lived, Santos reflected on the monkeys' mischief. "It's not just that we're dumb researchers and they can outsmart us," she says. "They're specifically trying to steal from us when we're not aware of what they're doing." Santos, a professor of psychology at Yale University, decided to study the monkeys' theft. She found that they selectively stole from the person who couldn't see them. "In other words, they're rationally calculating whether or not someone could detect that they're about to do something dastardly," she says. It was behavior befitting a human. Over the years Santos has discovered other similarities in how humans and non-human primates act. She's also pinpointed important differences, helping us understand which capacities are unique to humans. This comparison between humans and other animals, Santos says, is essential for making any claims that humans are unique. "There's no way to study what makes humans special if you only study humans. You actually have to turn to all the other critters in the animal kingdom," she says. © 2019 npr

Keyword: Evolution
Link ID: 26739 - Posted: 10.23.2019

By Jonathan Lambert Prozac, a commonly prescribed medication for kids and teens with autism, is no more effective than a placebo at treating obsessive-compulsive behaviors, a small study finds. The results of the randomized clinical trial, published October 22 in JAMA, cast further doubt on the widespread practice of prescribing a class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs, to treat children with autism who have these behaviors, says pediatric neurologist Ann Neumeyer. “We really don’t have any good medications that have yet been studied in children with autism for these behaviors,” says Neumeyer, the medical director of the Massachusetts General Hospital Lurie Center for Autism in Lexington, who wasn’t involved in the study. “That’s a problem.” Autism spectrum disorders encompass a diversity of symptoms, but common among them are obsessive-compulsive behaviors (SN: 10/16/18). Individuals with autism can become hyperfocused on specific ideas or objects and can engage in ritualistic “tics,” such as rocking or hand-waving. For many individuals, these symptoms interfere with everyday functioning. SSRI antidepressants account for a quarter to a third of all prescriptions to children and teens with autism, according to pediatrician Dinah Reddihough at the Murdoch Children’s Research Institute in Melbourne, Australia. “Despite their widespread use, there is no evidence of effectiveness of SSRIs for autism spectrum disorders in children,” she says. © Society for Science & the Public 2000–2019.

Keyword: Autism
Link ID: 26738 - Posted: 10.23.2019

Alexander D. Reyes Information in the brain is thought to be encoded as complex patterns of electrical impulses generated by thousands of neuronal cells. Each impulse, known as an action potential, is mediated by currents of charged ions flowing through a neuron’s membrane. But how the ions pass through the insulated membrane of the neuron remained a puzzle for many years. In 1976, Erwin Neher and Bert Sakmann developed the patch-clamp technique, which showed definitively that currents result from the opening of many channel proteins in the membrane1. Although the technique was originally designed to record tiny currents, it has since become one of the most important tools in neuroscience for studying electrical signals — from those at the molecular scale to the level of networks of neurons. By the 1970s, current flowing through the cell was generally accepted to result from the opening of many channels in the membrane, although the underlying mechanism was unknown. At that time, current was commonly recorded by impaling tissue with a sharp electrode — a pipette with a very fine point. Unfortunately, however, the signal recorded in this way was excessively noisy, and so only the large, ‘macroscopic’ current — the collective current mediated by many different types of channel — that flows through the tissue could be resolved. In 1972, Bernard Katz and Ricardo Miledi2, pioneers of the biology of the synaptic connections between cells, managed to infer from the macroscopic current certain properties of the membrane channels, but only after a heroic effort to exclude all possible confounding factors. The problem was that the macroscopic current could be influenced by factors not directly related to channel activity, such as cell geometry and modulatory processes that regulate cell excitability. Also troublesome was that interpretations of macroscopic-current features were based on unverified assumptions about the statistics of individual channel activity2,3. Despite Katz and Miledi’s careful analyses, there was a lingering doubt about whether their conclusions were correct. The crucial data were obtained by Neher and Sakmann using patch clamp. © 2019 Springer Nature Limited

Keyword: Brain imaging
Link ID: 26737 - Posted: 10.23.2019

Anna Azvolinsky Nearly 30 years ago, Kamran Khodakhah, now a neuroscientist at Albert Einstein College of Medicine, signed up for a TV repair course that met several times a week at night at a local community college in London. While many of the other students were attending with the obvious goal of repairing TVs and other appliances, Khodakhah had a different aim. He reasoned that if he could understand how a television worked, he could design new tools to study the rat brain slices he had collected. Khodakhah was working as a PhD student in the lab of neuroscientist David Ogden at the National Institute for Medical Research, trying to determine whether a particular signaling pathway—the inositol trisphosphate (InsP3)/calcium signaling pathway—could be activated in nerve cells called Purkinje neurons. They are found in the cerebellum and have a high density of InsP3 receptors. By taking the TV repair class, Khodakhah wanted to learn to build an electronic circuit to enhance his camera images in order to better visualize the Purkinje cells within slices of the cerebellum and to study the InsP3/calcium ion signaling pathway. He used the new imaging setup, combined with existing lab tools such as flash photolysis, to introduce inert precursor molecules of InsP3—called caged InsP3—into Purkinje neurons in cerebellar slices prepared from rat brains. When stimulated with light, a caged InsP3 molecule is rapidly converted into an active form that binds to InsP3 receptors. Khodakhah then used a fluorescent calcium indicator and recorded the calcium channel activity to see if the binding of InsP3 receptors caused release of calcium from internal stores. At the time, researchers knew that in liver and other non-neuronal cells, InsP3 molecules act as messengers, stimulating the release of calcium ions, which then activates internal cellular pathways. Whether something similar happened in Purkinje neurons wasn’t clear, but if it did, the process might reveal something about how the cerebellum coordinates movement, Khodakhah thought. © 1986–2019 The Scientist.

Keyword: Movement Disorders
Link ID: 26736 - Posted: 10.23.2019

By Laura Sanders CHICAGO — Light pulses from outside a monkey’s brain can activate nerve cells deep within. This external control, described October 20 at the annual meeting of the Society for Neuroscience, might someday help scientists treat brain diseases such as epilepsy. Controlling nerve cell behavior with light, a method called optogenetics, often requires thin optical fibers to be implanted in the brain (SN: 1/15/10). That invasion can cause infections, inflammation and tissue damage, says study coauthor Diego Mendoza-Halliday of MIT. He and his colleagues created a new light-responsive molecule, called SOUL, that detects extra dim light. After injecting SOUL into macaque monkeys’ brains, researchers shined blue light through a hole in the skull. SOUL-containing nerve cells, which were as deep as 5.8 millimeters in the brain, became active. A dose of orange light stopped this activity. SOUL can’t sense light coming from outside of the macaques’ skulls. But in mice, the system works through the skull, the researchers reported. LEDs implanted just under people’s skulls might one day be used to treat brain diseases. Such a system might be able to temporarily turn off nerve cells that are about to cause an epileptic seizure, for instance. “This is basically scooping out a piece of brain and then putting it back in a few seconds later,” when the risk of a seizure has dropped, Mendoza-Halliday says. © Society for Science & the Public 2000–2019.

Keyword: Brain imaging
Link ID: 26735 - Posted: 10.23.2019

By Pam Belluck About 10 days after what seemed like a garden-variety cold, Luca Waugh, a healthy 4-year-old, developed troubling symptoms. Suddenly, his neck became so weak that he fell backward. Then his right arm couldn’t move. Within days, recalled his mother, Dr. Riley Bove, he developed “head-to-toe paralysis, where he could kind of move his eyes a little bit and one side of his face.” Doctors diagnosed Luca with acute flaccid myelitis or A.F.M., a mysterious neurological condition that can cause limb weakness and polio-like paralysis, mostly in young children. A.F.M. is rare, but in 2014, when Luca became afflicted, health authorities identified a burst of 120 cases. Since then, A.F.M. has made headlines as cases have spiked every two years, and nearly 600 have been confirmed across the country since 2014. What exactly causes A.F.M. has eluded experts, frustrating attempts to prevent or treat it. Now, a study by a team that includes Luca’s mother, Dr. Bove, who happens to be a neurologist, provides strong evidence of a likely cause. It involved dozens of children with A.F.M., including Luca, whose paralysis improved after weeks of hospitalization but who remains disabled five years later. The research, published Monday in the journal Nature Medicine, points to a long-suspected culprit: enteroviruses, a group of common viruses that usually produce mild effects, but can sometimes cause neurological symptoms. Using sophisticated laboratory techniques, researchers found antibodies to enteroviruses in the cerebrospinal fluid of nearly 70 percent of the children with A.F.M., a sign their bodies had mobilized to defend against enterovirus infection. © 2019 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26734 - Posted: 10.22.2019

By Sofie Bates Make some noise for the white bellbirds of the Brazilian Amazon, now the bird species with the loudest known mating call. The birds (Procnias albus) reach about 125 decibels on average at the loudest point in one of their songs, researchers report October 21 in Current Biology. Calls of the previous record-holder — another Amazonian bird called the screaming piha (Lipaugus vociferans) — maxed out around 116 decibels on average. This difference means that bellbirds can generate a soundwave with triple the pressure of that made by pihas, says Jeff Podos, a behavioral ecologist at the University of Massachusetts Amherst, who did the research along with ornithologist Mario Cohn-Haft, of the National Institute of Amazon Research in Manaus, Brazil. The team measured sound intensity from three pihas and eight bellbirds. Each sounded off at different distances from the scientists. So to make an accurate comparison, the researchers used rangefinder binoculars, with lasers to measure distance, to determine how far away each bird was. Then, they calculated how loud the sound would be a meter from each bird to crown a winner. The small white bellbird, which weighs less than 250 grams, appears to be built for creating loud sounds, with thick abdominal muscles and a beak that opens extra wide. “Having this really wide beak helps their anatomy be like a musical instrument,” Podos says. Being the loudest may come with a cost: White bellbirds can’t hold a note for long because they run out of air in their lungs. Their loudest call sounds like two staccato beats of an air horn while the calls of screaming pihas gradually build to the highest point. © Society for Science & the Public 2000–2019

Keyword: Sexual Behavior; Hearing
Link ID: 26733 - Posted: 10.22.2019

By Jon Cohen On a lightly snowing Sunday evening, a potential participant in Denis Rebrikov’s controversial plans to create gene-edited babies meets with me at a restaurant in a Moscow suburb. She does not want to be identified beyond her patronymic, Yevgenievna. We sit at a corner table in an empty upstairs section of the restaurant while live Georgian music plays downstairs. Yevgenievna, in her late 20s, cannot hear it—or any music. She has been deaf since birth. But with the help of a hearing aid that’s linked to a wireless microphone, which she places on the table, she can hear some sounds, and she is adept at reading lips. She speaks to me primarily in Russian, through a translator, but she is also conversant in English. Yevgenievna and her husband, who is partially deaf, want to have children who will not inherit hearing problems. There is nothing illicit about our discussion: Russia has no clear regulations prohibiting Rebrikov’s plan to correct the deafness mutation in an in vitro fertilization (IVF) embryo. But Yevgenievna is uneasy about publicity. “We were told if we become the first couple to do this experiment we’ll become famous, and HBO already tried to reach me,” Yevgenievna says. “I don’t want to be well known like an actor and have people bother me.” She is also deeply ambivalent about the procedure itself, a pioneering and potentially risky use of the CRISPR genome editor. The couple met on vk.com, a Russian Facebook of sorts, in a chat room for people who are hearing impaired. Her husband could hear until he was 15 years old, and still gets by with hearing aids. They have a daughter—Yevgenievna asks me not to reveal her age—who failed a hearing test at birth. Doctors initially believed it was likely a temporary problem produced by having a cesarean section, but 1 month later, her parents took her to a specialized hearing clinic. “We were told our daughter had zero hearing,” Yevgenievna says. “I was shocked, and we cried.” © 2019 American Association for the Advancement of Science.

Keyword: Hearing; Genes & Behavior
Link ID: 26732 - Posted: 10.22.2019

By Eric A. Taub Like clockwork, the sound of the freight train came roaring through our bedroom in the middle of each night. Or at least what sounded like a freight train. In reality, it was me, snoring. And according to my wife, that freight train had gotten considerably louder over the years. Unfortunately, snoring frequency and volume is exacerbated by age, among other factors. While there’s nothing I can do about getting older, there are products and procedures available that can eliminate or significantly reduce the annoyance to one’s bed partner caused by all that nighttime snorting and wheezing. Snoring and sleep apnea are not the same, although severe snoring can be an indication of apnea. If sleep apnea is not present, snoring is simply the benign result of an obstructed airway. As we age, the uvula — that soft, floppy, fingerlike projection in the back of the throat — gets softer and floppier. At the same time, muscles under the tongue get lax. And the condition is exacerbated if we are overweight or drink too much alcohol. “With age, the muscle tone of our airways decreases. That decreased tone allows the tissues to move more readily and become more prone to collapse and to vibrate,” said Dr. Michael D. Olson, an ear, nose and throat doctor and sleep surgeon in the Mayo Clinic’s department of head and neck surgery. In addition, if the size of the airway decreases, air pressure increases, allowing for tissue vibration and snoring. “Combine that with nasal congestion, a big tongue and body fat, and that leads to an excessive collapse of the airways,” Dr. Olson said. Another cause of snoring: teeth extraction, a particular issue for baby boomers who had braces in their youth. With the removal of four bicuspids as a common practice at the time, boomers may now be suffering snoring because of a larger tongue in a smaller mouth. © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26731 - Posted: 10.22.2019

Emma Yasinski Delta waves, patterns of slow, synchronized brain activity that occur during deep sleep, have long been considered “periods of silence,” in which neurons in the cortex stop firing. But these intervals may not be silent after all, researchers reported yesterday in Science. In rats, some cortical neurons remain active during delta waves, and their firing may even be involved in consolidating memories. “The paper is absolutely fascinating and will have a large impact on the field of memory and sleep,” says Björn Rasch, a biopsychologist at the University of Fribourg in Switzerland who was not involved in the study. He suggests it might even help explain surprising results in his own research in humans published earlier this year that indicated participants may better remember words from a foreign language if they are replayed during delta wave sleep than if they are never repeated during sleep. The latest study “challenges our views on the potential function of down states [when cortical neurons seem silent] in memory consolidation processes.” When humans (and rats) are awake, a brain structure called the hippocampus records the ongoing episodes of our lives. When we sleep, the hippocampus replays this activity, which is transmitted to the cortex where it forms long-term memories. Afterward, the cortex seems to go silent. This quiet delta wave period is known to be important for memory consolidation, but researchers have wondered how it helps the process. © 1986–2019 The Scientist.

Keyword: Sleep; Learning & Memory
Link ID: 26730 - Posted: 10.22.2019

/ By Elizabeth Preston On the first page of Heinz Koop’s fecal analysis test results, a bar showed where he fell on a gradient from green to red. A label above said, in German: “Overall dysbiosis.” Koop was not in the green or even the yellow regions, but a worrisome orange. It was a bad result — but, he says, “I was kind of happy.” Doctors hadn’t given him a satisfying answer about his recurring bloody diarrhea and other gut troubles. But Koop had learned on Facebook that he could test his gut microbiome — the community of bacteria and other organisms living in his gastrointestinal tract — to look for problems. Koop ordered a test from a German laboratory called Medivere. The results said his gut microbes were imbalanced, which was something he thought he could treat. Soon he would be attempting to correct this imbalance by chauffering a friend’s fresh stool samples home to implant up his own colon. Trillions of microbes living on and in our bodies, especially our guts, make up our microbiome. The bugs in our bowel are not just there to slow down our poop, as one researcher speculated in 1970, but are intricately connected to our health. Gut microbes help us digest our food, make critical vitamins, and keep pathogens out. Over the past decade or so, research into the microbiome has exploded as researchers have tried to tease apart the complex connections between our diseases and our resident microbes. Today, at least 10 percent of published microbiome papers use the term dysbiosis to describe changes in the microbiome, estimates Katarzyna Hooks, a computational biologist now at Evotec, a global biotechnology company headquartered in Germany. Some scientists say the term is useful for communicating a specific finding, though they acknowledge its limitations. Other scientists hate it. Copyright 2019 Undark

Keyword: Obesity
Link ID: 26729 - Posted: 10.22.2019

Jon Hamilton Brain scientists are offering a new reason to control blood sugar levels: It might help lower your risk of developing Alzheimer's disease. "There's many reasons to get [blood sugar] under control," says David Holtzman, chairman of neurology at Washington University in St. Louis. "But this is certainly one." Holtzman moderated a panel Sunday at the Society for Neuroscience meeting in Chicago that featured new research exploring the links between Alzheimer's and diabetes. "The risk for dementia is elevated about twofold in people who have diabetes or metabolic syndrome (a group of risk factors that often precedes diabetes)," Holtzman says. "But what's not been clear is, what's the connection?" One possibility involves the way the brain metabolizes sugar, says Liqin Zhao, an associate professor in the school of pharmacy at the University of Kansas. Zhao wanted to know why people whose bodies produce a protein called ApoE2 are less likely to get Alzheimer's. Previous research has shown that these people are less likely to develop the sticky plaques in the brain associated with the disease. But Zhao looked at how ApoE2 affects glycolysis, a part of the process that allows brain cells to turn sugar into energy. So she gave ApoE2 to mice that develop a form of Alzheimer's. And sure enough, Zhao says, the substance not only improved energy production in brain cells but made the cells healthier overall. "All of this together increased the brain's resilience against Alzheimer's disease," she says. © 2019 npr

Keyword: Alzheimers; Obesity
Link ID: 26728 - Posted: 10.22.2019

By Austin Frakt To ward off age-related cognitive decline, you may be tempted to turn to brain training apps. Last year, consumers spent nearly $2 billion on them, some of which claim to improve cognitive skills. Evidence suggests you’d be better off spending more time exercising and less time staring at your phone. This year the World Health Organization released evidence-based guidelines on reducing risks of cognitive decline and dementia. Although it pointed to some systematic reviews that reported positive cognitive effects of brain training, the W.H.O. judged the studies to be of low quality. Among the studies’ limitations is that they measure only short-term effects and in areas targeted by the training. There is no long-term evidence of general improvement in cognitive performance. Instead of mind games, moving your body is among the most helpful things you can do. At least 150 minutes of moderate physical activity per week, including strength training, yields not just physical benefits but cognitive ones as well. But to be most effective, you need to do it before cognitive decline starts, according to the W.H.O. Some evidence to support this recommendation comes from short-term studies. Several randomized studies of tai chi for older adults found it yielded cognitive benefits. Likewise, randomized studies of aerobic exercise for older adults found short-term improvements in cognitive performance. A systematic review published this year in PLOS One examined 36 randomized studies of exercise programs that were as short as four weeks and as long as a year. It found cognitive benefits of activities such as bicycling, walking, jogging, swimming and weight training. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26727 - Posted: 10.21.2019

By Marlene Cimons In 1991, Karestan Koenen was a recent college graduate and Peace Corps volunteer who arrived in a village in Niger eager to help local women start small businesses. When her sister came to visit during Christmas, the two decided to travel north to Agadez, a city in the Sahara. There, on the morning of Dec. 27, two male traders stopped by, trying to sell them jewelry. Koenen’s sister went to the market with one of men to have a look. While she was gone, the second man grabbed Koenen, held her down and raped her. Traumatized by the experience, Koenen was medically evacuated to the United States two days later and resigned from the Peace Corps. She returned to New Jersey to live with her parents, but the assault continued to haunt her. Increasingly, she became depressed. A psychologist diagnosed Koenen with post-traumatic stress disorder, or PTSD, a condition triggered by a traumatic, scary or dangerous event, and, for reasons still unclear, seems to disproportionately afflict women. These assaults can include combat, sexual assault, gun violence, accidents, natural disasters, even the death of a loved one. “I lay in bed, unable to sleep, thinking of ways to kill myself,” she recalls. “When I did sleep, I had nightmares. I lost interest in everything. I couldn’t read and was too jumpy to sit through a movie or watch TV. I was irritable with my family. I was always on guard — angry — and couldn’t stop thinking about what had happened. I felt like I was stuck in a dark tunnel, moving more and more quickly, but it only got darker.”

Keyword: Stress; Sexual Behavior
Link ID: 26726 - Posted: 10.21.2019

by Emily Anthes The Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, launched by the U.S. National Institutes of Health (NIH) in 2013, has a lofty goal: to unravel the cellular basis of cognition and behavior. Since the initiative’s launch, the NIH has doled out about $1 billion to researchers who are developing tools and technologies to map, measure and observe the brain’s neural circuits. Along the way, the agency has also tried to explore the ethical implications of this research. Khara Ramos, who directs the neuroethics program at the NIH’s National Institute of Neurological Disorders and Stroke, described the emerging field of neuroethics today at the 2019 Society for Neuroscience annual meeting in Chicago, Illinois. Spectrum: Was discussion about ethics part of the BRAIN Initiative from the beginning? Khara Ramos: We knew that we needed to do something with neuroethics, but it took time for us to figure out what exactly, in part because neuroethics is a relatively new field. Bioethics is a broad field that covers all aspects of biomedicine, but there isn’t specialization of bioethics in kidney research or pulmonary research the way there is in neuroscience research, and that’s really because the brain is so intimately connected with who we are. Neuroscience research raises these unique ethical questions, such as: How might new neurotechnologies alter fundamental notions of agency or autonomy or identity? We’re starting to focus on data sharing and privacy from a philosophical, conceptual perspective: Is there something unique about brain data that is different from, for instance, genetic data? How do researchers themselves feel about data sharing and privacy? And how does the public view it? For instance, is my social security number more or less sensitive than the kinds of neural data that somebody might be able to get if I were participating in a clinical trial? © 2019 Simons Foundation

Keyword: Autism; Attention
Link ID: 26725 - Posted: 10.21.2019

By Perri Klass, M.D. It’s a pretty safe bet that most of our children, in high school and in college, will be in social situations in which people drink in unwise and sometimes downright dangerous ways. Even if they don’t drink, they will at least be exposed to friends and classmates and roommates who do. What makes alcohol more problematic for some kids — and some adults? There’s been a good deal of research on the development of what is now called alcohol use disorder, and its precursors — what do we now understand, and can that understanding help us as parents to worry less, or at least, to direct our worries in the right directions? Frances Wang, a postdoctoral scholar at the University of Pittsburgh who studies genetic and environmental causes of alcohol use disorders, said that often people blame only the home environment — that is to say, the parenting. But there are genetic risk factors that seem to be common across a number of disorders, she said, including alcohol use disorder, but also depression and conduct problems, like aggression and antisocial behavior, which can be predecessors of alcohol problems. Dr. Wang was the first author on a study published in 2018 in the journal Development and Psychopathology, which looks at a particular biological attribute — the functioning of serotonin, a neurotransmitter — determined by a combination of genetic factors. Investigating these common genetic risk factors might help us understand the connections. But bear in mind that there are no simple cause-and-effect stories here. And while there may be times when the home environment really is the driving force, Dr. Wang said, “for most people it’s the interaction between already having that genetic risk and an environment that increases genetic risk or makes genetic risk come out.” © 2019 The New York Times Company

Keyword: Drug Abuse
Link ID: 26724 - Posted: 10.21.2019

Zoë Corbyn At a time when women’s reproductive freedoms are under attack, any suggestion that the birth control pill could be problematic feels explosive. But Sarah E Hill, a professor of social psychology at the Texas Christian University in Fort Worth, Texas argues we need to talk about how oral contraceptives are affecting women’s thinking, emotions and behaviour. How the Pill Changes Everything: Your Brain on Birth Control is her new book about the science behind a delicate subject. Some US states have recently made it harder to get an abortion and the Trump administration is doing its best to chisel away at access to birth control. Is your book trying to dissuade women from using the pill? My institution was founded as a Christian school, but it doesn’t have a particular religious bent now. My goal with this book is not to take the pill away or alarm women. It is to give them information they haven’t had up until now so they can make informed decisions. The pill, along with safe, legalised abortions, are the two biggest keys to women’s rights. But we also have a blind spot when it comes to thinking about how changing women’s sex hormones – which is what the pill does – influences their brains. For a long time, women have been experiencing “psychological” side-effects on the pill but nobody was telling them why. The backlash we are seeing against the pill, particularly with millennial women walking away from it, I think is because women haven’t felt right on it and have grown weary of doctors patting them on their heads and telling them they are wrong. The more information women have, the more it will bring them back to the pill. © 2019 Guardian News & Media Limited

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 26723 - Posted: 10.19.2019