Iris Berent How can a cellist play like an angel? Why am I engrossed in my book when others struggle with reading? And while we’re at it, can you tell me why my child won’t stop screaming? Now neuroscience offers the answers—or so say the news headlines. The brains of musicians “really do” differ from those of the rest of us. People with dyslexia have different neural connections than people without the condition. And your screaming toddler’s tantrums originate from her amygdala, a brain region linked to emotions. It’s all in the brain! Neuroscience is fascinating. But it is not just the love of science that kindles our interest in these stories. Few of us care for the technical details of how molecules and electrical charges inthe brain give rise to our mental life. Furthermore, invoking the brain does not always improve our understanding. You hardly need a brain scan to tell that your toddler is enraged. Nor is it surprising that an amateur cellist’s brain works differently than Yo-Yo Ma’s—or that the brains of typical and dyslexic readers differ in some way. Where else would those differences reside? These sorts of science news stories speak to a bias: As numerous experiments have demonstrated, we have a blind spot for the brain. In classic work on the “seductive allure of neuroscience,” a team of researchers at Yale University presented participants with a psychological phenomenon (for instance, children learning new words), along with two explanations. One invoked a psychological mechanism, and the other was identical except it also dropped in a mention of a brain region. The brain details were entirely superfluous—they did nothing to improve the explanation, as judged by neuroscientists. Yet laypeople thought they did, so much so that once the brain was invoked, participants overlooked gross logical flaws in the accounts. © 2021 Scientific American,

Keyword: Attention
Link ID: 28105 - Posted: 12.11.2021

Monique Brouillette Last summer a group of Harvard University neuroscientists and Google engineers released the first wiring diagram of a piece of the human brain. The tissue, about the size of a pinhead, had been preserved, stained with heavy metals, cut into 5,000 slices and imaged under an electron microscope. This cubic millimeter of tissue accounts for only one-millionth of the entire human brain. Yet the vast trove of data depicting it comprises 1.4 petabytes’ worth of brightly colored microscopy images of nerve cells, blood vessels and more. “It is like discovering a new continent,” said Jeff Lichtman of Harvard, the senior author of the paper that presented these results. He described a menagerie of puzzling features that his team had already spotted in the human tissue, including new types of cells never seen in other animals, such as neurons with axons that curl up and spiral atop each other and neurons with two axons instead of one. These findings just scratched the surface: To search the sample completely, he said, would be a task akin to driving every road in North America. Lichtman has spent his career creating and contemplating these kinds of neural wiring diagrams, or connectomes — comprehensive maps of all the neural connections within a part or the entirety of a living brain. Because a connectome underpins all the neural activity associated with a volume of brain matter, it is a key to understanding how its host thinks, feels, moves, remembers, perceives, and much more. Don’t expect a complete wiring diagram for a human brain anytime soon, however, because it’s technically infeasible: Lichtman points out that the zettabyte of data involved would be equivalent to a significant chunk of the entire world’s stored content today. In fact, the only species for which there is yet a comprehensive connectome is Caenorhabditis elegans, the humble roundworm. Nevertheless, the masses of connectome data that scientists have amassed from worms, flies, mice and humans are already having a potent effect on neuroscience. And because techniques for mapping brains are getting faster, Lichtman and other researchers are excited that large-scale connectomics — mapping and comparing the brains of many individuals of a species — is finally becoming a reality. Share this article Simons Foundation All Rights Reserved © 2021

Keyword: Brain imaging
Link ID: 28104 - Posted: 12.08.2021

by Anna Goshua Mice that lack one copy of TBX1, a gene in the autism-linked 22q11.2 chromosomal region, produce too little myelin — the fatty insulation that surrounds neurons — and perform poorly on tasks that measure cognitive speed, according to a new study. The work, published 5 November in Molecular Psychiatry, may offer insight into the mechanisms that underlie impaired cognitive function in some people with a 22q11.2 deletion, and possibly other copy number variants (CNVs). “The myelin changes could potentially emerge as a common neuronal deficit that mediates cognitive changes among many CNV cases,” says lead investigator Noboru Hiroi, professor of pharmacology at the University of Texas Health Science Center at San Antonio. Neuronal axons — the projections that conduct nerve impulses — are coated with myelin, which serves to speed up electrical transmission. The brains of autistic people and several mouse models of autism have disruptions in myelin, previous research has shown. These connecting fibers are the “highways of the brain,” says Valerie Bolivar, research scientist at the New York State Department of Health’s Wadsworth Center in Albany. “If the highway doesn’t work, you can’t get your goods from one place to another as fast.” TBX1 encodes a protein that regulates the expression of other genes during brain development. Deleting one copy of TBX1 leads to social and communication deficits in mice, according to previous studies by Hiroi’s team. © 2021 Simons Foundation

Keyword: Autism; Glia
Link ID: 28103 - Posted: 12.08.2021

By Elizabeth Preston A person trying to learn the way around a new neighborhood might spend time studying a map. You would probably not benefit from being carried rapidly through the air, upside-down in the dark. Yet that’s how some baby bats learn to navigate, according to a study published last month in Current Biology. As their mothers tote them on nightly trips between caves and certain trees, the bat pups gain the skills they need to get around when they grow up. Mothers of many bat species carry their young while flying, said Aya Goldshtein, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Konstanz, Germany. Egyptian fruit bats, for example, are attached to their mothers continuously for the first three weeks of life. While a mother searches for food, her pup clings to her body with two feet and its jaw, latching its teeth around her nipple. Mothers can still be seen flying with older pups that weigh 40 percent of what they do. It hadn’t been clear why the moms go to this length, instead of leaving pups in the cave where they roost, as some other species do. Dr. Goldshtein worked with Lee Harten, a behavioral ecologist at Tel Aviv University in Israel, where both she and Dr. Goldshtein were graduate students at the time in the lab of Yossi Yovel, a study co-author, to make sense of this maternal mystery. The researchers captured Egyptian fruit bat mothers and pups from a cave just outside Tel Aviv. They attached a tag holding a radio transmitter and miniature GPS device to each bat’s fur that would drop off after a couple of weeks. Then, the researchers brought the bats back to their cave. To track the bats, Dr. Harten held an antenna while standing on the roof of a 10-story building with a view of the cave. She directed Dr. Goldshtein, who was on foot or in a car with her own antenna, to follow the radio signals of bat pairs as they flew out at night. But again and again, there was a problem: The pup’s movement would suddenly stop, while the mother’s signal disappeared. “At the beginning we thought that we were doing our job wrong, and just losing the bats,” Dr. Harten said. © 2021 The New York Times Company

Keyword: Learning & Memory; Animal Migration
Link ID: 28102 - Posted: 12.08.2021

L. Carol Ritchie U.S. Surgeon General Vivek Murthy has a warning about the mental health of young people. Murthy told Morning Edition that children and young adults were already facing a mental health crisis before the coronavirus pandemic began: One in three high school students reported persistent feelings of sadness or hopelessness, a 40% increase from 2009 to 2019, he said. Suicide rates went up during that time by 57% among youth ages 10 to 24. During the pandemic, rates of anxiety and depression have increased, he said. The pandemic has made the issues behind the mental health crisis only worse, he said. "This is a critical issue that we have to do something about now," he said. "We can't wait until after the pandemic is over." Murthy, who issued an advisory called "Protecting Youth Mental Health," also cites gun violence, the specter of climate change, racism and social conflict as sources of stress. "We also have to recognize that kids increasingly are experiencing bullying, not just in school but online, that they're growing up in a popular culture and a media culture that reminds kids often that they aren't good-looking enough, thin enough, popular enough, rich enough, frankly, just not enough," he said. Article continues after sponsor message "Even to this day, even though I have parents who I know unconditionally loved me, I never felt comfortable telling them about it because I thought that this was my fault. I don't want that to be the reality for my children, who are 4 and 5 and growing up, you know, in this very complicated world." © 2021 npr

Keyword: Depression
Link ID: 28101 - Posted: 12.08.2021

Alison Abbott There Is Life After the Nobel Prize Eric Kandel Columbia Univ. Press (2021) In 1996, Denise Kandel warned her husband that were he to win the Nobel prize for his pioneering work on memory, then it should be later rather than sooner. Laureates too often turn into socialites, she warned, and stop contributing to the intellectual life of science. Just four years later, Eric Kandel shared the 2000 Nobel Prize in Physiology or Medicine. He was then 71, an age when he could legitimately have rested on his laurels. But resting is not among Kandel’s many strengths. His new book, There Is Life After the Nobel Prize, outlines his achievements of the past couple of decades — numerous enough to dispel Denise’s fears, he writes. It is hard to disagree. The volume adds to Kandel’s respected literary oeuvre, which ranges from neuroscience textbooks to highly original popular science. But it is slight, and feels like a coda. In it, he summarises his post-Nobel research (on learning and memory deficits in addiction, schizophrenia and ageing), writing and public outreach. And he acknowledges colleagues and sponsors of his long career, particularly the Howard Hughes Medical Institute in Chevy Chase, Maryland, and Columbia University in New York City, where he remains a professor and institute director. A fuller and more poignant autobiography can be found in Kandel’s 2006 book In Search of Memory. There, he explains why his traumatic childhood in Austria drew him to study the mechanisms of memory. That book also presents a marvellous history of neuroscience. Making sense Kandel was born in 1929 in Vienna. His family was Jewish and owned a toy shop. When Hitler annexed Austria in 1938, his parents began their year-long effort to emigrate. They finally arrived in New York shortly before the outbreak of World War II, physically unharmed but psychologically traumatized. © 2021 Springer Nature Limited

Keyword: Learning & Memory
Link ID: 28100 - Posted: 12.08.2021

By Laura Sanders Kanu Caplash was lying on a futon in a medical center in Connecticut, wearing an eye mask and listening to music. But his mind was far away, tunneling down through layer upon layer of his experiences. As part of a study of MDMA, a psychedelic drug also known as molly or ecstasy, Caplash was on an inner journey to try to ease his symptoms of post-traumatic stress disorder. On this particular trip, Caplash, now 22, returned to the locked bathroom door of his childhood home. As a kid, he used to lock himself in to escape the yelling adults outside. But now, he was both outside the locked door, knocking, and inside, as his younger, frightened self. He started talking to his younger self. “I open the door, and my big version picks up my younger version of myself, and literally carries me out,” he says. “I carried myself out of there and drove away.” That self-rescue brought Caplash peace. “I got out of there. I’m alive. It’s all right. I’m OK.” For years, Caplash had experienced flashbacks, nightmares and insomnia from childhood trauma. He thought constantly about killing himself, he says. His experiences while on MDMA changed his perspective. “I still have the memory, but that anger and pain is not there anymore.” Caplash’s transcendent experiences, spurred by three therapy sessions on MDMA, happened in 2018 as part of a research project on PTSD. Along with a handful of other studies, that research suggests that when coupled with psychotherapy, mind-altering drugs bring some people immediate, powerful and durable relief. © Society for Science & the Public 2000–2021.

Keyword: Depression; Drug Abuse
Link ID: 28099 - Posted: 12.04.2021

By Pam Belluck AURORA, Ill. — There is sobering evidence of Samantha Lewis’s struggle with long Covid on her bathroom mirror. Above the sink, she has posted a neon pink index card scrawled with nine steps (4. Wet brush 5. Toothpaste) reminding her how to brush and floss her teeth. It is one of many strategies Ms. Lewis, 34, has learned from “cognitive rehab,” an intensive therapy program for Covid-19 survivors whose lives have been upended by problems like brain fog, memory lapses, dizziness and debilitating fatigue. Nearly two years into the pandemic, advances have been made in treating Covid itself, but long Covid — a constellation of lingering health problems that some patients experience — remains little understood. Post-Covid clinics around the country are trying different approaches to help patients desperate for answers, but there is little data on outcomes so far, and doctors say it is too soon to know what might work, and for which patients. While some physical symptoms of long Covid, like shortness of breath or nausea, can be addressed with medication, cognitive issues are more challenging. Few drugs exist, and while some deficits can rebound with time, they can also be exacerbated by resuming activities too soon or intensively. Over several months, The New York Times visited Ms. Lewis, interviewed her doctors, attended her therapy sessions and read her medical records. Before she was infected with the coronavirus in October 2020, experiencing a modest initial illness that did not require hospitalization, she was successfully juggling a demanding, detail-oriented job while raising a child with autism and attention deficit hyperactivity disorder. But this summer, she scored 25 on a 30-point assessment, placing her in a pre-dementia category called mild cognitive impairment. © 2021 The New York Times Company

Keyword: Learning & Memory
Link ID: 28098 - Posted: 12.04.2021

By Bob Goldstein On a cold, dry Tuesday in December, 1940, Rita Levi-Montalcini rode a train from the station near her home in Turin, Italy, for 80 miles to Milan to buy a microscope. Milan had not seen bombings for months. On her return to the Turin train station, two police officers stopped her and demanded to see inside the cake-sized box that she was carrying. With wartime food rationing, panettone cakes were only available illegally. The officers found her new microscope instead. They let her go. Just a week after her trip, British bombers hit Milan. Levi-Montalcini was a 31-year-old scientist who had been working at the University of Turin. Despite her father’s disapproval, she had trained in medicine, inspired by seeing a nanny succumb to cancer. In 1938, the Italian dictator Mussolini banned Jews from positions in universities. Levi-Montalcini was not raised in the Jewish religion, but her Jewish ancestry would have been evident from her surname. Mussolini’s ban had pushed Levi-Montalcini to leave Italy for Belgium in 1939, where she did research using fertilized chicken eggs as a source of material for her research topic: the developing nervous systems of vertebrate embryos. Levi-Montalcini also spent time with her older sister Nina, whose family was in Belgium as well. Rita wrote home to her mother of an “infinite desire to embrace you again,” but research at the university in Turin would have been impossible had she returned home. Her passion for research alternated with her frustration with challenges. When Hitler invaded Poland in September, launching war, her worst frustrations were realized. The “whole world was in danger,” Levi-Montalcini later wrote. In December 1939, she returned to Italy. © 2021 NautilusThink Inc,

Keyword: Apoptosis; Development of the Brain
Link ID: 28097 - Posted: 12.04.2021

By Emily Cataneo If you could upload your consciousness to the cloud and live forever as a mind in the metaverse, would you do it? Think carefully before answering. In “Feeling & Knowing: Making Minds Conscious,” neuroscientist Antonio Damasio argues that consciousness is far more than an algorithmic process. Uploading your consciousness to the cloud, he says, would be like experiencing a meal by reading a recipe rather than by eating. So then what is consciousness? That’s the question at the heart of this book. Damasio is a professor of neuroscience, philosophy, and psychology and the director of the Brain and Creativity Institute at the University of Southern California, Los Angeles, as well as the author of the 2018 book “The Strange Order of Things,” in which he extols the power of homeostasis, the force that keeps all living beings in equilibrium and therefore alive. Consciousness is such a slippery and ephemeral concept that it doesn’t even have its own word in many Romance languages, but nevertheless it’s a hot topic these days. “Feeling & Knowing” is the result of Damasio’s editor’s request to weigh in on the subject by writing a very short, very focused book. Over 200 pages, Damasio ponders profound questions: How did we get here? How did we develop minds with mental maps, a constant stream of images, and memories — mechanisms that exist symbiotically with the feelings and sensations in our bodies that we then, crucially, relate back to ourselves and associate with a sense of personhood?

Keyword: Consciousness
Link ID: 28096 - Posted: 12.04.2021

Daisy Yuhas Billions of people worldwide speak two or more languages. (Though the estimates vary, many sources assert that more than half of the planet is bilingual or multilingual.) One of the most common experiences for these individuals is a phenomenon that experts call “code switching,” or shifting from one language to another within a single conversation or even a sentence. This month Sarah Frances Phillips, a linguist and graduate student at New York University, and her adviser Liina Pylkkänen published findings from brain imaging that underscore the ease with which these switches happen and reveal how the neurological patterns that support this behavior are very similar in monolingual people. The new study reveals how code switching—which some multilingual speakers worry is “cheating,” in contrast to sticking to just one language—is normal and natural. Phillips spoke with Mind Matters editor Daisy Yuhas about these findings and why some scientists believe bilingual speakers may have certain cognitive advantages. Can you tell me a little bit about what drew you to this topic? I grew up in a bilingual household. My mother is from South Korea; my dad is African-American. So I grew up code switching a lot between Korean and English, as well as different varieties of English, such as African-American English and the more mainstream, standardized version. When you spend a lot of time code switching, and then you realize that this is something that is not well understood from a linguistic perspective, nor from a neurobiological perspective, you realize, “Oh, this is open territory.” © 2021 Scientific American

Keyword: Language
Link ID: 28095 - Posted: 12.01.2021

By Gretchen Reynolds Staying physically active as we age substantially drops our risk of developing dementia during our lifetimes, and it doesn’t require prolonged exercise. Walking or moving about, rather than sitting, may be all it takes to help bolster the brain, and a new study of octogenarians from Chicago may help to explain why. The study, which tracked how often older people moved or sat and then looked deep inside their brains after they passed away, found that certain vital immune cells worked differently in the brains of older people who were active compared to their more sedentary peers. Physical activity seemed to influence their brain’s health, their thinking abilities and whether they experienced the memory loss of Alzheimer’s disease. The findings add to growing evidence that when we move our bodies, we change our minds, no matter how advanced our age. Already, plenty of scientific evidence indicates that physical activity bulks up our brains. Older, sedentary people who begin walking for about an hour most days, for instance, typically add volume to their hippocampus, the brain’s memory center, reducing or reversing the shrinkage that otherwise commonly occurs there over the years. Active people who are middle-aged or older also tend to perform better on tests of memory and thinking skills than people of the same age who rarely exercise, and are nearly half as likely eventually to be diagnosed with Alzheimer’s disease. Almost as heartening, active people who do develop dementia usually show their first symptoms years later than inactive people do. But precisely how movement remodels our brains is still mostly mysterious, although scientists have hints from animal experiments. When adult lab mice and rats run on wheels, for example, they goose production of hormones and neurochemicals that prompt the creation of new neurons, as well as synapses, blood vessels and other tissues that connect and nurture those young brain cells. © 2021 The New York Times Company

Keyword: Alzheimers
Link ID: 28094 - Posted: 12.01.2021

by Charles Q. Choi One injection of a potential new gene therapy for Angelman syndrome forestalls many of the neurodevelopmental condition’s key traits, according to early tests in mice. “While additional pharmacology and safety studies are needed, our viral vector can potentially provide transformative therapeutic relief with a single dose,” says lead investigator Benjamin Philpot, professor of neuroscience at the University of North Carolina at Chapel Hill. Angelman syndrome, which affects about one in 20,000 children, is associated with significant developmental delays and, often, autism. It arises from mutations or deletions in the maternal copy of the UBE3A gene, which encodes a protein that helps regulate the levels of other important proteins. There are no treatments specifically for Angelman syndrome, but several gene therapies are under development. One in clinical trials requires repeat injections in the spine and has shown serious side effects at high doses. These therapies all aim to restore UBE3A function in neurons. One challenge, though, is that neurons produce several variants, or ‘isoforms,’ of the UBE3A protein that vary slightly in length; in mice, for example, neurons make two isoforms in a ratio of about four short forms for every long one. In contrast to other gene therapies, the new one generates short and long forms of the UBE3A protein at nearly the same ratio as is seen in mouse neurons. Such proportions “may be important for therapeutic efficacy,” says Eric Levine, professor of neuroscience at the University of Connecticut in Farmington, who was not involved in this study. © 2021 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28093 - Posted: 12.01.2021

By Ariana Remmel Scientists have finally sniffed out the molecules behind marijuana’s skunky aroma. The heady bouquet that wafts off of fresh weed is actually a cocktail of hundreds of fragrant compounds. The most prominent floral, citrusy and piney overtones come from a common class of molecules called terpenes, says analytical chemist Iain Oswald of Abstrax Tech, a private company in Tustin, Calif., that develops terpenes for cannabis products (SN: 4/30/18). But the source of that funky ganja note has been hard to pin down. Now, an analysis is the first to identify a group of sulfur compounds in cannabis that account for the skunklike scent, researchers report November 12 in ACS Omega. Oswald and colleagues had a hunch that the culprit may contain sulfur, a stinky element found in hops and skunk spray. So the team started by rating the skunk factor of flowers harvested from more than a dozen varieties of Cannabis sativa on a scale from zero to 10, with 10 being the most pungent. Next, the team created a “chemical fingerprint” of the airborne components that contributed to each cultivar’s unique scent using gas chromatography, mass spectroscopy and a sulfur chemiluminescence detector. As suspected, the researchers found small amounts of several fragrant sulfur compounds lurking in the olfactory profiles of the smelliest cultivars. The most dominant was a molecule called prenylthiol, or 3-methyl-2-butene-1-thiol, that gives “skunked beer” its notorious flavor (SN: 11/27/05). © Society for Science & the Public 2000–2021

Keyword: Chemical Senses (Smell & Taste); Drug Abuse
Link ID: 28092 - Posted: 12.01.2021

To eavesdrop on a brain, one of the best tools neuroscientists have is the fMRI scan, which helps map blood flow, and therefore the spikes in oxygen that occur whenever a particular brain region is being used. It reveals a noisy world. Blood oxygen levels vary from moment to moment, but those spikes never totally flatten out. “Your brain, even resting, is not going to be completely silent,” says Poortata Lalwani, a PhD student in cognitive neuroscience at the University of Michigan. She imagines the brain, even at its most tranquil, as kind of like a tennis player waiting to return a serve: “He’s not going to be standing still. He’s going to be pacing a little bit, getting ready to hit the backhand.” Many fMRI studies filter out that noise to find the particular spikes researchers want to scrutinize. But for Lalwani, that noise is the most telling signal of all. To her, it’s a signal of cognitive flexibility. Young, healthy brains tend to have signals with a lot of variability in blood oxygen levels from moment to moment. Older ones vary less, at least in certain regions of the brain. About a decade ago, scientists first showed the link between low neural signal variability and the kind of cognitive decline that accompanies healthy aging, rather than specific dementias. A brain’s noisiness is a solid proxy for details that are more abstract, Lalwani says: “How efficient information transfer is, how well-connected the neural networks are, in general how well-functioning the underlying neural network is.” But why that change happens with age has been a mystery. So has the question of whether it’s reversible. © 2021 Condé Nast.

Keyword: Attention; Alzheimers
Link ID: 28091 - Posted: 11.24.2021

By Kim Tingley When they first appeared in the United States in the mid-2000s, “electronic nicotine delivery systems” — e-cigarettes, vapes, e-liquids and other wares that contain the stimulant found in tobacco — were subject to little federal oversight. Their makers could incorporate countless other ingredients and flavorings. Like cigarettes before them, the devices proved extremely attractive to young people; in 2018, the surgeon general declared youth vaping an “epidemic” and noted that one in five high schoolers and one in 20 middle schoolers used e-cigarettes. Nicotine can harm the developing brain, and e-cigarettes contain potentially harmful toxins like heavy metals; the long-term effects of vaping — the heating of nicotine to create an inhaled aerosol — are uncertain. Despite these concerns, public-​health officials in the U.S. hope that, given a choice in the open market, people already addicted to nicotine will choose e-cigarettes over cigarettes — a deadly consumer product so successful at attracting and retaining users that it has killed as many as 24 million Americans over the past six decades. Because e-cigarettes generally contain fewer toxic chemicals than tobacco smoke, they are believed to be less damaging than cigarettes. If a sizable number of the one in seven adults in the U.S. who smoke switched to e-cigarettes, the theory goes, significantly fewer people might suffer from cancer and cardiovascular and respiratory diseases. In 2016, in an effort to mitigate the potential harms of e-cigarettes, the Food and Drug Administration began regulating them as “new tobacco products.” It became illegal to sell e-cigarettes to anyone under 18 (a cutoff that rose nationally to 21 in late 2019), and the agency was empowered to require warning labels. The F.D.A. also gained the authority to keep products out of the marketplace, unless it could be demonstrated that their public-health benefit outweighed their risks. (As a result of legislation passed in 2009, this condition applies to new tobacco products in general; cigarettes themselves, and other tobacco products on the market before Feb. 15, 2007, don’t have to meet the same standard.) As of last month, the agency had denied nearly a million applications. But a vaporizer and two liquids, in regular tobacco and menthol flavors, were authorized, after the F.D.A. declared that data submitted by their manufacturer showed that they were indeed less toxic than cigarettes and could, in the words of the agency’s news release, “benefit addicted adult smokers who switch to these products.” This would “outweigh the risk to youth” and lead to an overall “protection of the public health.” © 2021 The New York Times Company

Keyword: Drug Abuse
Link ID: 28090 - Posted: 11.24.2021

By Kelly Servick For patients whose depression resists treatment with drugs and electroconvulsive therapy, surgically implanted wires that stimulate the brain might bring relief. But in recent years, two randomized, controlled trials of this approach, known as deep brain stimulation (DBS), were halted after underwhelming results in interim analyses. “It was like the air was let out of the room,” Sameer Sheth, a neurosurgeon at Baylor College of Medicine, says of those results. “It was a big let-down.” Now, researchers are testing more sophisticated, personalized DBS techniques they hope will yield stronger results. The tests to date have involved just one or a few patients, far from proof of effectiveness. But researchers hope they’ll inform larger studies that finally cement the effectiveness of DBS in depression. “With all these irons in the fire … we will hopefully build up enough understanding and evidence,” says Sheth, an author of a case study published this week. DBS is already approved in the United States to treat epilepsy, obsessive compulsive disorder, and movement disorders such as Parkinson’s disease. Could it also shift patterns of abnormal activity in neural circuits that may drive depression symptoms? Early studies without control groups yielded promising results, but two randomized, controlled trials, sponsored by the medical device companies Medtronic and St. Jude Medical, Inc. (which was later acquired by Abbott Laboratories) did not show significant benefits after several months of DBS, teams reported in 2015 and 2017. Long-term follow-up of participants has revived some optimism. For example, many people in the 30-participant Medtronic trial improved over 1 year or more—beyond the timeline of the initial study, says Stanford University psychiatrist Mahendra Bhati, a co-investigator. Last month, he and colleagues published a follow-up study of eight trial patients, most of whom continue to use their implant about 10 years later. About one-half have had at least a 50% improvement over their pretreatment score on a depression scale. © 2021 American Association for the Advancement of Science.

Keyword: Depression
Link ID: 28089 - Posted: 11.24.2021

By Gretchen Reynolds Does being active make us ravenous afterward and prone to eating more than we perhaps should? Or does it blunt our appetites and make it easier for us to skip that last, tempting slice of pie? A new study provides timely, if cautionary, clues. The study, which involved overweight, sedentary men and women and several types of moderate exercise, found that people who worked out did not overeat afterward at an enticing buffet lunch. However, they also did not skip dessert or skimp on portions. The findings offer a reminder during the holidays that while exercise has countless health benefits, helping us eat less or lose weight may not be among them. For most of us, exercise affects our weight and hunger in unexpected and sometimes contradictory ways. According to multiple scientific studies, few people who start to exercise drop as many pounds as the number of calories they burn working out would foretell. Some recent research suggests this occurs because our bodies stubbornly try to hang on to our fat stores, an evolutionary adaptation that protects us against (unlikely) future famines. So, if we burn calories during exercise, our bodies might nudge us to sit more afterward or reallocate energy from some bodily systems to others, reducing our overall daily energy expenditure. In this way, our bodies unconsciously compensate for many of the calories we burn exercising, reducing our chances of dropping pounds by working out. But that caloric compensation happens slowly, over the course of weeks or months, and involves energy expenditure. It has been less clear whether and how exercise influences our energy intake — that is, how many servings of food we consume — especially in the hours immediately after a workout. The evidence so far has been mixed. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 28088 - Posted: 11.24.2021

By Sabrina Imbler The male Bornean rock frog cannot scream over the sound of a waterfall. Instead, he threatens other frogs with his feet. The frog intimidates his male competitors with a can-can-like gesture: kicking his leg up into the air, fully extending his splayed foot, and dragging it down toward the ground. This foot-flagging display may not sound threatening to a human, but its effect has to do with a frog’s visual perception. To a frog, the world contains two kinds of objects: things that are worms, and things that are not worms. If a frog sees a skinny object moving parallel to its long axis — like how a worm travels along the ground — it sees dinner. But if a frog sees a similar shape moving perpendicular its long axis — very unlike a worm — it sees a threat to flee from. Scientists call this latter movement the anti-worm stimulus, and it strikes fear into the hearts of frogs. Frogs likely evolved this visual system to hunt worms and stay safe from larger predators. Now, researchers suggest some male frogs have evolved to take advantage of their froggy brethren’s fears by kicking and lowering their legs in a gesture that looks a lot like an anti-worm signal, as a way to frighten their competition. In a paper published Wednesday in Proceedings of the Royal Society B, researchers reveal that they could amplify the foot-flagging behavior of Bornean rock frogs by giving the frogs a dose of testosterone. The hormone acts on the muscles in the frog’s leg to exaggerate the gesture, meaning the more testosterone coursing through the frog, the bigger the foot-flagging display. This flamboyant foot display, intensified by the sex hormone, suggests the frogs evolved a way to exploit their competitors’ unusual visual system to appear more dangerous to other frogs. © 2021 The New York Times Company

Keyword: Aggression; Hormones & Behavior
Link ID: 28087 - Posted: 11.20.2021

ByEmily Underwood Scientists have argued for decades over whether humans have pheromones, chemical compounds that trigger aggression and mating in insects and other animals. Although the notion has great popular appeal—search Amazon for “pheromone” and you’ll get the idea—there’s scant evidence for this kind of signal in our species. A new study could change that. Researchers have identified an odorless compound emitted by people—and in particular babies—called hexadecanal, or HEX, that appears to foster aggressive behavior in women and blunt it in men. “We cannot say that this is a pheromone,” says study author Noam Sobel, a neuroscientist at the Weizmann Institute of Science. “But we can say that it’s a molecule expressed by the human body that influences human behavior, specifically aggressive behavior, in a predicted manner.” Humans emit HEX from their skin, saliva, and feces, and it’s among the most abundant molecules babies emit from their heads. When researchers isolated the odorless compound and piped it into mouse cages, it had a relaxing effect on the animals, says Sobel, who studies the role of scent in human interactions. To test how HEX affects people, Eva Mishor, who earned her Ph.D. in Sobel’s lab, created a series of computer games designed to evoke intense frustration—and a measurable response to it—in 126 human participants. Half of the volunteers wore a HEX-infused adhesive strip on their upper lips while they played, whereas the other half wore strips that smelled identical but were HEX-free. In one task, participants negotiated with an unseen partner to divvy up a sum of virtual money. The participants thought they were playing with another person, but they were actually playing against computers. If a player offered their “partner” anything less than 90% of the whole amount, the computer rejected their proposals with a bright red “NO!” preventing them from earning any money. © 2021 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Aggression
Link ID: 28086 - Posted: 11.20.2021