Most Recent Links

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.

Links 1 - 20 of 28424

By Simon Makin Our thoughts and feelings arise from networks of neurons, brain cells that send signals using chemicals called neurotransmitters. But neurons aren't alone. They're supported by other cells called glia (Greek for “glue”), which were once thought to hold nerve tissue together. Today glia are known to help regulate metabolism, protect neurons and clean up cellular waste—critical but unglamorous roles. Now, however, neuroscientists have discovered a type of “hybrid” glia that sends signals using glutamate, the brain's most common neurotransmitter. These findings, published in Nature, breach the rigid divide between signaling neurons and supportive glia. “I hope it's a boost for the field to move forward, to maybe begin studying why certain [brain] circuits have this input and others don't,” says study co-author Andrea Volterra, a neuroscientist at the University of Lausanne in Switzerland. Around 30 years ago researchers began reporting that star-shaped glia called astrocytes could communicate with neurons. The idea was controversial, and further research produced contradictory results. To resolve the debate, Volterra and his team analyzed existing data from mouse brains. These data were gathered using a technique called single-cell RNA sequencing, which lets researchers catalog individual cells' molecular profiles instead of averaging them in a bulk tissue sample. Of nine types of astrocytes they found in the hippocampus—a key memory region—one had the cellular machinery required to send glutamate signals. The small numbers of these cells, present only in certain regions, may explain why earlier research missed them. “It's quite convincing,” says neuroscientist Nicola Hamilton-Whitaker of King's College London, who was not involved in the study. “The reason some people may not have seen these specialized functions is they were studying different astrocytes.” © 2023 SCIENTIFIC AMERICAN,

Keyword: Glia
Link ID: 29025 - Posted: 11.26.2023

Jon Hamilton If this year's turkey seems over brined, blame your brain. The question of when salty becomes too salty is decided by a special set of neurons in the front of the brain, researchers report in the journal Cell. A separate set of neurons in the back of the brain adjusts your appetite for salt, the researchers showed in a series of experiments on mice. "Sodium craving and sodium tolerance are controlled by completely different types of neurons," says Yuki Oka, an author of the study and a professor of biology at Caltech. The finding could have health implications because salt ingestion is a "major issue" in many countries, including the United States, says Nirupa Chaudhari, a professor of physiology and biology at the University of Miami's Miller School of Medicine. Too much salt can cause high blood pressure and raise the risk for heart disease and stroke, says Chaudhari, who was not involved in the study. Craving, to a point The study sought to explain the complicated relationship that people and animals have with salt, also known as sodium chloride. We are happy to drink sodas, sports drinks, and even tap water that contain a little salt, Oka says. "But if you imagine a very high concentration of sodium like ocean water, you really hate it." This aversion to super salty foods and beverages holds unless your body is really low on salt, something that's pretty rare in people these days. But experiments with mice found that when salt levels plummet, the tolerance for salty water goes up. "Animals start liking ocean water," Oka says. The reason for this change involves at least two different interactions between the body and brain, Oka's team found. When the concentration of sodium in the bloodstream begins to fall below healthy levels, a set of neurons in the back of the brain respond by dialing up an animal's craving for salt. "If you stimulate these neurons, then animals run to a sodium source and start eating," Oka says. Meanwhile, a different set of neurons in the front of the brain monitors the saltiness of any food or water the mice are consuming. And usually, these neurons will set an upper limit on saltiness. © 2023 npr

Keyword: Chemical Senses (Smell & Taste); Obesity
Link ID: 29024 - Posted: 11.26.2023

By Catherine Offord As millions in the United States settle down to Thanksgiving dinner this week, few will be pondering a major question in neuroscience: Why, when so much of life across the animal kingdom revolves around finding and consuming food, do we ever stop eating? Scientists have identified brain regions and even specific cells involved in terminating meals. But exactly how this process is coordinated remains murky. Now, using brain recordings from mice tucking into food, researchers have for the first time identified how specific neurons in a region called the caudal nucleus of the solitary tract (cNTS) switch on during a meal to slow down and eventually end eating. “Nobody has really been able to [do this] in awake, behaving animals” before, says Nicholas Betley, a neuroscientist at the University of Pennsylvania who was not involved in the work. The findings, published today in Nature, suggest the brain manages a coordinated sequence of behavioral responses to food as it travels from the mouth through the gastrointestinal tract, and could provide new insight into humans’ eating behaviors and disorders, he adds. Previous research on what causes animals to stop eating has largely focused on two types of cells located in the cNTS. One is prolactin-releasing hormone (PRLH) neurons, which have been linked to many functions, including the inhibition of feeding behavior. The other is GCG neurons, which produce glucagon-like peptide-1—the appetite-suppressing hormone mimicked by newly popular weight loss drugs such as Wegovy. Studies of anesthetized animals have found that both neuron types become active in response to the stomach filling, which researchers mimic by inflating a balloon in the stomach or by directly infusing food. But such techniques are a poor proxy for what happens in real life, says Zachary Knight, a neurobiologist and Howard Hughes Medical Institute investigator at the University of California, San Francisco (UCSF). “You don’t really have any sense of what’s happening dynamically.”

Keyword: Obesity
Link ID: 29023 - Posted: 11.26.2023

Nell Greenfieldboyce If you've got itchy skin, it could be that a microbe making its home on your body has produced a little chemical that's directly acting on your skin's nerve cells and triggering the urge to scratch. That's the implication of some new research that shows how a certain bacteria, Staphylococcus aureus, can release an enzyme that generates an itchy feeling. What's more, a drug that interferes with this effect can stop the itch in laboratory mice, according to a new report in the journal Cell. "That's exciting because it's a drug that's already approved for another condition, but maybe it could be useful for treating itchy skin diseases like eczema," says Isaac Chiu, a scientist at Harvard Medical School who studies interactions between microbes and nerve cells. He notes that eczema or atopic dermatitis is actually pretty common, affecting about 20% of children and 10% of adults. In the past, says Chiu, research on itchy skin conditions has focused on the role of the immune response and inflammation in generating the itch sensation. People with eczema often take medications aimed at immune system molecules. But scientists have also long known that people with eczema frequently have skin that's colonized by Staphylococcus aureus, says Chiu, even though it's never been clear what role the bacteria might play in this condition. Chiu's previous lab work had made him realize that bacteria can directly act on nerve cells to cause pain. "So this made us ask: Could certain microbes like Staphylococcus aureus also particularly be in some way linked to itch?" says Chiu. "Is there a role for microbes in talking to itch neurons?" He and his colleagues first found that putting this bacteria on the skin of mice resulted in vigorous scratching by these animals, leading to damaged skin that spread beyond the original exposure site. © 2023 npr

Keyword: Pain & Touch
Link ID: 29022 - Posted: 11.26.2023

By Erin Garcia de Jesús A new brain-monitoring device aims to be the Goldilocks of anesthesia delivery, dispensing drugs in just the right dose. No physician wants a patient to wake up during surgery — nor do patients. So anesthesiologists often give more drug than necessary to keep patients sedated during medical procedures or while on lifesaving machines like ventilators. But anesthetics can sometimes be harmful when given in excess, says David Mintz, an anesthesiologist at Johns Hopkins University. For instance, elderly people with cognitive conditions like dementia or age-related cognitive decline may be at higher risk of post-surgical confusion. Studies also hint that long periods of use in young children might cause behavioral problems. “The less we give of them, the better,” Mintz says. An automated anesthesia delivery system could help doctors find the right drug dose. The new device monitored rhesus macaques’ brain activity and supplied a common anesthetic called propofol in doses that were automatically adjusted every 20 seconds. Fluctuating doses ensured the animals received just enough drug — not too much or too little — to stay sedated for 125 minutes, researchers reported October 31 in PNAS Nexus. The study is a step toward devising and testing a system that would work for people. © Society for Science & the Public 2000–2023.

Keyword: Consciousness; Pain & Touch
Link ID: 29021 - Posted: 11.26.2023

By Sandra G. Boodman The first sign of trouble was difficulty reading. In late 2014 Cathy A. Haft, a New York real estate broker who divides her time between Brooklyn and Long Island, thought she needed new glasses. But an eye exam found that her prescription was largely unchanged. Bladder problems came next, followed by impaired balance, intermittent dizziness and unexplained falls. By 2018 Haft, unable to show properties because she was too unsteady on her feet, was forced to retire. For the next four years specialists evaluated her for neuromuscular and balance-related ear problems in an attempt to explain her worsening condition, which came to include cognitive changes her husband feared was Alzheimer’s disease. In August 2022 Haft, by then dependent on a walker, consulted a Manhattan neurosurgeon. After observing her gait and reviewing images from a recent brain scan, he sent her to a colleague. Less than eight weeks later Haft underwent brain surgery for a condition that is frequently unrecognized or misdiagnosed. The operation succeeded in restoring skills that had gradually slipped away, stunting Haft’s life. “It’s pretty astonishing that this disorder is not that uncommon and no one put the pieces together,” she said. In her case a confluence of confounding symptoms, a complex medical history and the possible failure to take a holistic approach may have led doctors to overlook a condition that can sometimes be reversed — with dramatic results.

Keyword: Movement Disorders; Alzheimers
Link ID: 29020 - Posted: 11.26.2023

By John Krakauer & Tamar Makin The human brain’s ability to adapt and change, known as neuroplasticity, has long captivated both the scientific community and the public imagination. It’s a concept that brings hope and fascination, especially when we hear extraordinary stories of, for example, blind individuals developing heightened senses that enable them to navigate through a cluttered room purely based on echolocation or stroke survivors miraculously regaining motor abilities once thought lost. For years, the notion that neurological challenges such as blindness, deafness, amputation or stroke lead to dramatic and significant changes in brain function has been widely accepted. These narratives paint a picture of a highly malleable brain that is capable of dramatic reorganization to compensate for lost functions. It’s an appealing notion: the brain, in response to injury or deficit, unlocks untapped potentials, rewires itself to achieve new capabilities and self-repurposes its regions to achieve new functions. This idea can also be linked with the widespread, though inherently false, myth that we only use 10 percent of our brain, suggesting that we have extensive neural reserves to lean on in times of need. But how accurate is this portrayal of the brain’s adaptive abilities to reorganize? Are we truly able to tap into reserves of unused brain potential following an injury, or have these captivating stories led to a misunderstanding of the brain’s true plastic nature? In a paper we wrote for the journal eLife, we delved into the heart of these questions, analyzing classical studies and reevaluating long-held beliefs about cortical reorganization and neuroplasticity. What we found offers a compelling new perspective on how the brain adapts to change and challenges some of the popularized notions about its flexible capacity for recovery. The roots of this fascination can be traced back to neuroscientist Michael Merzenich’s pioneering work, and it was popularized through books such as Norman Doidge’s The Brain That Changes Itself. Merzenich’s insights were built on the influential studies of Nobel Prize–winning neuroscientists David Hubel and Torsten Wiesel, who explored ocular dominance in kittens. © 2023 SCIENTIFIC AMERICAN,

Keyword: Learning & Memory; Regeneration
Link ID: 29019 - Posted: 11.22.2023

By Yasemin Saplakoglu From the moment you swallow a bite of food to the moment it exits your body, the gut is toiling to process this strange outside material. It has to break chunks down into small bits. It must distinguish healthy nutrients from toxins or pathogens and absorb only what is beneficial. And it does all this while moving the partially processed food one way through different factories of digestion — mouth, esophagus, stomach, through the intestines and out. “Digestion is required for survival,” said Marissa Scavuzzo, a postdoctoral researcher at Case Western Reserve University in Ohio. “We do it every day, but also, if you really think about it, it sounds very foreign and alien.” Breaking down food requires coordination across dozens of cell types and many tissues — from muscle cells and immune cells to blood and lymphatic vessels. Heading this effort is the gut’s very own network of nerve cells, known as the enteric nervous system, which weaves through the intestinal walls from the esophagus down to the rectum. This network can function nearly independently from the brain; indeed, its complexity has earned it the nickname “the second brain.” And just like the brain, it’s made up of two kinds of nervous system cells: neurons and glia. Glia, once thought to be mere glue that fills the space between neurons, were largely ignored in the brain for much of the 20th century. Clearly, neurons were the cells that made things happen: Through electrical and chemical signaling, they materialize our thoughts, feelings and actions. But in the last few decades, glia have shed their identity as passive servants. Neuroscientists have increasingly discovered that glia play physiological roles in the brain and nervous system that once seemed reserved for neurons. A similar glial reckoning is now happening in the gut. A number of studies have pointed to the varied active roles that enteric glia play in digestion, nutrient absorption, blood flow and immune responses. Others reveal the diversity of glial cells that exist in the gut, and how each type may fine-tune the system in previously unknown ways. One recent study, not yet peer-reviewed, has identified a new subset of glial cells that senses food as it moves through the digestive tract, signaling to the gut tissue to contract and move it along its way. All Rights Reserved © 2023

Keyword: Obesity; Glia
Link ID: 29018 - Posted: 11.22.2023

Claudia López Lloreda The idea that the nervous system passes messages from one nerve cell to another only through synapses — the points where the cells link up end to end — is changing. Two studies show how messages can pass between cells over longer distances, through a ‘wireless’ nerve network in the worm Caenorhabditis elegans. Researchers had not appreciated the extent of this wireless communication, which happens when a molecule called a neuropeptide is released by one neuron and intercepted by another some distance away. The new studies, published in Nature1 and in Neuron2, map out the entire network of neuropeptide communication in a model organism for the first time. “We knew that these chemical connections existed, but this is probably the most comprehensive study in an entire nervous system,” says Gáspár Jékely, a neuroscientist at Heidelberg University in Germany who was not involved in the work. And what the research shows, he adds, is that “it’s not all about the synapses”. Researchers had previously worked out anatomical wiring maps — connectomes — showing how all the neurons in the fruit fly (Drosophila melanogaster) and in C. elegans are linked by their synapses. However, William Schafer, a neuroscientist at the MRC Laboratory of Molecular Biology in Cambridge, UK, wondered about the role of neuropeptides, which had been considered merely helpers in nervous-system messaging. “When I first started talking about this,” he says, “some people wondered, ‘is it all just kind of a soup’” where neuropeptides randomly float from one neuron to the next, “or can you really think about it like a network?” He and his colleagues analysed which neurons in the C. elegans nervous system expressed genes for certain neuropeptides and which ones expressed genes for the receptors of those neuropeptides. Using this data, the team predicted which pairs of nerve cells might be communicating wirelessly. On the basis of these results, the researchers generated a potential map of wireless connections in the worm, finding dense connectivity that looks very different from the anatomical wiring diagram of C. elegans. They published their findings in Neuron2 last week. © 2023 Springer Nature Limited

Keyword: Hormones & Behavior
Link ID: 29017 - Posted: 11.22.2023

By Hannah Docter-Loeb Paxlovid can prevent severe illness from COVID-19, but it comes with a price: In many users, the antiviral drug leaves a weird, metallic aftertaste that can last for days—a condition nicknamed “Paxlovid mouth.” Now, researchers say they’ve figured out why. A component of Paxlovid activates one of the tongue’s bitter taste receptors even at low levels, which may draw out the yuck factor, the team reports this month in Biochemical and Biophysical Research Communications. The work could lead to ways to alleviate the unpleasant side effect. The study is a “good first step” in teasing apart the mechanism behind Paxlovid mouth, says Alissa Nolden, a sensory scientist at the University of Massachusetts Amherst who was not involved with the research. But she says more work will be needed to truly understand why the metallic taste lingers for so long. Paxlovid is composed of two antivirals: nirmatrelvir and ritonavir. Nirmatrelvir blocks a key protein that SARS-CoV-2 needs to replicate. Ritonavir helps maintain the level of nirmatrelvir in the blood. Scientists have suspected that ritonavir is the primary culprit behind Paxlovid mouth. It was originally used in HIV medications and was known to directly taste bitter. A recent study also demonstrated that the compound acts on several tongue receptors that respond to bitter taste. However, ritonavir’s bitterness is short-lived, says Peihua Jiang, a molecular biologist at the Monell Chemical Senses Center, an independent research institute. So in the new study, he and colleagues looked more closely at nirmatrelvir. They added the antiviral to various groups of cells, each collection with a different member of the 25 human bitter taste receptors. They then identified the receptors that responded most vigorously to the compound by changes in a fluorescence marker in the cells. Nirmatrelvir seemed to hone in on TAS2R1, one of the primary receptors responsible for the bitter aftertaste of antiviral medicines, the researchers found. The compound activated the receptor even when its concentration was relatively low, which could explain why Paxlovid causes a persistent bitter taste.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29016 - Posted: 11.22.2023

Lilly Tozer By analysing more than one million people’s genomes, researchers have identified stretches of DNA that could be linked to cannabis addiction. They also found that some of the same regions in the genome are associated with other health conditions, such as lung cancer and schizophrenia. The findings are evidence that cannabis addiction “could have substantial public-health risks if the usage increases”, says Daniel Levey, a medical neuroscientist at Yale University in New Haven, Connecticut, and a co-author of the study, published today in Nature Genetics1. Taking cannabis recreationally is legal in at least 8 countries, and 48 countries have legalized medicinal use of the drug for conditions including chronic pain, cancer and epilepsy. But one-third of people who take cannabis end up becoming addicted, or using the drug in a way that is damaging to their health. Previous studies have suggested that there is a genetic component, and have shown links between problematic cannabis use and some cancers and psychiatric disorders. Weighing the dangers of cannabis Drug taking and addiction can be influenced both by people’s genes and by their environment, which makes them extremely difficult to study, says Levey. But the team was able to build on data from previous work2 by including genetic information from additional sources, predominantly the Million Veteran Program — a US-based biobank with a large genetic database that aims to improve health care for former military service members. The analysis encompassed multiple ethnic groups, a first for a genetic study looking at cannabis misuse. As well as identifying regions of the genome that might be involved, the researchers saw a bi-directional link between excessive cannabis use and schizophrenia, meaning that the two conditions can influence each other. This finding is intriguing, says Marta Di Forti, a psychiatrist-scientist at King’s College London. Cannabis use “is the most preventable risk factor” for schizophrenia, she says, adding that the type of genetic data examined in the study could be used in future to identify and support people at increased risk of developing psychiatric disorders through cannabis use. © 2023 Springer Nature Limited

Keyword: Drug Abuse; Genes & Behavior
Link ID: 29015 - Posted: 11.22.2023

By Annie Roth A few years ago, Nicolas Fasel, a biologist at the University of Lausanne in Switzerland, and his colleagues developed a fascination with the penises of serotine bats, a species found in woodlands and the attics of old buildings across Europe and Asia. Serotine bats sport abnormally long penises with wide, heart-shaped heads. When erect, the members are around seven times longer than the female’s vagina, and their bulbous heads are seven times wider than the female’s vaginal opening. “We wondered: How does that work? How can they use that for copulation?” Dr. Fasel recalled. What they discovered has overturned an assumption about mammalian reproduction, namely that procreation must always involve penetration. In a study, published Monday in the journal Current Biology, Dr. Fassel and his colleagues presented evidence that serotine bats mate without penetration, making them the first mammals known to do so. Instead of using their penises to penetrate their partners, the scientists found, the male bats use them to push their partner’s tail membrane out of the way so they can align their openings and engage in contact mating, a behavior similar to one found in birds and known as “cloacal kissing.” To learn how these bats overcome their substantial genital size difference, Dr. Fasel and his colleagues analyzed nearly 100 videos of serotine bats mating. The videos were provided by a bat rehabilitation center in Ukraine and a citizen scientist filming bats in the attic of a church in the Netherlands. The footage revealed a mating strategy unlike any other used by mammals. While the two bats hang upside down, the male climbs on the female’s back and grasps the nape of her neck. Once he has a firm hold, the male will use his erect penis to push the female’s tail membrane to the side and probe between her legs until he has located her vulva. The male then presses the heart-shaped head of his penis to the female’s vulva and holds it there until the deed is done. While this process took less than an hour for most of the couples the researchers observed, one pair went at it for nearly 13 hours. “It’s a really weird reproductive strategy, but bats are weird and have a lot of weird reproductive strategies,” said Patty Brennan, a biologist at Mount Holyoke College in Massachusetts who studies the evolution of genital morphology but was not involved in the study. © 2023 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 29014 - Posted: 11.22.2023

Jon Hamilton MICHEL MARTIN, HOST: If you are thinking about brining that turkey for Thanksgiving - and full disclosure here, I will be doing that - here is something to consider. Food and drinks that are really salty can be appealing one day and off-putting the next. And scientists think they've figured out why. NPR's Jon Hamilton reports on a study that found two separate brain circuits that affect the taste for salt. JON HAMILTON, BYLINE: Our relationship with salt is complicated. Yuki Oka, a scientist at Caltech, says sodas, sports drinks and even tap water all contain a little salt, also known as sodium chloride. YUKI OKA: You enjoy low-sodium water, but if you imagine very high concentration of sodium, like ocean water, you really hate it. HAMILTON: Unless your body is really low on salt. That's pretty rare in people these days, but Oka says experiments with animals show that when salt levels plummet, the tolerance for salty water goes up. OKA: If your body needs sodium, then animals immediately start liking ocean water. HAMILTON: They crave sodium, and they can tolerate it in high concentrations they would normally avoid. Oka wanted to know how this system works in the brain, so he and a team of scientists studied mice. They showed that one set of neurons toward the back of the brain regulates the craving for salt. OKA: If you stimulate these neurons, then animals run to sodium source and then start eating. HAMILTON: Another group of neurons toward the front of the brain normally sets an upper limit on salt tolerance, but when salt levels get low enough, Oka says, these neurons get switched off. OKA: This means that the sodium craving and the sodium tolerance are controlled by completely different types of neurons. HAMILTON: The finding, which appears in the journal Cell, is part of a growing field of study called interoception. It deals with internal sensations like hunger and pain. Stephen Liberles, a cell biologist at Harvard Medical School, says scientists already know a lot about how the brain deals with sensory information coming from the eyes, ears, nose and skin. © 2023 npr

Keyword: Obesity
Link ID: 29013 - Posted: 11.22.2023

By Laura Sanders WASHINGTON — Brain scans could be used to predict how teenagers’ mental health will fare during a stressful time, an analysis that spanned the COVID-19 pandemic suggests. The findings, presented November 13 in a news briefing at the annual meeting of the Society for Neuroscience, may help explain why some people succumb to stress while others are more resilient. For a lot of research, “the study happens, and you report on the results, and that’s about it,” says Margot Wagner, a bioengineer at the University of California, San Diego who was not involved in the new work. But this research followed hundreds of teenagers over time, a study design that “means you can intervene and help way sooner than otherwise,” Wagner says. The pandemic was particularly tough for many teenagers, as isolation, worry and upheaval of daily routines affected them in ways that scientists are just now starting to see (SN: 1/3/23). A record number of young people are struggling with depression and anxiety, a mental health crisis that some scientists are calling “the second pandemic” (SN: 6/30/23). While many teenagers struggled during the pandemic, others did OK. Computational neuroscientist Caterina Stamoulis of Harvard Medical School and Boston Children’s Hospital investigated why responses differed using data collected as part of the Adolescent Brain Cognitive Development, or ABCD, study. That larger study — involving scientists at 21 research sites across the United States — aims to figure out how teenagers’ brains grow over the years. “This is the first time in history we’re looking at thousands of participants and getting these measures over time,” Wagner says. “It’s truly remarkable.” The ABCD study, begun in 2015, was well under way when COVID hit, so researchers possessed brain scans from before the pandemic. “Without the pandemic, we would not have been able to understand the impact of a long-lasting adverse event” that deeply affected the participants’ lives, changing their interactions with their family and friends, Stamoulis says. © Society for Science & the Public 2000–2023.

Keyword: Development of the Brain; Stress
Link ID: 29012 - Posted: 11.18.2023

By Carl Zimmer Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. If a troop of baboons encounters another troop on the savanna, they may keep a respectful distance or they may get into a fight. But human groups often do something else: They cooperate. Tribes of hunter-gatherers regularly come together for communal hunts or to form large-scale alliances. Villages and towns give rise to nations. Networks of trade span the planet. Human cooperation is so striking that anthropologists have long considered it a hallmark of our species. They have speculated that it emerged thanks to the evolution of our powerful brains, which enable us to use language, establish cultural traditions and perform other complex behaviors. But a new study, published in Science on Thursday, throws that uniqueness into doubt. It turns out that two groups of apes in Africa have regularly mingled and cooperated with each other for years. “To have extended, friendly, cooperative relationships between members of other groups who have no kinship ties is really quite extraordinary,” said Joan Silk, a primatologist at Arizona State University who was not involved in the study. The new research comes from long-term observations of bonobos, an ape species that lives in the forests of the Democratic Republic of Congo. A century ago, primatologists thought bonobos were a slender subspecies of chimpanzee. But the two species are genetically distinct and behave in some remarkably different ways. Among chimpanzees, males hold a dominant place in society. They can be extremely violent, even killing babies. In bonobo groups, however, females dominate, and males have never been observed to commit infanticide. Bonobos often defuse conflict with sex, a strategy that primatologists have not observed among chimpanzees. Scientists made most of their early observations of bonobos in zoos. But in recent years they’ve conducted long-term studies of the apes in the wild. © 2023 The New York Times Company

Keyword: Evolution; Aggression
Link ID: 29011 - Posted: 11.18.2023

By Timmy Broderick Smell is probably our most underappreciated sense. “If you ask people which sense they would be most willing to give up, it would be the olfactory system,” says Michael Leon, a neurobiologist at the University of California, Irvine. But a loss of smell has been linked to health complications such as depression and cognitive decline. And mounting evidence shows that olfactory training, which involves deliberately smelling strong scents on a regular basis, may help stave off that decline. Now a team of researchers led by Leon has successfully boosted cognitive performance by exposing people to smells while they sleep. Twenty participants—all older than 60 years and generally healthy—received six months of overnight olfactory enrichment, and all significantly improved their ability to recall lists of words compared with a control group. The study appeared in Frontiers in Neuroscience. The scientists are unsure about how the overnight odors may have produced this result, but Leon notes that the neurons involved in olfaction have “direct superhighway access” to brain regions related to memory and emotion. In participants who received the treatment, the study authors observed physical changes in a brain structure that connects the memory and emotional centers—a pathway that often deteriorates as people age, especially in those with Alzheimer's disease. Previous successful attempts to boost memory with odors typically relied on complicated interventions with multiple exposures a day. If the nighttime treatment proves successful in larger trials, it promises to be a less intrusive way to achieve similar effects, says Vidya Kamath, a neuropsychologist at the Johns Hopkins University School of Medicine, who was not involved in the recent study. Larger trials may also help answer some remaining questions. The new study used widely available essential oils such as rose and eucalyptus, but researchers aren't sure if just any odor would get the same results. They don't know how much an odor's qualities—whether it's foul or pleasant to people, for example—affects the cognitive gains. It is also unclear how much novelty plays a role, says Michał Pieniak, a psychology researcher at the University of Wroclaw in Poland who has studied olfactory training. © 2023 SCIENTIFIC AMERICAN,

Keyword: Sleep; Learning & Memory
Link ID: 29010 - Posted: 11.18.2023

By Emily Cataneo It’s 1922. You’re a scientist presented with a hundred youths who, you’re told, will grow up to lead conventional adult lives — with one exception. In 40 years, one of the one hundred is going to become impulsive and criminal. You run blood tests on the subjects and discover nothing that indicates that one of them will go off the rails in four decades. And yet sure enough, 40 years later, one bad egg has started shoplifting and threatening strangers. With no physical evidence to explain his behavior, you conclude that this man has chosen to act out of his own free will. Now, imagine the same experiment starting in 2022. This time, you use the blood samples to sequence everyone’s genome. In one, you find a mutation that codes for something called tau protein in the brain and you realize that this individual will not become a criminal in 40 years out of choice, but rather due to dementia. It turns out he did not shoplift out of free will, but because of physical forces beyond his control. Now, take the experiment a step further. If a man opens fire in an elementary school and kills scores of children and teachers, should he be held responsible? Should he be reviled and punished? Or should observers, even the mourning families, accept that under the right circumstances, that shooter could have been them? Does the shooter have free will while the man with dementia does not? Can you explain why? These provocative, even disturbing questions about similar scenarios underlie two new books about whether humans have control over our personalities, opinions, actions, and fates. “Free Agents: How Evolution Gave Us Free Will,” by professor of genetics and neuroscience Kevin J. Mitchell, and “Determined: A Science of Life Without Free Will,” by biology and neurology professor Robert M. Sapolsky, both undertake the expansive task of using the tools of science to probe the question of whether we possess free will, a question with stark moral and existential implications for the way we structure human society.

Keyword: Consciousness
Link ID: 29009 - Posted: 11.18.2023

By Tina Hesman Saey WASHINGTON — Scientists have uncovered a clue about why it takes so long for Huntington’s disease to develop. And they may have a lead on how to stop the fatal brain disease. Huntington’s is caused by a mistakenly repeated bit of a gene called HTT. Until recently, researchers thought the number of repeats a person is born with doesn’t change, though repeats may expand when passed to future generations. But in some brain cells, the repeats can grow over time to hundreds of copies, geneticist Bob Handsaker reported November 2 at the annual meeting of the American Society of Human Genetics. Once the number of repeats passes a certain point, the activity of thousands of other genes in the brain cells changes drastically, leading the cells to die. These findings suggest that adding repeats to the HTT gene in vulnerable brain cells is what is driving Huntington’s disease, says Handsaker, of the Broad Institute of MIT and Harvard in Cambridge, Mass. The research also suggests that preventing the repeats from growing may stop the development of the disease. The new work gives “serious insight into the disease mechanism,” says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the work. About 41,000 people in the United States have symptomatic Huntington’s disease, and another 200,000 are at risk of developing it. Inheriting just one copy of a repeat-riddled HTT gene produces symptoms. Even though individuals are born with the disease-causing gene, symptoms don’t usually appear until people are in their 30s to 50s. Those symptoms include depression, mood swings, forgetfulness, balance problems, involuntary movements and slurred speech. Eventually, a person with the disease may be paralyzed and can die from complications such as pneumonia or heart failure. © Society for Science & the Public 2000–2023.

Keyword: Huntingtons
Link ID: 29008 - Posted: 11.15.2023

Sean O'Donnell Human-driven climate change is increasingly shaping the Earth’s living environments. Rising temperatures, rapid shifts in rainfall and seasonality, and ocean acidification are presenting altered environments to many animal species. How do animals adjust to these new, often extreme, conditions? Animal nervous systems play a central role in both enabling and limiting how they respond to changing climates. Two of my main research interests as a biologist and neuroscientist involve understanding how animals accommodate temperature extremes and identifying the forces that shape the structure and function of animal nervous systems, especially brains. The intersection of these interests led me to explore the effects of climate on nervous systems and how animals will likely respond to rapidly shifting environments. All major functions of the nervous system – sense detection, mental processing and behavior direction – are critical. They allow animals to navigate their environments in ways that enable their survival and reproduction. Climate change will likely affect these functions, often for the worse. Changing temperatures shift the energy balance of ecosystems – from plants that produce energy from sunlight to the animals that consume plants and other animals – subsequently altering the sensory worlds that animals experience. It is likely that climate change will challenge all of their senses, from sight and taste to smell and touch. Animals like mammals perceive temperature in part with special receptor proteins in their nervous systems that respond to heat and cold, discriminating between moderate and extreme temperatures. These receptor proteins help animals seek appropriate habitats and may play a critical role in how animals respond to changing temperatures.

Keyword: Biological Rhythms
Link ID: 29007 - Posted: 11.15.2023

By Sean Cummings If a bite of dandelion greens or extra-dark chocolate makes you pucker, there’s good reason. Bitterness can indicate the presence of toxins in potential foods, and animals long ago honed the ability to ferret out harsh tastes. But the ability to sense bitterness may be even older than many presumed, a new study finds. It likely first evolved in vertebrates roughly 460 million years ago, when sharks and other cartilaginous fishes separated from bony vertebrates like ourselves, researchers report today in the Proceedings of the National Academy of Sciences. The bitter taste receptor identified in a pair of shark species may mirror a sort of all-purpose bitterness detector that our common ancestor possessed. “Given how quickly taste receptors change, to have this one receptor conserved over 460 million years, that’s pretty astounding,” says Craig Montell, a neurobiologist at the University of California, Santa Barbara who was not involved in the study. “The ability to react to the particular bitter chemicals that activate it must be really important.” Humans and other bony vertebrates experience bitterness thanks to taste 2 receptors, or T2Rs, which are proteins that transmit taste information to the brain. But scientists had never found T2Rs in cartilaginous vertebrates such as sharks and rays. That led many to assume these receptors had evolved after their lineage split from the bony vertebrates. Yet sharks and other cartilaginous fish do have smell receptors closely related to bitter taste receptors. That made Sigrun Korsching, a neurobiologist at the University of Cologne, wonder: Could bitter taste perception be even older than most believed? To find out, she and colleagues examined 17 genomes from various species of sharks, skates, and sawfish. Twelve of these had genes that coded for taste receptors similar to T2Rs, which they dubbed T2R1s. In the lab, the researchers implanted genes for these receptors from two of the species—bamboo sharks and catsharks—into human kidney cells, then exposed them to 94 bitter substances. These included resveratrol, found in foods such as grapes, peanuts, and cranberries, and amarogentin, a compound from the gentian plant considered one of the most astringent tastes in the world.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 29006 - Posted: 11.15.2023