By Cara Giaimo Platypuses do it. Opossums do it. Even three species of North American flying squirrel do it. Tasmanian devils, echidnas and wombats may also do it, although the evidence is not quite so robust. And, breaking news: Two species of rabbit-size rodents called springhares do it. That is, they glow under black light, that perplexing quirk of certain mammals that is baffling biologists and delighting animal lovers all over the world. Springhares, which hop around the savannas of southern and eastern Africa, weren’t on anyone’s fluorescence bingo card. Like the other glowing mammals, they are nocturnal. But unlike the other creatures, they are Old World placental mammals, an evolutionary group not previously represented. Their glow, a unique pinkish-orange the authors call “funky and vivid,” forms surprisingly variable patterns, generally concentrated on the head, legs, rear and tail. Fluorescence is a material property rather than a biological one. Certain pigments can absorb ultraviolet light and re-emit it as a vibrant, visible color. These pigments have been found in amphibians and some birds, and are added to things like white T-shirts and party supplies. But mammals, it seems, don’t tend to have these pigments. A group of researchers, many associated with Northland College in Ashland, Wis., has been chasing down exceptions for the past few years — ever since one member, the biologist Jonathan Martin, happened to wave a UV flashlight at a flying squirrel in his backyard. It glowed eraser pink. © 2021 The New York Times Company

Keyword: Vision; Evolution
Link ID: 27697 - Posted: 02.19.2021

By Gary Stix A consensus has emerged in recent years that psychotherapies—in particular, cognitive behavioral therapy (CBT)—rate comparably to medications such as Prozac and Lexapro as treatments for depression. Either option, or the two together, may at times alleviate the mood disorder. In looking more closely at both treatments, CBT—which delves into dysfunctional thinking patterns—may have a benefit that could make it the better choice for a patient.The reason may be rooted in our deep evolutionary past. Scholars suggest humans may become depressed to help us focus attention on a problem that might cause someone to fall out of step with family, friends, clan or the larger society—an outcast status that, especially in Paleolithic times, would have meant an all-but-certain tragic fate. Depression, by this account, came about as a mood state to make us think long and hard about behaviors that may have caused us to become despondent because some issue in our lives is socially problematic. A recent article in American Psychologist, the flagship publication of the American Psychological Association, weighs what the possible evolutionary origins of depression might mean for arguments about the merits of psychotherapy versus antidepressants. In the article, Steven D. Hollon, a professor of psychology at Vanderbilt University, explores the implications of helping a patient come to grips with the underlying causes of a depression—which is the goal of CBT, and is also in line with an evolutionary explanation. The anodyne effects of an antidepressant, by contrast, may divert a patient from engaging in the reflective process for which depression evolved—a reason perhaps that psychotherapy appears to produce a more enduring effect than antidepressants. Scientific American spoke with Hollon about his ideas on the topic.

Keyword: Depression
Link ID: 27696 - Posted: 02.17.2021

By Cathleen O’Grady As Samuel West combed through a paper that found a link between watching cartoon violence and aggression in children, he noticed something odd about the study participants. There were more than 3000—an unusually large number—and they were all 10 years old. “It was just too perfect,” says West, a Ph.D. student in social psychology at Virginia Commonwealth University. Yet West added the 2019 study, published in Aggressive Behavior and led by psychologist Qian Zhang of Southwest University of Chongqing, to his meta-analysis after a reviewer asked him to cast a wider net. West didn’t feel his vague misgivings could justify excluding it from the study pool. But after Aggressive Behavior published West’s meta-analysis last year, he was startled to find that the journal was investigating Zhang’s paper while his own was under review. It is just one of many papers of Zhang’s that have recently been called into question, casting a shadow on research into the controversial question of whether violent entertainment fosters violent behavior. Zhang denies any wrongdoing, but two papers have been retracted. Others live on in journals and meta-analyses—a “major problem” for a field with conflicting results and entrenched camps, says Amy Orben, a cognitive scientist at the University of Cambridge who studies media and behavior. And not just for the ivory tower, she says: The research shapes media warning labels and decisions by parents and health professionals. © 2021 American Association for the Advancement of Science.

Keyword: Aggression; Development of the Brain
Link ID: 27695 - Posted: 02.17.2021

In a study led by National Institutes of Health researchers, scientists found that five genes may play a critical role in determining whether a person will suffer from Lewy body dementia, a devastating disorder that riddles the brain with clumps of abnormal protein deposits called Lewy bodies. Lewy bodies are also a hallmark of Parkinson’s disease. The results, published in Nature Genetics, not only supported the disease’s ties to Parkinson’s disease but also suggested that people who have Lewy body dementia may share similar genetic profiles to those who have Alzheimer’s disease. “Lewy body dementia is a devastating brain disorder for which we have no effective treatments. Patients often appear to suffer the worst of both Alzheimer’s and Parkinson’s diseases. Our results support the idea that this may be because Lewy body dementia is caused by a spectrum of problems that can be seen in both disorders,” said Sonja Scholz, M.D., Ph.D., investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and the senior author of the study. “We hope that these results will act as a blueprint for understanding the disease and developing new treatments.” The study was led by Dr. Scholz’s team and researchers in the lab of Bryan J. Traynor, M.D., Ph.D., senior investigator at the NIH’s National Institute on Aging (NIA). Lewy body dementia usually affects people over 65 years old. Early signs of the disease include hallucinations, mood swings, and problems with thinking, movements, and sleep. Patients who initially have cognitive and behavioral problems are usually diagnosed as having dementia with Lewy bodies, but are sometimes mistakenly diagnosed with Alzheimer’s disease. Alternatively, many patients, that are initially diagnosed with Parkinson’s disease, may eventually have difficulties with thinking and mood caused by Lewy body dementia. In both cases, as the disease worsens, patients become severely disabled and may die within eight years of diagnosis.

Keyword: Alzheimers; Parkinsons
Link ID: 27694 - Posted: 02.17.2021

By Isobel Whitcomb It began with a pulled muscle. Each day after school, as the sun sank dusky purple over the hills of my hometown, I’d run with my track teammates. Even on our easy days, I’d bound ahead, leaving them behind. It wasn’t that I thought myself better than them—it’s that when I ran fast, and focused on nothing but the cold air burning my lungs and my feet pounding, my normally anxious thoughts turned to white noise. Until, one day, something popped in my leg. I stopped. I limped a little, and then tried running again: sharp, hot pain radiated down my thigh. Panic flooded me, as I imagined weeks without running: weeks without a predictable break from my own thoughts, weeks immersed in adolescent loneliness. I was 14. Pain was about to define a decade of my life. Advertisement First, I took a break from the sport—five months of stretching, icing, and waiting for the leg to heal. I returned to running, but soon after, I developed a throbbing pain in my back. The cycle repeated. Less than a year later, the pain showed up again, this time in my foot. My focus on healing my body became singular: I tried physical therapy and massage and acupuncture. I researched conditions that could lead to repeat injury. Maybe I had a rare soft-tissue disorder, I thought, or maybe early-onset rheumatoid arthritis. I let an osteopath stick a giant needle into my spinal ligaments, and inject me with sugar water, which is just as painful as it sounds. After a chiropractor recommended an anti-inflammatory diet, I subsisted on only meat and vegetables. I’d get a few good months—a joyful summer, a successful cross-country season. Then the pain would return again. As I prepared to leave home for college, my knees and ankles throbbed. For several months, my hip hurt so badly I dreaded even walking to the dining hall. Then, while scrambling to finish my senior thesis, neck spasms prevented me from leaving my bed for days. When I saw doctors, I hoped that they would discover something terribly wrong. They never did. “Have you tried psychotherapy?” one asked me. I had. I’d been in therapy for years. © 2021 The Slate Group LLC.

Keyword: Pain & Touch; Attention
Link ID: 27693 - Posted: 02.15.2021

By Sabrina Imbler Over the course of her 32 years, Cheyenne the red-bellied lemur has had many soul mates. Her first was a mate in the traditional sense, a male red-bellied lemur who lived monogamously with Cheyenne for many years at the Duke Lemur Center in Durham, N.C. When he died, the elderly Cheyenne moved on to Geb, a geriatric crowned lemur; his young mate, Aria, had recently left him for a an even younger lemur. Cheyenne and Geb shared several years of peaceful, platonic companionship until Geb died in 2018 at the venerable age of 26. Cheyenne now lives with Chloris, a 32-year-old ring-tailed lemur who has full cataracts in one eye and arthritis in her tail. The two spend their days as many couples do, elderly or not: sleeping, hanging out, grooming each other and cuddling. “Right now Chloris and Cheyenne are snuggled up like a yin-yang symbol,” Britt Keith, the head lemur keeper, said on a call from the D wing of the center, which houses many of the center’s geriatric lemurs. The goal of Cheyenne and Chloris’s pairing is not for them to breed; the lemurs are both post-reproductive females. Rather, it is companionship, the comfort of having someone to spend your twilight days with and a soft body to snuggle up to at night — and, in Cheyenne and Chloris’s case, also during the day. “They sleep a lot,” Ms. Keith said. In the wild, lemurs generally do not want for company. Red-bellied lemurs form extremely tight, long-term bonds with their mates, and pairs rarely stray more than than three dozen feet apart, according to Stacey Tecot, a lemur primatologist at the University of Arizona. Crowned lemurs like Geb and ring-tailed lemurs like Chloris are not monogamous but have rich social lives, said Nicholas Grebe, a postdoctoral researcher who studies lemur behavior at Duke University and who knows Cheyenne and Chloris. © 2021 The New York Times Company

Keyword: Emotions; Pain & Touch
Link ID: 27692 - Posted: 02.15.2021

By William Weir There are a few ways we perceive food, and not all are particularly well-understood. We know that much of it happens in the olfactory bulb, a small lump of tissue between the eyes and behind the nose, but how the stimuli arrive at this part of the brain is still being worked out. How these stimuli are processed in the brain plays a major role in our daily life. Fully understanding how our perceptions of food are formed is critical, Fahmeed Hyder said, but getting a clear picture of what our brains do when we smell has been tricky. “Knowing which exact pathways are affected and teaching our brain to appreciate and acknowledge both modes of perception in understanding the flavor is a part of our culture that we haven’t fully exploited yet,” he said. A better understanding of how smells get to our brain would not only tell us a lot about our eating habits, he said, it could even potentially help patients of certain diseases. Hyder, professor of biomedical engineering and radiology & biomedical imaging, has taken a detailed look at the function of the olfactory bulb. It may not be one of the most talked-about regions of the brain, but it helps us make sense of the outside world by taking in molecules from food — known as food volatiles — and then sending these signals further into the brain. It serves a pivotal role as the gateway for chemical stimuli to the rest of the brain — specifically the piriform cortex, amygdala, and hippocampus. To see exactly how it does that, Hyder and his team mapped the activity in the entire olfactory bulb. It’s the first time that this has ever been done for the two independent routes of odor delivery — that is, the orthonasal and retronasal routes. The results were published in NeuroImage. Copyright © 2021 Yale University

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27691 - Posted: 02.15.2021

By Leslie Nemo Ironically, this tangle of brain cells is helping scientists tease apart a larger problem: how to help people with Alzheimer’s disease. Matheus Victor, a researcher at the Massachusetts Institute of Technology, photographed these neurons after coaxing them to life in a petri dish in the hope that the rudimentary brain tissue will reveal why a new therapy might alleviate Alzheimer’s symptoms. In humans and mice, a healthy memory is associated with a high level of synced neurons that turn on and off simultaneously. Those with neurological conditions such as Alzheimer’s and Parkinson’s disease often have fewer brain cells blinking unanimously. A couple of years ago Victor’s lab leader Li-Huei Tsai and her team at M.I.T. found that when they surrounded mice genetically predisposed to Alzheimer’s with sound pulses beating 40 times a second, the rodents performed better on memory-related tasks. The animals also lost some amyloid plaques, protein deposits in the brain that are characteristic of the disease. The researchers had previously performed a similar study with light flickering at the same rate, and the mice were found to experience additional improvements when the sound and light pulses were combined. Astoundingly, the mouse neurons synced up to the 40-beats-per-second rhythm of the audio pulses, though the mechanism behind this result and the reason the shift improves symptoms remain a mystery. To help solve it, the researchers want to watch how brain tissue responds to the stimulants at the cellular level. The goal is to one day understand how this exposure treatment might work for people, so the team is growing human brain cells in the lab and engineering them to respond to sound and light without eyes and ears. “We are trying to mimic the sensory stimulation in mice but missing a lot of the hardware that makes it possible. So this is a bit of a hack,” Victor says. © 2021 Scientific American

Keyword: Alzheimers; Brain imaging
Link ID: 27690 - Posted: 02.15.2021

By Alex Vadukul In the early 1970s, the field of neuroradiology was still in its formative years, and among its early practitioners was Dr. John Bentson, at UCLA Medical Center in Los Angeles. As he helped patients with the aid of new technology like the CT scan and computer imaging, he saw an opportunity for innovation. A subspecialty of radiology, neuroradiology involves diagnosing and treating ailments in the brain, spinal cord and nerves. One tool used in treatment is the combination of an angiographic guidewire and catheter, essentially a slender wire and tube. Inserted through the leg, it can aid with the injection of contrast dye for diagnostic brain imaging and the treatment of aneurysms. At the time, however, guidewires were rigid and at worst could injure a blood vessel. Dr. Bentson decided to design a better type. He conceived of a more supple guidewire that also featured a flexible tip, and after UCLA built an early prototype for him, other neuroradiologists started using his model. Cook Medical began manufacturing the device in 1973, and it’s still in use today, commonly known as a Bentson guidewire. Dr. Bentson died at 83 on Dec. 28 at a hospital in Los Angeles. The cause was complications of Covid-19, his daughter Dr. Erika Drazan said. “He liked to push boundaries if he thought he could help the patient,” she said. “He liked saying that the vessels in the body are just like a tree, and that he could get where he wanted through them by feel.” Thousands of patients have benefited from his innovation, The American Society of Neuroradiology said after his death. John Reinert Bentson was born on May 15, 1937, in Viroqua, Wis., to Carl and Stella (Hagen) Bentson, who were of Norwegian heritage. He was raised on his family’s dairy farm, going to school in the winter on wooden skis. His mother prepared Norwegian fare like lutefisk. © 2021 The New York Times Company

Keyword: Brain imaging; Stroke
Link ID: 27689 - Posted: 02.15.2021

By Gina Kolata For the first time, a drug has been shown so effective against obesity that patients may dodge many of its worst consequences, including diabetes, researchers reported on Wednesday. The drug, semaglutide, made by Novo Nordisk, already is marketed as a treatment for Type 2 diabetes. In a clinical trial published in the New England Journal of Medicine, researchers at Northwestern University in Chicago tested semaglutide at a much higher dose as an anti-obesity medication. Nearly 2,000 participants, at 129 centers in 16 countries, injected themselves weekly with semaglutide or a placebo for 68 weeks. Those who got the drug lost close to 15 percent of their body weight, on average, compared with 2.4 percent among those receiving the placebo. More than a third of the participants receiving the drug lost more than 20 percent of their weight. Symptoms of diabetes and pre-diabetes improved in many patients. Those results far exceed the amount of weight loss observed in clinical trials of other obesity medications, experts said. The drug is a “game-changer,” said Dr. Robert F. Kushner, an obesity researcher at Northwestern University Feinberg School of Medicine, who led the study. “This is the start of a new era of effective treatments for obesity.” Dr. Clifford Rosen of Maine Medical Center Research Institute, who was not involved in the trial, said, “I think it has a huge potential for weight loss.” Gastrointestinal symptoms among the participants were “really marginal — nothing like with weight loss drugs in the past,” added Dr. Rosen, an editor at the New England Journal of Medicine and a co-author of an editorial accompanying the study. For decades, scientists have searched for ways to help growing numbers of people struggling with obesity. Five currently available anti-obesity drugs have side effects that limit their use. The most effective, phentermine, brings about a 7.5 percent weight loss, on average, and can be taken only for a short time. After it is stopped, even that amount of weight is regained. © 2021 The New York Times Company

Keyword: Obesity
Link ID: 27688 - Posted: 02.13.2021

Ariana Remmel Researchers have created tiny, brain-like ‘organoids’ that contain a gene variant harboured by two extinct human relatives, Neanderthals and Denisovans. The tissues, made by engineering human stem cells, are far from being true representations of these species’ brains — but they show distinct differences from human organoids, including size, shape and texture. The findings, published1 in Science on 11 February, could help scientists to understand the genetic pathways that allowed human brains to evolve. Can lab-grown brains become conscious? “It’s an extraordinary paper with some extraordinary claims,” says Gray Camp, a developmental biologist at the University of Basel in Switzerland, whose lab last year reported2 growing brain organoids that contained a gene common to Neanderthals and humans. The latest work takes the research further by looking at gene variants that humans lost in evolution. But Camp remains sceptical about the implications of the results, and says the work opens more questions that will require investigation. Humans are more closely related to Neanderthals and Denisovans than to any living primate, and some 40% of the Neanderthal genome can still be found spread throughout living humans. But researchers have limited means to study these ancient species’ brains — soft tissue is not well preserved, and most studies rely on inspecting the size and shape of fossilized skulls. Knowing how the species’ genes differ from humans’ is important because it helps researchers to understand what makes humans unique — especially in our brains. © 2021 Springer Nature Limited

Keyword: Development of the Brain; Evolution
Link ID: 27687 - Posted: 02.13.2021

By Carolyn Gramling The fin whale’s call is among the loudest in the ocean: It can even penetrate into Earth’s crust, a new study finds. Echoes in whale songs recorded by seismic instruments on the ocean floor reveal that the sound waves pass through layers of sediment and underlying rock. These songs can help probe the structure of the crust when more conventional survey methods are not available, researchers report in the Feb. 12 Science. Six songs, all from a single whale that sang as it swam, were analyzed by seismologists Václav Kuna of the Czech Academy of Sciences in Prague and John Nábělek of Oregon State University in Corvallis. They recorded the songs, lasting from 2.5 to 4.9 hours, in 2012 and 2013 with a network of 54 ocean-bottom seismometers in the northeast Pacific Ocean. The songs of fin whales (Balaenoptera physalus) can be up to 189 decibels, as noisy as a large ship. Seismic instruments detect the sound waves of the song, just like they pick up pulses from earthquakes or from air guns used for ship-based surveys. The underwater sounds can also produce seismic echoes: When sound waves traveling through the water meet the ground, some of the waves’ energy converts into a seismic wave (SN: 9/17/20). Those seismic waves can help scientists “see” underground: As the penetrating waves bounce off different rock layers, researchers can estimate the thickness of the layers. Changes in the waves’ speed can also reveal what types of rocks the waves traveled through. © Society for Science & the Public 2000–2021.

Keyword: Hearing; Animal Communication
Link ID: 27686 - Posted: 02.13.2021

By Warren Cornwall Prozac might need a new warning label: “Caution: This antidepressant may turn fish into zombies.” Researchers have found that long-term exposure to the drug makes guppies act more alike, wiping out some of the typical behavioral differences that distinguish them. That could be a big problem when the medication—technically named fluoxetine—washes into streams and rivers, potentially making fish populations more vulnerable to predators and other threats. In recent decades, scientists have uncovered a plethora of ways that pharmaceuticals affect animals in the lab and in the wild, such as by altering courtship, migration, and anxiety. The drugs find their way into the environment through water that pours from sewage treatment plants, which is rarely filtered to remove the chemicals. But the findings are usually based on an average taken from combining measurements of all the individual animals in a group. Giovanni Polverino, a behavioral ecologist at the University of Western Australia, Perth, and colleagues wondered whether this calculation obscured important but subtle insights about individual animals. Did the drug change behavior similarly in all the creatures in a group? Or were certain kinds of “personalities” affected more strongly? To find out, Polverino’s team captured 3600 guppies (Poecilia reticulata)—a common silvery fish often used in labs that grows to half the length of an average human’s pinkie—from a creek in northeastern Australia. In the laboratory, the fish and their offspring—as many as six generations—spent 2 years in tanks filled with either freshwater, water with fluoxetine at levels common in the wild, or a higher dose similar to places near sewage outflows. © 2021 American Association for the Advancement of Science.

Keyword: Depression; Neurotoxins
Link ID: 27685 - Posted: 02.13.2021

Elizabeth Landau At a sleep research symposium in January 2020, Janna Lendner presented findings that hint at a way to look at people’s brain activity for signs of the boundary between wakefulness and unconsciousness. For patients who are comatose or under anesthesia, it can be all-important that physicians make that distinction correctly. Doing so is trickier than it might sound, however, because when someone is in the dreaming state of rapid-eye movement (REM) sleep, their brain produces the same familiar, smoothly oscillating brain waves as when they are awake. Lendner argued, though, that the answer isn’t in the regular brain waves, but rather in an aspect of neural activity that scientists might normally ignore: the erratic background noise. Some researchers seemed incredulous. “They said, ‘So, you’re telling me that there’s, like, information in the noise?’” said Lendner, an anesthesiology resident at the University Medical Center in Tübingen, Germany, who recently completed a postdoc at the University of California, Berkeley. “I said, ‘Yes. Someone’s noise is another one’s signal.’” Lendner is one of a growing number of neuroscientists energized by the idea that noise in the brain’s electrical activity could hold new clues to its inner workings. What was once seen as the neurological equivalent of annoying television static may have profound implications for how scientists study the brain. All Rights Reserved © 2021

Keyword: Sleep; Attention
Link ID: 27684 - Posted: 02.13.2021

By Jamie Talan When Fred “Rusty” Gage began his career in neuroscience more than four decades ago, the general thinking was that adult human brain cells just don’t reproduce and that their numbers are fixed. You lose them, they are gone forever. But Gage’s studies on adult human brain cells in the 1990s surprised everyone, including himself, when he and his colleagues found that exercise — such as running — and enriched, complex and variable environments can give rise to new populations of cells that serve the brain well. He has been a serious runner most of his life, so this was good news on every level. Now 70 and president of the Salk Institute for Biological Sciences in the La Jolla neighborhood in San Diego, Gage is still trying to figure out how adults can continue to make new brain cells and keep their brains healthier and resistant to disease. As head of the institute, he also supports his colleagues’ broader work in novel approaches to treating cancer, how the properties in the food we eat shape our brains, the effect of isolation on brain functioning, and plant biology and climate change. The Washington Post spoke with Gage on a video conference call recently to talk about growing up overseas, including in Frankfurt, Germany, and Rome; honing his interests in various labs; and giving mice a running wheel in their cages that sparked a key finding in understanding neuron growth in the brain © 1996-2021 The Washington Post

Keyword: Neurogenesis
Link ID: 27683 - Posted: 02.13.2021

Bevil R. Conway Danny Garside Is the red I see the same as the red you see? At first, the question seems confusing. Color is an inherent part of visual experience, as fundamental as gravity. So how could anyone see color differently than you do? To dispense with the seemingly silly question, you can point to different objects and ask, “What color is that?” The initial consensus apparently settles the issue. But then you might uncover troubling variability. A rug that some people call green, others call blue. A photo of a dress that some people call blue and black, others say is white and gold. You’re confronted with an unsettling possibility. Even if we agree on the label, maybe your experience of red is different from mine and – shudder – could it correspond to my experience of green? How would we know? Neuroscientists, including us, have tackled this age-old puzzle and are starting to come up with some answers to these questions. One thing that is becoming clear is the reason individual differences in color are so disconcerting in the first place. Scientists often explain why people have color vision in cold, analytic terms: Color is for object recognition. And this is certainly true, but it’s not the whole story. The color statistics of objects are not arbitrary. The parts of scenes that people choose to label (“ball,” “apple,” “tiger”) are not any random color: They are more likely to be warm colors (oranges, yellows, reds), and less likely to be cool colors (blues, greens). This is true even for artificial objects that could have been made any color. © 2010–2021, The Conversation US, Inc.

Keyword: Vision; Attention
Link ID: 27682 - Posted: 02.08.2021

By Brooke N. Dulka Think back to years past. When you were a kid, you most likely had more friends than you do now. There were probably a lot of children on the playground you considered a friend, but not all of these friendships were very deep. As you grew up, your friendship circle most likely grew smaller. Instead of having many superficial relationships, you now have just a few really important friendships. This is normal. When we are older, we tend to focus on maintaining positive, meaningful relationships. One idea suggests that we become more selective about our friends because we become increasingly aware of our own mortality. In other words, we have future-oriented cognition. However, a recent study published in Science on the wild chimpanzees living in Uganda’s Kibale National Park suggests that our friendships may not actually be tied to thinking about the future. Alexandra Rosati, an evolutionary psychologist at the University of Michigan and one of the study’s lead investigators, had heard about this long-term field study in Uganda. “It seemed like it all could sort of fit together, in this cool way, this primatology data to actually test this idea about human cognition,” she says. Advertisement In this study, a team of researchers analyzed 78,000 hours of observations of 21 male chimpanzees made between 1995 and 2016 at the Kibale National Park. According to Rosati, a unique feature of this study is the value that exists in the long-term collection of data. “We used 20 years of data for this paper. [It] lets us look at this really detailed information about what's going on in these chimpanzees’ social lives,” she says. The findings surprised her. © 2021 Scientific American

Keyword: Stress; Development of the Brain
Link ID: 27681 - Posted: 02.08.2021

by Peter Hess A new engineered protein that glows in the presence of serotonin enables researchers to track the neurotransmitter’s levels and location in the brains of living mice, according to a new study. This ‘serotonin sensor’ could help elucidate serotonin’s role in autism, experts say. Serotonin helps regulate mood, circulation and digestion, among other functions. Some people with autism have elevated levels of serotonin in their blood. Other evidence links serotonin to social behavior in mice. “Serotonin is wildly important both for basic research and human health. And for the longest time, ways to measure it were very indirect,” says co-lead researcher Loren Looger, professor of neuroscience at the University of California, San Diego. “Only with sensors like this can one follow it in vivo, which is critical.” Unlike other tools for measuring serotonin, the sensor can also show changes in serotonin activity over time, making it an exciting tool for autism research, says Jeremy Veenstra-VanderWeele, professor of psychiatry at Columbia University, who was not involved in the study. “This tool will make it possible to understand the relationships between serotonin release and complex behaviors, including in different genetic mouse models related to autism,” he says. “I imagine that this tool will come into fairly broad use.” Programmable protein: The new sensor originated from one described last year that detects a different neurotransmitter, acetylcholine. Looger and his team used a computer algorithm to redesign the acetylcholine-binding portion of the sensor protein so that it could attach to serotonin instead. © 2021 Simons Foundation

Keyword: Depression; Obesity
Link ID: 27680 - Posted: 02.08.2021

By Laura Sanders In the late 1800s, Santiago Ramón y Cajal, a Spanish brain scientist, spent long hours in his attic drawing elaborate cells. His careful, solitary work helped reveal individual cells of the brain that together create wider networks. For those insights, Cajal received a Nobel Prize for physiology or medicine in 1906. Now, a group of embroiderers has traced those iconic cell images with thread, paying tribute to the pioneering drawings that helped us see the brain clearly. The Cajal Embroidery Project was launched in March of 2020 by scientists at the University of Edinburgh. Over a hundred volunteers — scientists, artists and embroiderers — sewed panels that will ultimately be stitched into a tapestry, a project described in the December Lancet Neurology. Catherine Abbott, a neuroscientist at the University of Edinburgh, had the idea while talking with her colleague Jane Haley, who was planning an exhibit of Cajal’s drawings. These meticulous drawings re-created nerve cells, or neurons, and other types of brain cells, including support cells called astrocytes. “I said, off the cuff, ‘Wouldn’t it be lovely to embroider some of them?’” © Society for Science & the Public 2000–2021.

Keyword: Brain imaging
Link ID: 27679 - Posted: 02.08.2021

Cassandra Willyard In 2006, soon after she launched her own laboratory, neuroscientist Jane Foster discovered something she felt sure would set her field abuzz. She and her team were working with two groups of mice: one with a healthy selection of microorganisms in their guts, and one that lacked a microbiome. They noticed that the mice without gut bacteria seemed less anxious than their healthy equivalents. When placed in a maze with some open paths and some walled-in ones, they preferred the exposed paths. The bacteria in the gut seemed to be influencing their brain and behaviour. Foster, at McMaster University in Toronto, Canada, wrote up the study and submitted it for publication. It was rejected. She rewrote it and sent it out again. Rejected. “People didn’t buy it. They thought it was an artefact,” she says. Finally, after three years and seven submissions, she got an acceptance letter1. John Cryan, a neuroscientist at University College Cork in Ireland, joined the field about the same time as Foster did, and knows exactly how she felt. When he began talking about the connections between bacteria living in the gut and the brain, “I felt very evangelical”, he says. He recalls one Alzheimer’s disease conference at which he presented in 2014. “I’ve never given a talk in a room where there was less interest.” Today, however, the gut–brain axis is a feature at major neuroscience meetings, and Cryan says he is no longer “this crazy guy from Ireland”. Thousands of publications over the past decade have revealed that the trillions of bacteria in the gut could have profound effects on the brain, and might be tied to a whole host of disorders. Funders such as the US National Institutes of Health are investing millions of dollars in exploring the connection. © 2021 Springer Nature Limited

Keyword: Obesity; Alzheimers
Link ID: 27678 - Posted: 02.03.2021