by Rachel Zamzow The X chromosome holds stronger-than-expected genetic sway over the structure of several brain regions, a new study finds. The X-linked genes that may underlie this oversized influence have ties to autism and intellectual disability. “There were already hints that the X chromosome was likely to be conspicuous, with how involved it is with the brain,” says lead investigator Armin Raznahan, chief of the section on developmental neurogenomics at the U.S. National Institute of Mental Health. Many X chromosome genes — including those at the root of several autism-related conditions, such as fragile X syndrome and Rett syndrome — are expressed in the brain, for example. But the new findings suggest that the X chromosome, despite containing only 5 percent of the human genome, has a privileged role in shaping the brain — one that may be particularly relevant to developmental conditions. What’s more, this influence may be stronger in men than in women, the study shows. “What they’re showing is X is fundamentally different,” says David Glahn, professor of psychology at Harvard University, who was not involved in the new study. “It’s off the scale.” Research over the past decade has linked genetic variation to shifts in brain features, such as overall size or patterns of connectivity between regions, Glahn says. But “the X chromosome and the Y chromosome are fundamentally understudied,” because including them requires extra analytical legwork, he says. © 2021 Simons Foundation

Keyword: Development of the Brain; Genes & Behavior
Link ID: 27992 - Posted: 09.15.2021

By Husseini Manji, Joseph Hayes Depression affects more than 264 million people of all ages globally. The World Health Organization ranks depression as one of the most debilitating diseases to society. It is the leading cause of disability worldwide and the psychiatric diagnosis most commonly associated with suicide, which accounts for nearly 800,000 deaths globally each year. Individuals suffering from depression may face an inability to manage life’s demands and maintain social connections, affecting all aspects of their experiences, from school and employment to relationships and overall quality of life. When it comes to treatment, approximately one third of those suffering from depression do not respond to two or more antidepressants and are considered treatment-resistant. Treatment-resistant depression is a chronic condition that places an increased emotional, functional and economic burden on the individual, their loved ones and society. It is also associated with greater morbidity, higher health care costs and various comorbid conditions. While a number of antidepressants exist, they all work through changing the levels of brain-signaling molecules called monoaminergic neurotransmitters. New drug development for depression had stalled for a number of years, and many pharmaceutical companies have withdrawn from neuroscience entirely. But recent scientific advances have led to the development of novel antidepressants working via completely different mechanisms. The brain is the most advanced, adaptive information processing system in existence—in large part because of its tremendous plasticity. Scientists have been building upon these neuroscience advances to develop completely novel, rapid-acting antidepressants. In this regard, considerable evidence has demonstrated that the regulation of two receptors—AMPA and NMDA—on many neurons that respond to the neurotransmitter glutamate control changes in the tiny junctions, or synapses, between neurons. © 2021 Scientific American

Keyword: Depression
Link ID: 27991 - Posted: 09.15.2021

Andrew Gregory Health editor Millions of people with eye conditions including age-related macular degeneration, cataracts and diabetes-related eye disease have an increased risk of developing dementia, new research shows. Vision impairment can be one of the first signs of the disease, which is predicted to affect more than 130 million people worldwide by 2050. Previous research has suggested there could be a link between eye conditions that cause vision impairment, and cognitive impairment. However, the incidence of these conditions increases with age, as do systemic conditions such as diabetes, high blood pressure, heart disease, depression and stroke, which are all accepted risk factors for dementia. That meant it was unclear whether eye conditions were linked with a higher incidence of dementia independently of systemic conditions. Now researchers have found that age-related macular degeneration, cataracts and diabetes-related eye disease are independently associated with increased risk of dementia, according to a new study published in the British Journal of Ophthalmology. The research examined data from 12,364 British adults aged 55 to 73, who were taking part in the UK Biobank study. They were assessed in 2006 and again in 2010 with their health information tracked until early 2021. More than 2,300 cases of dementia were documented, according to the international team of experts led by academics from the Guangdong Eye Institute in China. After assessing health data, researchers found those with age-related macular degeneration had a 26% increased risk of developing dementia. Those with cataracts had an 11% increased risk and people with diabetes-related eye disease had a 61% heightened risk. Glaucoma was not linked to a significant increase in risk. © 2021 Guardian News & Media Limited

Keyword: Alzheimers; Vision
Link ID: 27990 - Posted: 09.15.2021

Jon Hamilton The visual impairment known as "lazy eye" can be treated in kids by covering their other eye with a patch. Scientists may have found a way to treat adults with the condition using a pufferfish toxin. MARY LOUISE KELLY, HOST: Children who develop the visual impairment often called lazy eye can be treated by covering their other eye with a patch. Now researchers think they have found a way to treat adults using a toxin found in deadly puffer fish. The approach has only been tried in animals so far, but NPR's Jon Hamilton reports the results are encouraging. JON HAMILTON, BYLINE: A lazy eye isn't really lazy. The term refers to amblyopia, a medical condition that occurs when the brain starts ignoring the signals from one eye. Existing treatments restrict use of the strong eye in order to force the brain to pay attention to the weak one. But Mark Bear, a neuroscientist at MIT, says that approach has limits. MARK BEAR: There are a very significant number of adults with amblyopia where the treatment either didn't work or it was initiated too late. HAMILTON: After a critical period that ends at about age 10, the connections between eye and brain become less malleable. They lose what scientists call plasticity. So for several decades, Bear and a team of researchers have been trying to answer a question. BEAR: How can we rejuvenate these connections? How can they be brought back online? HAMILTON: To find out, Bear's team studied adults with amblyopia who lost their strong eye to a disease or an injury. © 2021 npr

Keyword: Vision; Development of the Brain
Link ID: 27989 - Posted: 09.15.2021

James M. Gaines Young macaques given the popular antidepressant fluoxetine for two years had lower levels of certain fatty acids and other lipids in their brains than ones not given the drug, finds a recent study (July 28) in International Journal of Molecular Sciences. The findings may help explain why younger people sometimes experience adverse side effects when taking the drug. Fluoxetine, often sold under the brand name Prozac, is a prescription medication that can be given to adults as well as children as young as 7 or 8 years old. But there’s not good literature on the long-term impact of fluoxetine and other psychoactive drugs that we use to treat adult symptoms in the young brain, says Bita Moghaddam, a behavioral neuroscientist at Oregon Health & Science University who was not involved in the study, “so [it] was really nice to see that there is this level of focus.” While genes and neurotransmitters may get the lion’s share of the attention in neuroscience research, brains are mostly made of up fats and other lipids. But lipids, it turns out, can be hard to study. So, when University of California Davis brain scientist Mari Golub and her colleagues wanted to know what was going on with the fats in the brains of the monkeys they were studying, they reached out to the brain lab at the Skoltech Institute of Science and Technology in Moscow where Anna Tkachev—the lead author on the new paper—works. “We happen to specialize in lipids in particular,” says Tkachev. For years, Golub and her colleagues had been using macaques to investigate the effects of fluoxetine. The antidepressant can be an effective treatment for maladies such as depression and obsessive-compulsive disorder. However, some studies suggest that the drug can occasionally cause serious, long-term side effects, and perhaps counter-intuitively for an antidepressant, it’s been linked to an increased risk of suicidal thinking and behavior, particularly in young people. © 1986–2021 The Scientist.

Keyword: Depression; Development of the Brain
Link ID: 27988 - Posted: 09.13.2021

Christie Wilcox If it walks like a duck and talks like a person, it’s probably a musk duck (Biziura lobata)—the only waterfowl species known that can learn sounds from other species. The Australian species’ facility for vocal learning had been mentioned anecdotally in the ornithological literature; now, a paper published September 6 in Philosophical Transactions of the Royal Society B reviews and discusses the evidence, which includes 34-year-old recordings made of a human-reared musk duck named Ripper engaging in an aggressive display while quacking “you bloody fool.” Ripper quacking "you bloody fool" while being provoked by a person separated from him by a fence The Scientist spoke with the lead author on the paper, Leiden University animal behavior researcher Carel ten Cate, to learn more about these unique ducks and what their unexpected ability reveals about the evolution of vocal learning. The Scientist: What is vocal learning? Carel ten Cate: Vocal learning, as it is used in this case, is that animals and humans, they learn their sounds from experience. So they learn from what they hear around them, which will usually be the parents, but it can also be other individuals. And if they don’t get that sort of exposure, then they will be unable to produce species-specific vocalizations, or in the human case, speech sounds and proper spoken language. © 1986–2021 The Scientist.

Keyword: Language; Evolution
Link ID: 27987 - Posted: 09.13.2021

Abby Olena Most people enjoy umami flavor, which is perceived when a taste receptor called T1R1/T1R3 senses the amino acid glutamate. In some other mammals, such as mice, however, this same receptor is much less sensitive to glutamate. In a new study published August 26 in Current Biology, researchers uncover the molecular basis for this difference. They show that the receptor evolved in humans and some other primates away from mostly binding free nucleotides, which are common in insects, to preferentially binding glutamate, which is abundant in leaves. The authors argue that the change facilitated a major evolutionary shift in these primates toward a plant-heavy diet. “The question always comes up about the evolution of umami taste: In humans, our receptor is narrowly tuned to glutamate, and we never had a good answer for why,” says Maude Baldwin, a sensory biologist at the Max Planck Institute for Ornithology in Germany. She was not involved in the new work, but coauthored a 2014 study with Yasuka Toda, who is also a coauthor on the new paper, showing that the T1R1/T1R3 receptor is responsible for sweet taste in hummingbirds. In the new study, the authors find “that this narrow tuning has evolved convergently multiple times [and] that it’s related to folivory,” she says, calling the paper “a hallmark, fantastic study, and one that will become a textbook example of how taste evolution can relate to diet and how to address these types of questions in a rigorous, comprehensive manner.” In 2011, Toda, who was then at the University of Tokyo and now leads a group at Meiji University in Japan, and Takumi Misaka of the University of Tokyo developed a strategy to use cultured cells to analyze the function of taste receptors. They used the technique to tease out the parts of the human T1R1/T1R3 that differed from that of mice and thus underlie the high glutamate sensitivity in the human receptor, work that they published in 2013. © 1986–2021 The Scientist.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 27986 - Posted: 09.13.2021

Sophie Fessl The hormone irisin is necessary for the cognitive benefits of exercise in healthy mice and can rescue cognitive decline associated with Alzheimer’s disease, according to a study published August 20 in Nature Metabolism. According to the authors, these results support the hypothesis that irisin undergirds the cognitive benefits of exercise—a link that has been long debated. In addition, this study has “paved the way for thinking whether irisin could be a therapeutic agent against Alzheimer’s disease,” says biologist Steffen Maak with the Leibniz Institute for Farm Animal Biology in Germany, who has been critical of the methods used to study irisin in the past and was not involved in the study. Many studies have found that exercise is good for the brain, but the molecular mechanisms responsible for the cognitive boost have remained elusive. During her postdoctoral studies, neuroscientist Christiane Wrann found that the gene that codes for irisin becomes highly expressed in the brain during exercise—one of the first studies linking irisin with the brain. See “Irisin Skepticism Goes Way Back” When she joined the faculties at Massachusetts General Hospital and Harvard Medical School, she decided to investigate the hormone further. Wrann, who holds a patent related to irisin and is academic cofounder and consultant for Aevum Therapeutics, a company developing drugs that harness the protective molecular mechanisms of exercise to treat neurodegenerative and neuromuscular disorders, began to investigate whether irisin mediates the positive effects of exercise on the brain. © 1986–2021 The Scientist.

Keyword: Learning & Memory; Hormones & Behavior
Link ID: 27985 - Posted: 09.13.2021

By Nicholas Bakalar Many animals are known to use tools, but a bird named Bruce may be one of the most ingenious nonhuman tool inventors of all: He is a disabled parrot who has designed and uses his own prosthetic beak. Bruce is a kea, a species of parrot found only in New Zealand. He is about 9 years old, and when wildlife researchers found him as a baby, he was missing his upper beak, probably because it had been caught in a trap made for rats and other invasive mammals the country was trying to eliminate. This is a severe disability, as kea use their dramatically long and curved upper beaks for preening their feathers to get rid of parasites and to remove dirt and grime. But Bruce found a solution: He has taught himself to pick up pebbles of just the right size, hold them between his tongue and his lower beak, and comb through his plumage with the tip of the stone. Other animals use tools, but Bruce’s invention of his own prosthetic is unique. Researchers published their findings Friday in the journal Scientific Reports. Studies of animal behavior are tricky — the researchers have to make careful, objective observations and always be wary of bias caused by anthropomorphizing, or erroneously attributing human characteristics to animals. “The main criticism we received before publication was, ‘Well, this activity with the pebbles may have been just accidental — you saw him when coincidentally he had a pebble in his mouth,’” said Amalia P.M. Bastos, an animal cognition researcher at the University of Auckland and the study’s lead author. “But no. This was repeated many times. He drops the pebble, he goes and picks it up. He wants that pebble. If he’s not preening, he doesn’t pick up a pebble for anything else.” Dorothy M. Fragaszy, an emerita professor of psychology at the University of Georgia who has published widely on animal behavior but was unacquainted with Bruce’s exploits, praised the study as a model of how to study tool use in animals. © 2021 The New York Times Company

Keyword: Intelligence; Evolution
Link ID: 27984 - Posted: 09.11.2021

By Carolyn Wilke Babies may laugh like some apes a few months after birth before transitioning to chuckling more like human adults, a new study finds. Laughter links humans to great apes, our evolutionary kin (SN: 6/4/09). Human adults tend to laugh while exhaling (SN: 6/10/15), but chimpanzees and bonobos mainly laugh in two ways. One is like panting, with sound produced on both in and out breaths, and the other has outbursts occurring on exhales, like human adults. Less is known about how human babies laugh. So Mariska Kret, a cognitive psychologist at Leiden University in the Netherlands, and colleagues scoured the internet for videos with laughing 3- to 18-month-olds, and asked 15 speech sound specialists and thousands of novices to judge the babies’ laughs. After evaluating dozens of short audio clips, experts and nonexperts alike found that younger infants laughed during inhalation and exhalation, while older infants laughed more on the exhale. That finding suggests that infants’ laughter becomes less apelike with age, the researchers report in the September Biology Letters. Humans start to laugh around 3 months of age, but early on, “it hasn’t reached its full potential,” Kret says. Both babies’ maturing vocal tracts and their social interactions may influence the development of the sounds, the researchers say.

Keyword: Language; Evolution
Link ID: 27983 - Posted: 09.11.2021

by Niko McCarty Brain scans from 16 mouse models of autism reveal at least four distinct patterns of brain activity, a new study suggests. The findings lend fresh support to the popular idea that autism is associated with a range of brain ‘signatures.’ Telltale neural signatures of autism have long proved elusive, with functional magnetic resonance imaging (fMRI) and other brain scanning technologies shouldering the blame for scattered and inconsistent results. “One big question is whether there’s a single signature of dysfunction in the brain of people with autism. And many people consider that to be, like, something that there must be,” says study investigator Alessandro Gozzi, senior researcher at the Istituto Italiano di Tecnologia in Rovereto, Italy. “If we’ve not found it yet, the blame must be on the method: fMRI.” The method gauges small changes in blood flow and oxygenation as an indirect measure of brain activity. For the new study, published in Molecular Psychiatry in August, Gozzi and his colleagues used fMRI to study brain connectivity patterns — or which brain regions ‘talk’ to each other, and to what degree. Brain regions are considered to be in communication if they have synchronous oscillations in blood flow. To tackle the question of reproducibility in fMRI, the researchers conducted their analysis in mice, anesthetizing the animals and fixing their heads in place to prevent any motion that could perturb brain signals. “We moved to a model organism where we can control, in exquisite detail, many of the factors that are considered to be at the basis of this variability, this unreliability in imaging,” Gozzi says. © 2021 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 27982 - Posted: 09.11.2021

By Lisa Sanders, M.D. The young woman was awakened by the screams of her 39-year-old husband. “Please make it stop!” he shouted, leaping from the bed. “It hurts!” He paced back and forth across the room, arms crossed over his chest as if to protect himself. Two days earlier, he had inhaled a breath mint when his wife startled him. He felt it move slowly down his throat as he swallowed repeatedly. His chest had hurt ever since. But not like this. The man squirmed miserably throughout the short drive to the emergency room at Westerly Hospital, near the Rhode Island and Connecticut border. No position was comfortable. Everything hurt. Even breathing was hard. Although the doctors in the E.R. immediately determined that the young man wasn’t having a heart attack, it was clear something was very wrong. His blood pressure was so low that it was hard to measure. A normal blood pressure may be 120/80. On arrival, his was 63/32. With a pressure this low, blood couldn’t get everywhere it was needed — a condition known as shock. His lips, hands and feet had a dusky hue from this lack of well-​oxygenated blood. He was given intravenous fluids to bring up his pressure, and when that didn’t work, he was started on medications for it. Three hours later, he was on two of these medicines and his fourth liter of fluid. Despite that, his pressure remained in the 70s. He had to be put on a breathing machine to help him keep up with his body’s demand for more oxygen. The most common cause of shock is infection. But this man, as sick as he was, had no signs of infection. The medical team started him on antibiotics anyway. Could the painful mint have torn his esophagus? Up to 50 percent of patients with that injury will die. A CT scan showed no evidence of perforation or of fluid in his chest. What else could this be? There was no sign of a clot keeping blood from entering the lungs, another cause of deadly low blood pressure. An ultrasound of the heart showed that he had some fluid in the sac called the pericardium, which contains and protects the heart, but not enough to interfere with how well it was beating. He was tested for Covid and for recreational drugs — both negative. © 2021 The New York Times Company

Keyword: Hormones & Behavior; Neuroimmunology
Link ID: 27981 - Posted: 09.08.2021

By Baland Jalal Obsessive-compulsive disorder (OCD) has puzzled artists and scientists for centuries. Afflicting one in 50 people, OCD can take several forms, such as compulsively putting things in just the right order or checking if the stove is turned off 10 times in a row. One type of OCD that affects nearly half of those with the condition entails irresistible washing urges. People with this type can spend hours scrubbing their hands in agitation after touching something as trivial as a doorknob even though they know this makes no sense. There is currently a shortage of effective therapies for OCD: 40 percent of patients do not benefit from existing treatments. A major issue is that today’s treatments are often too stressful. First-line “nonpharmacological therapies” involve telling patients to repeatedly touch things such as toilet seats and then refrain from washing their hands. But recent work by my colleagues and me has found something surprising: people diagnosed with OCD appear to have a more malleable “sense of self,” or brain-based “self-representation” or “body image”—the feeling of being anchored here and now in one’s body—than those without the disorder. This finding suggests new ways to treat OCD and perhaps unexpected insights into how our brain creates a distinction between “self” and “other.” In our recent experiments, for example, we showed that people with and without OCD responded differently to a well-known illusion. In our first study, a person without OCD watched as an experimenter used a paintbrush to stroke a rubber hand and the subject’s hidden real hand in precise synchrony. This induces the so-called rubber hand illusion: the feeling that a fake hand is your hand. When the experimenter stroked the rubber hand and the real one out of sync, the effect was not induced (or was greatly diminished). This compelling illusion illustrates how your brain creates your body image based on statistical correlations. It’s extremely unlikely for such stroking to be seen on a rubber hand and simultaneously felt on a hidden real one by chance. So your brain concludes, however illogically, that the rubber hand is part of your body. © 2021 Scientific American

Keyword: OCD - Obsessive Compulsive Disorder; Pain & Touch
Link ID: 27980 - Posted: 09.08.2021

By Sarah Lyall In the winter of 1995, the Brazilian neuroscientist Sidarta Ribeiro moved to New York to pursue his Ph.D. at Rockefeller University. His arrival, he writes in his fascinating, discursive new book, “The Oracle of Night,” precipitated one of the strangest periods of his life. Overcome by a sudden, inexplicable lassitude, Ribeiro did little but attend classes, read and sleep. But his sleep was exciting and revelatory, full of vivid, evocative dreams that enriched his waking hours. “I began to dream in English,” he writes, “and my dreams became even more intense, with representations of epic narratives through unnaturally deserted New York streets on the sunny, icy morning of an endless Sunday.” This period lasted for several months and then abruptly ended. When Ribeiro re-entered the world, as if emerging from hibernation, he was refreshed and alert, energized by a “cognitive transformation” that he felt had been enhanced by his dreaming imagination. He became fascinated by dreams — why do we have them, what do they say about us, what role do they play in our lives? — and embarked on a lifetime of study of this most interesting of topics. (He wears many hats. He got his Ph.D. in animal behavior; he is the founder and vice director of the Brain Institute at the Federal University of Rio Grande do Norte in Brazil.) “The Oracle of Night” makes a resounding case for the mystery, beauty and cognitive importance of dreams. Ribeiro marshals prodigious evidence to bolster his case that a dream is not simply “fragments of memory assembled at random” (as he summarizes Francis Crick’s dismissive position), but instead is a “privileged moment for prospecting the unconscious” — a phenomenon that, in Carl Jung’s words, “prepares the dreamer for the events of the following day.” © 2021 The New York Times Company

Keyword: Sleep
Link ID: 27979 - Posted: 09.08.2021

Allison Whitten Our mushy brains seem a far cry from the solid silicon chips in computer processors, but scientists have a long history of comparing the two. As Alan Turing put it in 1952: “We are not interested in the fact that the brain has the consistency of cold porridge.” In other words, the medium doesn’t matter, only the computational ability. Today, the most powerful artificial intelligence systems employ a type of machine learning called deep learning. Their algorithms learn by processing massive amounts of data through hidden layers of interconnected nodes, referred to as deep neural networks. As their name suggests, deep neural networks were inspired by the real neural networks in the brain, with the nodes modeled after real neurons — or, at least, after what neuroscientists knew about neurons back in the 1950s, when an influential neuron model called the perceptron was born. Since then, our understanding of the computational complexity of single neurons has dramatically expanded, so biological neurons are known to be more complex than artificial ones. But by how much? To find out, David Beniaguev, Idan Segev and Michael London, all at the Hebrew University of Jerusalem, trained an artificial deep neural network to mimic the computations of a simulated biological neuron. They showed that a deep neural network requires between five and eight layers of interconnected “neurons” to represent the complexity of one single biological neuron. All Rights Reserved © 2021

Keyword: Brain imaging; Vision
Link ID: 27978 - Posted: 09.04.2021

by Angie Voyles Askham Male mice exposed to atypically low levels of a placental hormone in the womb have altered brain development and asocial behaviors, according to a new study. The findings may help explain why preterm birth — which coincides with a deficiency in hormones made by the placenta — is linked to an increased likelihood of having autism. The hormone, called allopregnanolone, crosses the blood-brain barrier, binds to receptors for the chemical messenger gamma-aminobutyric acid (GABA) and helps regulate aspects of neurodevelopment, including the growth of new neurons. Its levels typically peak in the fetus during the second half of gestation. In the new study, researchers engineered a mouse model to have low fetal levels of allopregnanolone, mimicking the hormone’s loss due to preterm birth or placental dysfunction. The male mice in particular have structural changes in the cerebellum, a brain region known for balance and motor control, and exhibit more pronounced autism-like traits than control mice or female model mice. The new model “has a good translational potential for understanding the underlying mechanisms of sex differences in neurodevelopmental conditions such as autism,” says Amanda Kentner, professor of psychology at the Massachusetts College of Pharmacy and Health Sciences in Boston, who was not involved in the work. Injecting a pregnant mouse with allopregnanolone partway through gestation decreased the likelihood that its offspring would have autism-like traits, the researchers found. © 2021 Simons Foundation

Keyword: Autism; Development of the Brain
Link ID: 27977 - Posted: 09.04.2021

By Laura Sanders Clumps of brain cells grown from the stem cells of two people with a neurological syndrome show signs of the disorder. The results, published August 23 in Nature Neuroscience, suggest that personalized brain organoids could be powerful tools to understand complex disorders. Researchers are eager to create brain organoids, human stem cells coaxed into becoming 3-D blobs of brain cells, because of their ability to mimic human brains in the lab (SN: 2/20/18). In the current study, researchers grew two kinds of brain organoids. One kind, grown from healthy people’s stem cells, produced complex electrical activity that echoed the brain waves a full-sized brain makes. These waves, created by the coordinated firing of many nerve cells, are part of how the brain keeps information moving (SN: 3/13/18). The researchers also grew organoids using cells from a 25-year-old woman and a 5-year-old girl with Rett syndrome, a developmental disorder marked by seizures, autism and developmental lags. Rett syndrome is thought to be caused by changes in a gene called MECP2, mutations that the lab-grown organoids carried as well. These organoids looked like those grown from healthy people, but behaved differently in some ways. Their nerve cells fired off signals that were too synchronized and less varied. Some of the brain waves these organoids produced are reminiscent of a brain having a seizure, in which a bolus of electrical activity scrambles normal brain business. © Society for Science & the Public 2000–2021.

Keyword: Development of the Brain
Link ID: 27976 - Posted: 09.04.2021

Jordana Cepelewicz Faced with a threat, the brain has to act fast, its neurons making new connections to learn what might spell the difference between life and death. But in its response, the brain also raises the stakes: As an unsettling recent discovery shows, to express learning and memory genes more quickly, brain cells snap their DNA into pieces at many key points, and then rebuild their fractured genome later. The finding doesn’t just provide insights into the nature of the brain’s plasticity. It also demonstrates that DNA breakage may be a routine and important part of normal cellular processes — which has implications for how scientists think about aging and disease, and how they approach genomic events they’ve typically written off as merely bad luck. The discovery is all the more surprising because DNA double-strand breaks, in which both rails of the helical ladder get cut at the same position along the genome, are a particularly dangerous kind of genetic damage associated with cancer, neurodegeneration and aging. It’s more difficult for cells to repair double-strand breaks than other kinds of DNA damage because there isn’t an intact “template” left to guide the reattachment of the strands. Yet it’s also long been recognized that DNA breakage sometimes plays a constructive role, too. When cells are dividing, double-strand breaks allow for the normal process of genetic recombination between chromosomes. In the developing immune system, they enable pieces of DNA to recombine and generate a diverse repertoire of antibodies. Double-strand breaks have also been implicated in neuronal development and in helping turn certain genes on. Still, those functions have seemed like exceptions to the rule that double-strand breaks are accidental and unwelcome. All Rights Reserved © 2021

Keyword: Learning & Memory; Epigenetics
Link ID: 27975 - Posted: 09.01.2021

Virginia Morell Goffin’s cockatoos (Cacatua goffiniana) are so smart they’ve been compared to 3-year-old humans. But what 3-year-old has made their own cutlery set? Scientists have observed wild cockatoos, members of the parrot family, crafting the equivalent of a crowbar, an ice pick, and a spoon to pry open one of their favorite fruits. This is the first time any bird species has been seen creating and using a set of tools in a specific order—a cognitively challenging behavior previously known only in humans, chimpanzees, and capuchin monkeys. The work “supports the idea that parrots have a general [type of] intelligence that allows them to innovate creative solutions to the problems they run into in nature,” says Alex Taylor, a biologist who studies New Caledonian crows at the University of Auckland. “[It] establishes this species as one of the avian family’s most proficient wild tool users.” The discovery happened serendipitously when behavioral ecologist Mark O’Hara was working with wild but captive birds in a research aviary on Yamdena Island in Indonesia. “I’d just turned away, and when I looked back, one of the birds was making and using tools,” says O’Hara, of the Messerli Research Institute. “I couldn’t believe my eyes!” The Goffin’s cockatoo is known for being a clever and innovative social learner. In captivity, the birds have solved complex puzzle boxes and invented rakelike tools to retrieve objects. Several other birds, including hyacinth macaws and New Caledonian crows, make and use tools in the wild, often to extract food, but none seems to make a set of tools. For the new study, O’Hara and his colleagues traveled to this cockatoo’s home on Indonesia’s Tanimbar Islands. The birds live high in the tropical forest canopy, making them difficult to observe. The scientists spent almost 900 hours looking up to watch wild cockatoos feed, but didn’t witness tool use.

Keyword: Learning & Memory; Intelligence
Link ID: 27974 - Posted: 09.01.2021

Nicola Davis Premature babies appear to feel less pain during medical procedures when they are spoken to by their mothers, researchers have found. Babies that are born very early often have to spend time in neonatal intensive care units, and may need several painful clinical procedures. The situation can also mean lengthy separation from parents. Now researchers say they have found the sound of a mother’s voice seems to decrease the pain experienced by their baby during medical procedures. Dr Manuela Filippa, of the University of Geneva and first author of the study, said the research might not only help parents, by highlighting that they can play an important role while their baby is in intensive care, but also benefit the infants. Advertisement Last man out: the haunting image of America’s final moments in Afghanistan “We are trying to find non-pharmacological ways to lower the pain in these babies,” she said, adding that there was a growing body of evidence that parental contact with preterm babies could be important for a number of reasons, including attachment. Filippa said the team focused on voice because it was not always possible for parents to hold their babies in intensive care, while voice could be a powerful tool to share emotion. Mothers’ voices were studied in particular because infants would already have heard it in the womb. But Filippa said that did not mean a father’s voice could not become as familiar over time. “We are [also] running studies on fathers’ vocal contacts,” she said. Writing in the journal Scientific Reports, Filippa and colleagues at the University of Geneva, Parini hospital in Italy and the University of Valle d’Aosta, report how they examined the pain responses of 20 premature babies in neonatal intensive care to a routine procedure in which the foot is pricked and a few drops of blood collected. © 2021 Guardian News & Media Limited

Keyword: Pain & Touch; Development of the Brain
Link ID: 27973 - Posted: 09.01.2021