Finding Flavor - Odor Detectors - Motor Neuron Plasticity - Idiot Savants

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Oct 11, 2025, 7:46:29 AM (10 days ago) Oct 11
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https://www.sciencenews.org/article/brain-scans-flavor-insula-taste-smell Brain scans reveal where taste and smell become flavor By Siddhant Pusdekar Taste and smell are so intimately connected that a whiff of well-loved foods evokes their taste without any conscious effort. Now, brain scans and machine learning have for the first time pinpointed the region responsible for this sensory overlap in humans, a region called the insula, researchers report September 12 in Nature Communications. The findings could explain why people crave certain foods or are turned away from them, says Ivan de Araujo, a neuroscientist at Max Planck Institute for Biological Cybernetics in Tübingen, Germany. Smell and taste become associated from the moment we bite into something, says Putu Agus Khorisantono, a neuroscientist at Karolinska Institutet in Stockholm. Some food chemicals activate sweet, salty, sour, bitter or umami taste receptors on the tongue. Others travel through the roof of the mouth, activating odor receptors in the back of the nose. These “retronasal odors” are what distinguish mangoes from peaches, for example. Both taste mostly sour, Khorisantono says, “but it’s really the aroma that differentiates them.” The brain combines these signals to create our sense of flavor, but scientists have struggled to identify where this happens in the brain. In the new study, Khorisantono and colleagues gave 25 people drops of beverages designed to activate only their taste or retronasal receptors, while scanning brain activity over multiple sessions. Previously, the participants had learned to associate the combination of smells and tastes with particular flavors. © Society for Science & the Public 2000–2025. -------------------- https://www.science.org/content/article/perfume-scientists-tweak-cells-having-sense-smell Perfume scientists tweak cells into having ‘sense of smell’ By Jennie Erin Smith The marine whiff of ambergris. The citrusy tang of grapefruit. The must of “corked” wine. The human nose can detect a virtually infinite palette of odors, some at vanishingly low concentrations. But puzzlingly, our bodies only use about 400 receptor proteins to interpret them. Now, fragrance researchers in Switzerland have landed on a new way to study the proteins in the laboratory—and their results, they say, challenge a foundational theory of how smell works. For decades, scientists have struggled to get cells commonly used in laboratory settings to express the genes that encode olfactory receptors (ORs), proteins primarily found on neurons in our nasal cavities. Using a process they describe today in Current Biology, researchers at the Swiss fragrance and flavorings company Givaudan say they have tweaked lab-friendly cells into readily expressing ORs. The result was an in vitro system for identifying specific ORs, including those that strongly respond to molecules in ambergris, grapefruit, and corked wine. The Swiss group’s discovery, other olfaction researchers say, stands to make ORs much easier to study. But more controversially, the group also claims to have observed patterns of receptor activity that call into question combinatorial coding, a long-standing hypothesis of olfaction that helped Linda Buck and Richard Axel win a Nobel Prize in 2004. Combinatorial coding holds that multiple ORs act in concert to pick up different parts of an odorant molecule, creating patterns or codes that are recognized by the brain. Beyond that, says neuroscientist Joel Mainland of the Monell Chemical Senses Center, the model is “pretty vague on the details.” It has been hard to test, because olfactory neurons can’t be cultured in the lab. Determining which OR detects which odorant required extensive tests in rodents, and it’s not ideal “to have to sacrifice an animal each time you want to do an experiment,” says Claire de March, a chemist at CNRS, the French national research agency. As a result, investigators were left with many so-called orphan receptors whose ligands, or binding molecules, are unknown. © 2025 American Association for the Advancement of Science. -------------------- https://www.thetransmitter.org/neurodegenerative-disorders/new-questions-around-motor-neurons-and-plasticity/ New questions around motor neurons and plasticity By David Adam In February of this year, George Mentis and his colleagues published data from a small clinical trial they said showed that degraded motor neurons aren’t irreparable. In the study, electrical stimulation to the spine in three people with spinal muscular atrophy (SMA) appeared to resuscitate lost motor neurons, the authors said, as well as restore some of the cellular processes needed to activate muscle. “It was incredible,” says Mentis, professor of pathology and cell biology (in neurology) at Columbia University. “We’re unleashing or tapping on the potential of dysfunctional neurons to show plasticity.” The authors wrote that the results showed it was possible to “effectively rescue motor neuron function” and that the electrical stimulation had rebuilt neuronal circuitry and reversed—at least for a while—some degeneration. Mentis and his team think their results are coalescing into a theory, even if they don’t fully understand it yet. The researchers are essentially altering the electrical properties of the motor neurons so they start to behave better and closer to normal, says Genís Prat-Ortega, a postdoctoral associate in the Rehab Neural Engineering Labs at the University of Pittsburgh and an investigator on the study. “The motor neurons change and repair,” he says. “Somehow, we are reversing a neurodegenerative process.” Not everyone is so sure. Tim Hagenacker, professor of neurology at the University of Duisburg-Essen, says rebuilding the neural circuit is “not entirely convincing” as an explanation for the study’s results. He thinks that “other cell types play a crucial co-role” in restoring neuronal plasticity or that dysfunctional motor neurons could exist in some form of hibernation. © 2025 Simons Foundation -------------------- https://aeon.co/essays/historys-shaming-fascination-for-the-so-called-idiot-savant The puzzle of the ‘idiot savant’ Violeta Ruiz On 25 November 1915, the American newspaper The Review published the extraordinary case of an 11-year-old boy with prodigious mathematical abilities. Perched on a hill close to a set of railroad tracks, he could memorise all the numbers of the train carriages that sped by at 30 mph, add them up, and provide the correct total sum. What was remarkable about the case was not just his ability to calculate large numbers (and read them on a moving vehicle), but the fact that he could barely eat unassisted or recognise the faces of people he met. The juxtaposition between his supposed arrested development and his numerical facility made his mathematical feats even more impressive. ‘How can you account for it?’ asked the article’s author. The answer took the form of a medical label: the boy was what 19th-century medicine termed an ‘idiot savant’. He possessed an exceptional talent, despite a profound impairment of the mental faculties that affected both his motor and social skills. A century after The Review relayed the prodigious child’s mathematical abilities, trying to understand ‘how they do it’ still drives psychological research into savantism or ‘savant syndrome’ to this day. The SSM Health Treffert Centre in Wisconsin – named after Darold Treffert (1933-2020), one of the leading experts in the field – defines the savant phenomenon as ‘a rare condition in which persons with various developmental disorders, including autistic disorder, have an amazing ability and talent’. Today, savantism is largely comprehended through the lens of neurodivergence, since the association between savantism and autism is strong: roughly one in 10 people with autism exhibit some savant skills, while savantism in the absence of autism is much rarer. Psychological studies by Simon Baron-Cohen and Michael Lombardo, for example, have focused on the neurological basis of ‘systemising’, where exceptional mathematical or musical skills exist among people diagnosed with autism: such people are ‘hypersystemisers’, that is, they are especially good at identifying ‘laws, rules, and/or regularities’. It is believed that their brain’s systemising mechanisms are ‘tuned to very high levels’, making them acutely sensitive to sensory input and also capable of intense attentional focus and rule-learning. © Aeon Media Group Ltd. 2012-2025. -------------------- https://www.nature.com/articles/d41586-025-03280-5 Dangerous ‘nitazene’ opioids are on the rise    Mohana Basu The opioid class of drugs includes heroin and morphine. Unlike those drugs, which are derived from naturally occurring opium, nitazenes are synthesized from scratch in a laboratory. The first nitazenes were developed as painkillers in the 1950s, but were never approved for medical use because they carried a high risk of dangerous side effects such loss of consciousness, coma and death. But since 2019, there has been a rise in the reported use of nitazenes, according to the World Drug Report 2025, which was released in June. In 2023, the report states, 20 different nitazenes were seized by authorities across 28 countries and reported to the United Nations Office on Drugs and Crime (UNODC) Early Warning Advisory on New Psychoactive Substances. Nitazenes can be as much as 500 times more potent than opium-derived drugs. For example, butonitazene is 2.5 times more potent than heroin, whereas isotonitazene and etonitazene are 250 and 500 times more potent, respectively. This means that just a tiny amount can be deadly. In the United Kingdom, there were 179 confirmed deaths from nitazene overdoses in the year to 31 May 2024. And reports suggest that thousands of people might have died from nitazene overdoses in the United States since 2019. In Australia, researchers note that the unpredictable presence of nitazenes in various drugs is increasing the risk of overdose in the country. Most nitazene overdoses are unintentional, says Suzanne Nielsen, an addiction researcher at Monash University in Melbourne, Australia. Overdose tends to occur when nitazenes are sold as other drugs, such as heroin, oxycodone and MDMA (also known as ecstasy). Overdoses can be treated with naloxone, a drug that has long been used to treat other opioid overdoses. More awareness of this among drug users and their families could help save lives, Nielsen adds. © 2025 Springer Nature Limited --------------------



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