By Kelly Servick Do old and damaged cells remember what it was like to be young? That’s the suggestion of new study, in which scientists reprogrammed neurons in mouse eyes to make them more resistant to damage and able to regrow after injury—like the cells of younger mice. The study suggests that hallmarks of aging, and possibly the keys to reversing it, lie in the epigenome, the proteins and other compounds that decorate DNA and influence what genes are turned on or off. The idea that aging cells hold a memory of their young epigenome “is very provocative,” says Maximina Yun, a regenerative biologist at the Dresden University of Technology who was not involved in the work. The new study “supports that [idea], but by no means proves it,” she adds. If researchers can replicate these results in other animals and explain their mechanism, she says, the work could lead to treatments in humans for age-related disease in the eye and beyond. Epigenetic factors influence our metabolism, our susceptibility to various diseases, and even the way emotional trauma is passed through generations. Molecular biologist David Sinclair of Harvard Medical School, who has long been on the hunt for antiaging strategies, has also looked for signs of aging in the epigenome. “The big question was, is there a reset button?” he says. “Would cells know how to become younger and healthier?” In the new study, Sinclair and his collaborators aimed to rejuvenate cells by inserting genes that encode “reprogramming factors,” which regulate gene expression—the reading of DNA to make proteins. The team chose three of the four factors scientists have used for more than 10 years to turn adult cells into induced pluripotent stem cells, which resemble the cells of an early embryo. (Exposing animals to all four factors can cause tumors.) © 2020 American Association for the Advancement of Science.

Keyword: Vision
Link ID: 27608 - Posted: 12.05.2020

By Lisa Sanders, M.D. “You need to call an ambulance,” the familiar voice from her doctor’s office urged the frightened 59-year-old woman. “Or should I do it for you?” No, she replied shakily. I can do it. The woman looked down at the phone in her hand; there were two of them. She closed one eye and the second phone disappeared. Then she dialed 911. It had been a hellish few days. Five days earlier, she noticed that she was having trouble walking. Her legs couldn’t or wouldn’t follow her brain’s instructions. She had to take these ungainly baby steps to get anywhere. Her muscles felt weak; her feet were inert blocks. Her hands shook uncontrollably. She vomited half a dozen times a day. The week before, she decided to stop drinking, and she recognized the shaking and vomiting as part of that process. The trouble walking, that was new. But that’s not why she called her doctor. The previous day, she was driving home and was just a block away when suddenly there were two of everything. Stone-cold sober and seeing double. There were two dotted lines identifying the middle of her quiet neighborhood street in South Portland, Maine. Two sets of curbs in front of two sets of sidewalks. She stopped the car, rubbed her eyes and discovered that the second objects slid back into the first when one eye stayed covered. She drove home with her face crinkled in an awkward wink. At home, she immediately called her doctor’s office. They wanted to send an ambulance right then. But she didn’t have health insurance. She couldn’t afford either the ambulance or the hospital. She would probably be better by the next day, she told the young woman on the phone. But the next day was the same. And when she called the doctor’s office this time, the medical assistant’s suggestion that she call an ambulance made a lot more sense. The woman was embarrassed by the siren and flashing lights. Her neighbors would be worried. But she couldn’t deny the relief she felt as she watched the ambulance pull up. The E.M.T.s helped her to her feet and onto the stretcher, then drove her to nearby Northern Light Mercy Hospital. © 2020 The New York Times Company

Keyword: Language
Link ID: 27607 - Posted: 12.05.2020

By Mekado Murphy Creating an audioscape for a movie about a musician losing his hearing is more complicated than it may seem. The filmmakers behind the new drama “Sound of Metal” wanted to take audiences into the experience of its lead character, Ruben (Riz Ahmed), a punk-metal drummer who is forced to look at his life differently as he goes deaf. Judging by the overwhelmingly positive reviews, the filmmakers pulled off that difficult feat. In The New York Times, Jeannette Catsoulis raved about “an extraordinarily intricate sound design that allows us to borrow Ruben’s ears.” The film (streaming on Amazon) often places us in Ruben’s aural perspective as he navigates his new reality. (It’s worth watching with headphones or a good sound system.) “I had many conversations with people who have lost their hearing and not two people’s experience is the same,” said Darius Marder, the film’s co-writer and director. “But one thing that’s pretty much true for all people who are deaf is that they don’t lose sound entirely. It isn’t silence.” Instead, Marder and his sound designer, Nicolas Becker, wanted to capture those low-frequency vibrations and other tones. The approach was adjusted for different moments in Ruben’s experience. In separate Zoom interviews, Marder and Becker focused on three scenes as they spoke about some of the techniques and ideas they used to tap into Ruben’s aural experience, including putting microphones inside skulls and mouths. If the first times there’s a notable change in Ruben’s hearing comes before a show, as he is setting up the merchandise table with his bandmate and girlfriend, Lou (Olivia Cooke). At one point, he experiences a high-pitched ringing, then voices are muffled. Ahmed’s response in that moment isn’t just acting. The filmmakers had custom-fit earpieces made for the actor so they could feed him a high-frequency sound they had created. © 2020 The New York Times Company

Keyword: Hearing
Link ID: 27606 - Posted: 12.05.2020

By Veronique Greenwood The ibis and the kiwi are dogged diggers, probing in sand and soil for worms and other buried prey. Sandpipers, too, can be seen along the shore excavating small creatures with their beaks. It was long thought that these birds were using trial and error to find their prey. But then scientists discovered something far more peculiar: Their beaks are threaded with cells that can detect vibrations traveling through the ground. Some birds can feel the movements of their distant quarry directly, while others pick up on waves bouncing off buried shells — echolocating like a dolphin or a bat, in essence, through the earth. There’s one more odd detail in this story of birds’ unusual senses: Ostriches and emus, birds that most definitely do not hunt this way, have beaks with a similar interior structure. They are honeycombed with pits for these cells, though the cells themselves are missing. Now, scientists in a study published Wednesday in Proceedings of the Royal Society B report that prehistoric bird ancestors dating nearly as far back as the dinosaurs most likely were capable of sensing vibrations with their beaks. The birds that use this remote sensing today are not closely related to one another, said Carla du Toit, a graduate student at the University of Cape Town in South Africa and an author of the paper. That made her and her co-authors curious about when exactly this ability evolved, and whether ostriches, which are close relatives of kiwis, had an ancestor that used this sensory ability. “We had a look to see if we could find fossils of early birds from that group,” Ms. du Toit said. “And we’re very lucky.” There are very well-preserved fossils of birds called lithornithids dating from just after the event that drove nonavian dinosaurs to extinction. © 2020 The New York Times Company

Keyword: Pain & Touch; Evolution
Link ID: 27605 - Posted: 12.05.2020

A study led by researchers at the National Institutes of Health has made a surprising connection between frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS), two disorders of the nervous system, and the genetic mutation normally understood to cause Huntington’s disease. This large, international project, which included a collaboration between the National Institute of Neurological Disorders and Stroke (NINDS) and the National Institute on Aging (NIA), opens a potentially new avenue for diagnosing and treating some individuals with FTD or ALS. Several neurological disorders have been linked to “repeat expansions,” a type of mutation that results in abnormal repetition of certain DNA building blocks. For example, Huntington’s disease occurs when a sequence of three DNA building blocks that make up the gene for a protein called huntingtin repeats many more times than normal. These repeats can be used to predict whether someone will develop the illness and even when their symptoms are likely to appear, because the more repeats in the gene, the earlier the onset of disease. “It has been recognized for some time that repeat expansion mutations can give rise to neurological disorders,” said Sonja Scholz, M.D., Ph.D., investigator, NINDS Intramural Research Program. “But screening for these mutations throughout the entire genome has traditionally been cost-prohibitive and technically challenging.” Taking advantage of technology available at NIH, the researchers screened the entire genomes from large cohorts of FTD/ALS patients and compared them to those of age-matched healthy individuals. While several patients had a well-established genetic marker for FTD/ALS, a small subset surprisingly had the same huntingtin mutation normally associated with Huntington’s disease. Remarkably, these individuals did not show the classical symptoms of Huntington’s but rather those of ALS or FTD.

Keyword: ALS-Lou Gehrig's Disease ; Huntingtons
Link ID: 27604 - Posted: 12.05.2020

By Emily Willingham When a male sand-sifting sea star in the coastal waters of Australia reaches out a mating arm to its nearest neighbor, sometimes that neighbor is also male. Undaunted, the pair assume their species’ pseudocopulation position and forge ahead with spawning. Mating, pseudo or otherwise, with a same-sex neighbor obviously does not transfer a set of genes to the next generation—yet several sea star and other echinoderm species persist with the practice. They are not alone. From butterflies to birds to beetles, many animals exhibit same-sex sexual behaviors despite their offering zero chance of reproductive success. Given the energy expense and risk of being eaten that mating attempts can involve, why do these behaviors persist? One hypothesis, hotly debated among biologists, suggests this represents an ancient evolutionary strategy that could ultimately enhance an organism’s chances to reproduce. In results published recently in Nature Ecology & Evolution, Brian Lerch and Maria R. Servedio, from the University of North Carolina, Chapel Hill, offer theoretical support for this proposed explanation. They created a mathematical model that calculated scenarios in which mating attempts, regardless of partner sex, might be worth it. The results predicted that, depending on life span and mating chances, indiscriminate mating with any available candidates could in fact yield a better reproductive payoff than spending precious time and energy sorting out one sex from the other. Although this study does not address sexual orientation or attraction, both of which are common among vertebrate species, it does get at some persistent evolutionary questions: when did animals start distinguishing mates by sex, based on specific cues, and why do some animals apparently remain indiscriminate in their choices? © 2020 Scientific American

Keyword: Sexual Behavior; Evolution
Link ID: 27603 - Posted: 12.05.2020

Abby Olena The smallest terrestrial mammal, the Etruscan shrew (Suncus etruscus), is about as big as a person’s thumb and no heavier than a couple of paper clips. To have enough energy to survive, it must eat eight or more times its body weight daily and therefore doesn’t hibernate. Instead, according to a study published November 30 in PNAS, in winter, these shrews lose 28 percent of the volume from their somatosensory cortex, which likely helps them conserve energy. “This phenomenon of an animal that is not a hibernator still implementing these energy saving strategies is just stunning,” says Christine Schwartz, a neuroscientist who studies hibernation at the University of Wisconsin La Crosse and was not involved in the work. Scientists have shown before that red-toothed shrews, which belong to a group separate from the Etruscan shrew, are born and grow to their full body size in a single summer. Then in autumn, they start to shrink all over—in their spine length, skull, brain, bones, organs such as the liver, and body weight—reaching their smallest size in the winter. Somewhere around February, they start to grow again and reach a second size peak as they sexually mature in the spring. Then they reproduce just once, and, shortly after, die. This cycle is known as Dehnel’s phenomenon. When Saikat Ray was a graduate student in Michael Brecht's lab at the Bernstein Center for Computational Neuroscience in Berlin, he was curious to see if Dehnel’s phenomenon also exists in white-toothed shrews, the subfamily that includes the Etruscan shrew. They already had a colony of Etruscan shrews in the lab, says Ray, who is now a postdoc in Nachum Ulanovsky’s lab at the Weizmann Institute in Israel, because the animals’ tiny brains are a helpful model system for studying more of the brain at once than are the brains of larger mammals, such as mice or rats. © 1986–2020 The Scientist.

Keyword: Neurogenesis
Link ID: 27602 - Posted: 12.05.2020

By Sabrina Imbler In the spring of 2018 at the Montreal Insectarium, Stéphane Le Tirant received a clutch of 13 eggs that he hoped would hatch into leaves. The eggs were not ovals but prisms, brown paper lanterns scarcely bigger than chia seeds. They were laid by a wild-caught female Phyllium asekiense, a leaf insect from Papua New Guinea belonging to a group called frondosum, which was known only from female specimens. Phyllium asekiense is a stunning leaf insect, occurring both in summery greens and autumnal browns. As Royce Cumming, a graduate student at the City University of New York, puts it, “Dead leaf, live leaf, semi-dried leaf.” Mr. Le Tirant, the collections manager of the insectarium since 1989, specializes in scarab beetles; he estimates that he has 25,000 beetles in his private collection at home. But he had always harbored a passion for leaf insects and had successfully bred two species, a small one from the Philippines and a larger one from Malaysia. A Phyllium asekiense — rare, beautiful and, most important, living — would be a treasure in any insectarium. In the insect-rearing laboratory, Mario Bonneau and other technicians nestled the 13 eggs on a mesh screen on a bed of coconut fibers and spritzed them often with water. In the fall, and over the course of several months, five eggs hatched into spindly black nymphs. The technicians treated the baby nymphs with utmost care, moving them from one tree to another without touching the insects, only whatever leaf they clung to. “Other insects, we just grab them,” Mr. Le Tirant said. “But these small leaf insects were so precious, like jewels in our laboratory.” The technicians offered the nymphs a buffet of fragrant guava, bramble and salal leaves. Two nymphs refused to eat and soon died. The remaining three munched on bramble, molted, munched, molted, and molted some more. One nymph grew green and broad, just like her mother. © 2020 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 27601 - Posted: 12.05.2020

By Benedict Carey At a recent visit to the Veterans Affairs clinic in the Bronx, Barry, a decorated Vietnam veteran, learned that he belonged to a very exclusive club. According to a new A.I.-assisted algorithm, he was one of several hundred V.A. patients nationwide, of six million total, deemed at imminent risk of suicide. The news did not take him entirely off guard. Barry, 69, who was badly wounded in the 1968 Tet offensive, had already made two previous attempts on his life. “I don’t like this idea of a list, to tell you the truth — a computer telling me something like this,” Barry, a retired postal worker, said in a phone interview. He asked that his surname be omitted for privacy. “But I thought about it,” Barry said. “I decided, you know, OK — if it’s going to get me more support that I need, then I’m OK with it.” For more than a decade, health officials have watched in vain as suicide rates climbed steadily — by 30 percent nationally since 2000 — and rates in the V.A. system have been higher than in the general population. The trends have defied easy explanation and driven investment in blind analysis: machine learning, or A.I.-assisted algorithms that search medical and other records for patterns historically associated with suicides or attempts in large clinical populations. Doctors have traditionally gauged patients’ risks by looking at past mental health diagnoses and incidents of substance abuse, and by drawing on experience and medical instinct. But these evaluations fall well short of predictive, and the artificially intelligent programs explore many more factors, like employment and marital status, physical ailments, prescription history and hospital visits. These algorithms are black boxes: They flag a person as at high risk of suicide, without providing any rationale. But human intelligence isn’t necessarily better at the task. “The fact is, we can’t rely on trained medical experts to identify people who are truly at high risk,” said Dr. Marianne S. Goodman, a psychiatrist at the Veterans Integrated Service Network in the Bronx, and a clinical professor of medicine at the Icahn School of Medicine at Mount Sinai. “We’re no good at it.” © 2020 The New York Times Company

Keyword: Depression
Link ID: 27600 - Posted: 11.30.2020

By Jelena Kecmanovic Across the spectrum, mental health problems seem to be on the rise. One-quarter of Americans reported moderate to severe depression this summer and another quarter said they suffered from mild depression, a recent study reported. These findings are similar to surveys done by the Census Bureau and the Centers for Disease Control and Prevention. A third of Americans now show signs of clinical anxiety or depression, Census Bureau finds. Former first lady Michelle Obama highlighted the problem for many when she said in August that she has been dealing with “low-grade depression.” As a psychologist, I hear almost daily how the combination of coronavirus, racial unrest, economic uncertainty and political crisis are leading many people to feel a lot worse than usual. “It is not at all surprising that we are seeing the significant increase in distress. It’s a normal reaction to an abnormal situation,” said Judy Beck, president of the Beck Institute for Cognitive Behavior Therapy in Philadelphia and author of the widely used mental health textbook “Cognitive Behavior Therapy: Basics and Beyond.” But an important difference exists between having depressive symptoms — such as sadness, fatigue and loss of motivation — and a full-blown major depressive episode that can affect your ability to function at work and home for weeks or months. The amount and duration of the symptoms, as well as the degree to which they impair one’s life all play a role in diagnosing clinical depression. Extensive research suggests that certain ways of thinking and behaving can hasten the plunge into clinical depression, while others can prevent it. As we head into winter, which can stress the coping skills of many people, here are some strategies that can help you resist the depressive downward spiral. 1. Reduce overthinking. When we feel down, we tend to think about the bad things repeatedly, often trying to figure out why they’ve happened. Research shows that some people are especially prone to this kind of “depressive rumination.” They overanalyze everything, hoping to think their way out of feeling bad, and fret about consequences of their sadness.

Keyword: Depression; Emotions
Link ID: 27599 - Posted: 11.30.2020

by Laura Dattaro Autistic boys with large brains in early childhood still have large brains in adolescence, according to a new study. Autistic girls, too, have brains that grow differently from those of their non-autistic peers. The findings challenge the long-standing idea that brain enlargement in autism is temporary. Previous studies indicated that young children on the spectrum have larger brains than their non-autistic peers but older people with autism do not. To explain the difference, researchers speculated that a pruning process follows early brain overgrowth. But the changes are a mirage, the researchers behind the new study say: Because having a large brain is associated with a low intelligence quotient (IQ) and severe autism traits, and because older children with such characteristics are often excluded from imaging studies, the prior results reflect only a lack of older participants with large brains. “This whole idea of this early overgrowth followed by normalization is just an artifact of sampling bias,” says lead investigator Christine Wu Nordahl, associate professor of psychiatry and behavioral sciences at the University of California, Davis MIND Institute. “It was sort of like, ‘Wow, why didn’t we ever think about this before?’ But it’s pretty clear that that’s what’s happening.” Autistic and non-autistic children also show different development patterns in their white matter — fibers that connect regions of the brain — in early childhood, a second study from Nordahl’s group shows. Some of the differences correlate with changes in the children’s autism traits over time. © 2020 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 27598 - Posted: 11.30.2020

Janet M. Gibson Amusement and pleasant surprises – and the laughter they can trigger – add texture to the fabric of daily life. Those giggles and guffaws can seem like just silly throwaways. But laughter, in response to funny events, actually takes a lot of work, because it activates many areas of the brain: areas that control motor, emotional, cognitive and social processing. As I found when writing “An Introduction to the Psychology of Humor,” researchers now appreciate laughter’s power to enhance physical and mental well-being. People begin laughing in infancy, when it helps develop muscles and upper body strength. Laughter is not just breathing. It relies on complex combinations of facial muscles, often involving movement of the eyes, head and shoulders. Laughter – doing it or observing it – activates multiple regions of the brain: the motor cortex, which controls muscles; the frontal lobe, which helps you understand context; and the limbic system, which modulates positive emotions. Turning all these circuits on strengthens neural connections and helps a healthy brain coordinate its activity. By activating the neural pathways of emotions like joy and mirth, laughter can improve your mood and make your physical and emotional response to stress less intense. For example, laughing may help control brain levels of the neurotransmitter serotonin, similar to what antidepressants do. By minimizing your brain’s responses to threats, it limits the release of neurotransmitters and hormones like cortisol that can wear down your cardiovascular, metabolic and immune systems over time. Laughter’s kind of like an antidote to stress, which weakens these systems and increases vulnerability to diseases. © 2010–2020, The Conversation US, Inc.

Keyword: Emotions; Neuroimmunology
Link ID: 27597 - Posted: 11.30.2020

By Concepción de León Pat Quinn, who helped raise $220 million to fight amyotrophic lateral sclerosis, or A.L.S., by promoting the Ice Bucket Challenge in 2014, died on Sunday, seven years after he learned he had the disease. He was 37. His death, at St. John’s Riverside Hospital in Yonkers, N.Y., was confirmed by the A.L.S. Association and in a post on his official Facebook page. Mr. Quinn did not create the challenge, in which people dumped buckets of ice water on their heads while pledging to donate money to fight A.L.S. But he and his friend Pete Frates, who also had A.L.S., are credited with amplifying it and helping to make it a sensation in the summer and fall of 2014, raising tens of millions of dollars for research and, perhaps nearly as important, wider awareness of the disease. “Pat changed the trajectory of the fight against A.L.S. forever,” Calaneet Balas, the president and chief executive of the A.L.S. Association, said in a statement on Sunday. “He inspired millions to get involved and care about people who are living with A.L.S.” A.L.S., also called Lou Gehrig’s disease, is a progressive neurodegenerative disorder that attacks the nerve cells that control voluntary muscle movements and leads to full paralysis. People with the disease typically live three to five years from the time of diagnosis, according to the National Institute of Neurological Disorders and Stroke. Shortly after Mr. Quinn learned he had A.L.S. in 2013, he created Quinn for the Win, a Facebook group, to raise awareness of the disease and to raise money to fight for a cure. Mr. Frates created his own page, Team Frate Train, with the same goal. In July 2014, Mr. Quinn and Mr. Frates saw another A.L.S. patient, Anthony Senerchia, do the Ice Bucket Challenge online. They created their own ice-bucket videos and shared the challenge with their followers. (Mr. Frates died last year at age 34.) In Her Words: Where women rule the headlines. From there, the campaign spread wildly, with Lady Gaga, Oprah Winfrey, LeBron James and scores of other celebrities participating and donating to the cause. The challenge raised $115 million for the A.L.S. Association and $220 million around the world for A.L.S. research in the span of just six weeks, the A.L.S. Association said. © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27596 - Posted: 11.30.2020

by Josh Wilbur Jake Haendel was a hard-partying chef from a sleepy region of Massachusetts. When he was 28, his heroin addiction resulted in catastrophic brain damage and very nearly killed him. In a matter of months, Jake’s existence became reduced to a voice in his head. Jake’s parents had divorced when he was young. He grew up between their two homes in a couple of small towns just beyond reach of Boston, little more than strip malls, ailing churches and half-empty sports bars. His mother died of breast cancer when he was 19. By then, he had already been selling marijuana and abusing OxyContin, an opioid, for years. “Like a lot of kids at my school, I fell in love with oxy. If I was out to dinner with my family at a restaurant, I would go to the bathroom just to get a fix,” he said. He started culinary school, where he continued to experiment with opioids and cocaine. He hid his drug use from family and friends behind a sociable, fun-loving front. Inside, he felt anxious and empty. “I numbed myself with partying,” he said. After culinary school, he took a job as a chef at a local country club. At 25, Jake tried heroin for the first time, with a co-worker (narcotics are notoriously prevalent in American kitchens). By the summer of 2013, Jake was struggling to find prescription opioids. For months, he had been fending off the symptoms of opioid withdrawal, which he likened to “a severe case of the flu with an added feeling of impending doom”. Heroin offered a euphoric high, staving off the intense nausea and shaking chills of withdrawal. Despite his worsening addiction, Jake married his girlfriend, Ellen, in late 2016. Early in their relationship, Ellen had asked him if he was using heroin. He had lied without hesitation, but she soon found out the truth, and within months, the marriage was falling apart. “I was out of control, selling lots of heroin, using even more, spending a ridiculous amount of money on drugs and alcohol,” he said. In May 2017, Ellen noticed that he was talking funnily, his words slurred and off-pitch. “What’s up with your voice?” she asked him repeatedly.

Keyword: Consciousness; Drug Abuse
Link ID: 27595 - Posted: 11.27.2020

By Bethany Brookshire A hungry brain craves food. A lonely brain craves people. After spending a day completely isolated from anyone else, people’s brains perked up at the sight of social gatherings, like a hungry person’s brain seeing food, scientists report November 23 in Nature Neuroscience. Cognitive neuroscientist Livia Tomova, then at MIT, and her colleagues had 40 participants fast for 10 hours. At the end of the day, certain nerve cells in the midbrain fired up in response to pictures of pizza and chocolate cake. Those neurons — in the substantia nigra pars compacta and ventral tegmental area — produce dopamine, a chemical messenger associated with reward (SN: 8/27/15). On a different day, the same people underwent 10 hours of isolation (no friends, no Facebook and no Instagram). That evening, neurons in the same spot activated in response to pictures of people chatting or playing team sports. The more hunger or isolation the subject reported, the stronger the effect (SN: 10/4/17). In people who reported that they were generally more lonely, the social responses were blunted. “We don’t really know what causes that,” Tomova says. “Maybe being isolated doesn’t really affect them as much, because it’s something that is not that different, perhaps, from their everyday life.” The midbrain, which plays an important role in people’s motivation to seek food, friends, gambling or drugs, responds to food and social signals even when people aren’t hungry or lonely. After all, a person always could eat or hang out. But hunger and loneliness increased the reaction and made people’s responses specific to the thing they were missing. The findings “speak to our current state,” says Tomova, now at the University of Cambridge. COVID-19 has left many more socially isolated, putting mental as well as physical health at stake (SN: 3/29/20) and leaving people with cravings for more than food. “It’s important to look at the social dimension of this kind of crisis.” L. Tomova et al. Acute social isolation evokes midbrain craving responses similar to hunger. Nature Neuroscience. Published online November 23, 2020. doi: 10.1038/s41593-020-00742-z. = © Society for Science & the Public 2000–2020

Keyword: Stress; Obesity
Link ID: 27594 - Posted: 11.27.2020

By Lisa Feldman Barrett Five hundred million years ago, a tiny sea creature changed the course of history: It became the first predator. It somehow sensed the presence of another creature nearby, propelled or wiggled its way over, and deliberately ate it. This new activity of hunting started an evolutionary arms race. Over millions of years, both predators and prey evolved more complex bodies that could sense and move more effectively to catch or elude other creatures. Eventually, some creatures evolved a command center to run those complex bodies. We call it a brain. This story of how brains evolved, while admittedly just a sketch, draws attention to a key insight about human beings that is too often overlooked. Your brain’s most important job isn’t thinking; it’s running the systems of your body to keep you alive and well. According to recent findings in neuroscience, even when your brain does produce conscious thoughts and feelings, they are more in service to the needs of managing your body than you realize. And in stressful times like right now, this curious perspective on your mental life may actually help to lessen your anxieties. Much of your brain’s activity happens outside your awareness. In every moment, your brain must figure out your body’s needs for the next moment and execute a plan to fill those needs in advance. For example, each morning as you wake, your brain anticipates the energy you’ll need to drag your sorry body out of bed and start your day. It proactively floods your bloodstream with the hormone cortisol, which helps make glucose available for quick energy. Your brain runs your body using something like a budget. A financial budget tracks money as it’s earned and spent. The budget for your body tracks resources like water, salt and glucose as you gain and lose them. Each action that spends resources, such as standing up, running, and learning, is like a withdrawal from your account. Actions that replenish your resources, such as eating and sleeping, are like deposits. The scientific name for body budgeting is allostasis. It means automatically predicting and preparing to meet the body’s needs before they arise. © 2020 The New York Times Company

Keyword: Stress
Link ID: 27593 - Posted: 11.27.2020

By Katherine J. Wu For a rodent that resembles the love child of a skunk and a steel wool brush, the African crested rat carries itself with a surprising amount of swagger. The rats “very much have the personality of something that knows it’s poisonous,” says Sara Weinstein, a biologist at the University of Utah and the Smithsonian Conservation Biology Institute who studies them. In sharp contrast to most of their skittish rodent kin, Lophiomys imhausi lumber about with the languidness of porcupines. When cornered, they fluff up the fur along their backs into a tip-frosted mohawk, revealing rows of black-and-white bands that run like racing stripes down their flanks — and, at their center, a thicket of specialized brown hairs with a honeycomb-like texture. Those spongy hairs contain a poison powerful enough to bring an elephant to its knees, and are central to Dr. Weinstein’s recent research, which confirmed ideas about how this rat makes itself so deadly. Give them a chance and African crested rats will take nibbles from the branch of a poison arrow tree. It’s not for nutrition. Instead, they will chew chunks of the plants and spit them back out into their fur, anointing themselves with a form of chemical armor that most likely protects them from predators like hyenas and wild dogs. The ritual transforms the rats into the world’s only known toxic rodents, and ranks them among the few mammals that borrow poisons from plants. Dr. Weinstein’s research, which was published last week in the Journal of Mammalogy, is not the first to document the crested rats’ bizarre behavior. But the new paper adds weight to an idea described nearly a decade ago, and offers an early glimpse into the animals’ social lives. First documented in the scientific literature in 1867, the rarely-glimpsed African crested rat “has captured so much interest for so long,” said Kwasi Wrensford, a behavioral ecologist at the University of California, Berkeley who wasn’t involved in the study. “We’re now just starting to unpack what makes this animal tick.” © 2020 The New York Times Company

Keyword: Neurotoxins; Learning & Memory
Link ID: 27592 - Posted: 11.27.2020

By Lindsay Gray When Herbert Weinstein stood trial for the murder of his wife in 1992, his attorneys were struck by the measured calm with which he recounted her death and the events leading up to it. He made no attempt to deny that he was culpable, and yet his stoicism in the face of his wildly uncharacteristic actions led his defense to suspect that he might not be. Weinstein underwent neuroimaging tests, which confirmed what his attorneys had suspected: a cyst had impinged upon large parts of Weinstein’s frontal lobe, the seat of impulse control in the brain. On these grounds, they reasoned he should be found not guilty by reason of insanity, despite Weinstein’s free admission of guilt. Guilt is difficult to define, but it pervades every aspect of our lives, whether we’re chastising ourselves for skipping a workout, or serving on the jury of a criminal trial. Humans seem to be hardwired for justice, but we’re also saddled with a curious compulsion to diagram our own emotional wiring. This drive to assign a neurochemical method to our madness has led to the generation of vast catalogs of neuroimaging studies that detail the neural underpinnings of everything from anxiety to nostalgia. In a recent study, researchers now claim to have moved us one step closer to knowing what a guilty brain looks like. Since guilt carries different weight depending on context or culture, the authors of the study chose to define it operationally as the awareness of having harmed someone else. A series of functional magnetic resonance imaging (fMRI) experiments across two separate cohorts, one Swiss and one Chinese, revealed what they refer to as a “guilt-related brain signature” that persists across groups. Since pervasive guilt is a common feature in severe depression and PTSD, the authors suggest that a neural biomarker for guilt could offer more precise insight into these conditions and, potentially, their treatment. But brain-based biomarkers for complex human behaviors also lend themselves to the more ethically fraught discipline of neuroprediction, an emergent branch of behavioral science that combines neuroimaging data and machine learning to forecast how an individual is likely to act based on how their brain scans compare to those of other groups. © 2020 Scientific American,

Keyword: Stress; Brain imaging
Link ID: 27591 - Posted: 11.21.2020

by Peter Hess / Mutations in a top autism gene called SYNGAP1 slow the rate at which zebrafish digest food and pass waste. The findings may explain why some people with SYNGAP1 mutations have gastrointestinal (GI) problems. Researchers presented the unpublished work on Tuesday and Wednesday at the 2020 International SYNGAP1 Scientific Conference, which took place virtually because of the coronavirus pandemic. They also began recruiting people with SYNGAP1 mutations at the meeting for an ongoing study of gut function. “It’s been in the literature, this link between GI symptoms and [autism], for a long time, with not a lot of progress on the mechanisms,” says lead researcher Julia Dallman, associate professor of biology at the University of Miami in Florida, who presented the findings on Wednesday. In the brain, SYNGAP1 functions mainly at synapses, or the junctions between neurons, and helps the cells exchange chemical messages. Mutations in the gene are strongly linked to autism, seizures, intellectual disability and sleep problems. Prompted by families’ anecdotal reports of constipation, reflux and overeating in people with SYNGAP1 mutations, Dallman and her colleagues decided to explore the gene’s role in the gut. The young zebrafish’s transparent skin allowed the researchers to trace the movement of microscopic fluorescent beads — mixed into the fish’s food — through the gut. In this way, they measured how quickly and how strongly the digestive tract moves food and waste. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27590 - Posted: 11.21.2020

By Kashmir Hill and Jeremy White There are now businesses that sell fake people. On the website Generated.Photos, you can buy a “unique, worry-free” fake person for $2.99, or 1,000 people for $1,000. If you just need a couple of fake people — for characters in a video game, or to make your company website appear more diverse — you can get their photos for free on ThisPersonDoesNotExist.com. Adjust their likeness as needed; make them old or young or the ethnicity of your choosing. If you want your fake person animated, a company called Rosebud.AI can do that and can even make them talk. These simulated people are starting to show up around the internet, used as masks by real people with nefarious intent: spies who don an attractive face in an effort to infiltrate the intelligence community; right-wing propagandists who hide behind fake profiles, photo and all; online harassers who troll their targets with a friendly visage. The A.I. system sees each face as a complex mathematical figure, a range of values that can be shifted. Choosing different values — like those that determine the size and shape of eyes — can alter the whole image. For other qualities, our system used a different approach. Instead of shifting values that determine specific parts of the image, the system first generated two images to establish starting and end points for all of the values, and then created images in between. The creation of these types of fake images only became possible in recent years thanks to a new type of artificial intelligence called a generative adversarial network. In essence, you feed a computer program a bunch of photos of real people. It studies them and tries to come up with its own photos of people, while another part of the system tries to detect which of those photos are fake. The back-and-forth makes the end product ever more indistinguishable from the real thing. The portraits in this story were created by The Times using GAN software that was made publicly available by the computer graphics company Nvidia. © 2020 The New York Times Company

Keyword: Attention
Link ID: 27589 - Posted: 11.21.2020