by Grace Huckins In 1961, the late psychiatrist Daniel Freedman made what would become one of the most replicated — and most mysterious — discoveries in the history of autism research. Comparing blood levels of the neurotransmitter serotonin in 4 non-autistic and 23 autistic children, he found significantly higher levels among the latter group. Since then, researchers have repeatedly identified this trait, called hyperserotonemia, in about a third of autistic people tested. It’s not difficult to theorize how hyperserotonemia might be linked to a range of autism traits. Neurons that release serotonin extend into practically every part of the brain, where they modulate signals sent among other neurons. Selective serotonin reuptake inhibitors (SSRIs), drugs that raise levels of serotonin in the brain’s synapses, treat psychiatric conditions, such as anxiety and obsessive-compulsive disorder, that can co-occur with autism. And serotonin prompts the gut to contract and facilitate digestion, which is often impaired in autistic people. So when Edwin Cook, professor of psychiatry at the University of Illinois at Chicago, began to study the biology of autism in the 1980s, hyperserotonemia seemed like an obvious place to start. “We didn’t have much [else],” he says. “There were plenty of mothers of older patients I saw who had been labeled refrigerator mothers,” a term that refers to the discredited idea that unaffectionate mothers cause autism. The serotonin finding offered a tangible, biological clue. Even today, with decades more autism research to look back on, the hyperserotonemia result stands out. “It’s one of the few robust biological clues that we’ve had in autism,” says Jeremy Veenstra-VanderWeele, professor of psychiatry at Columbia University and a former advisee of Cook’s. But so far, it has escaped explanation. Nor have researchers been able to definitively link hyperserotonemia to specific genetic, anatomical or behavioral traits in autistic people. This apparent lack of progress has led some to disregard work on the neurotransmitter, according to serotonin researcher Georgianna Gould, associate professor of physiology at the University of Texas Health Science Center at San Antonio. “I’ve actually seen reviews come back that say that serotonin has nothing to do with autism,” she says. © 2023 Simons Foundation

Keyword: Autism; Obesity
Link ID: 28998 - Posted: 11.11.2023

Liam Drew In a laboratory in San Francisco, California, a woman named Ann sits in front of a huge screen. On it is an avatar created to look like her. Thanks to a brain–computer interface (BCI), when Ann thinks of talking, the avatar speaks for her — and in her own voice, too. In 2005, a brainstem stroke left Ann almost completely paralysed and unable to speak. Last year, neurosurgeon Edward Chang, at the University of California, San Francisco, placed a grid of more than 250 electrodes on the surface of Ann’s brain, on top of the regions that once controlled her body, face and larynx. As Ann imagined speaking certain words, researchers recorded her neural activity. Then, using machine learning, they established the activity patterns corresponding to each word and to the facial movements Ann would, if she could, use to vocalize them. The system can convert speech to text at 78 words per minute: a huge improvement on previous BCI efforts and now approaching the 150 words per minute considered average for regular speech1. Compared with two years ago, Chang says, “it’s like night and day”. In an added feat, the team programmed the avatar to speak aloud in Ann’s voice, basing the output on a recording of a speech she made at her wedding. “It was extremely emotional for Ann because it was the first time that she really felt that she was speaking for almost 20 years,” says Chang. This work was one of several studies in 2023 that boosted excitement about implantable BCIs. Another study2 also translated neural activity into text at unprecedented speed. And in May, scientists reported that they had created a digital bridge between the brain and spinal cord of a man paralysed in a cycling accident3. A BCI decoded his intentions to move and directed a spinal implant to stimulate the nerves of his legs, allowing him to walk. © 2023 Springer Nature Limited

Keyword: Brain imaging; Language
Link ID: 28997 - Posted: 11.11.2023

By Azeen Ghorayshi Doctors and patients have long known that antidepressants can cause sexual problems. No libido. Pleasureless orgasms. Numb genitals. Well over half of people taking the drugs report such side effects. Now, a small but vocal group of patients is speaking out about severe sexual problems that have endured even long after they stopped taking selective serotonin reuptake inhibitors, the most popular type of antidepressants. The drugs’ effects have been devastating, they said, leaving them unable to enjoy sex or sustain romantic relationships. “My clitoris feels like a knuckle,” said Emily Grey, a 27-year-old in Vancouver, British Columbia, who took one such drug, Celexa, for depression from age 17 to 23. “It’s not a normal thing to have to come to terms with.” The safety label on Prozac, one of the most widely prescribed S.S.R.I.s, warns that sexual problems may persist after the drug is discontinued. And health authorities in Europe and Canada recently acknowledged that the medications can lead to lasting sexual issues. But researchers are only just beginning to quantify how many people have these long-term problems, known as post-S.S.R.I. sexual dysfunction. And the chronic condition remains contested among some psychiatrists, who point out that depression itself can curb sexual desire. Clinical trials have not followed people after they stop the drugs to determine whether such sexual problems stem from the medications. “I think it’s depression recurring. Until proven otherwise, that’s what it is,” said Dr. Anita Clayton, the chief of psychiatry at the University of Virginia School of Medicine and a leader of an expert group that will meet in Spain next year to formally define the condition. Dr. Clayton published some of the earliest research showing that S.S.R.I.s come with widespread sexual side effects. © 2023 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 28996 - Posted: 11.11.2023

Catherine Sweeney - WPLN NASHVILLE, Tenn. — High school classes start so early around this city that some kids get on buses at 5:30 in the morning. Just 10% of public schools nationwide start before 7:30 a.m., according to federal statistics. But in Nashville, classes start at 7:05 — a fact the new mayor, Freddie O'Connell, has been criticizing for years. "It's not a badge of honor," he said when he was still a city council member. Since his election in September, O'Connell has announced that pushing back school start times is a cornerstone of the education policy he is promoting. He and others around the country have been trying to stress that teenagers aren't lazy or to blame for getting too little sleep. It's science. Sponsor Message "All teenagers have this shift in their brain that causes them to not feel sleepy until about 10:45 or 11 at night," said Kyla Wahlstrom, a senior research fellow at the University of Minnesota in the College of Education and Human Development. She studies how education policy affects learning, and she used to be a teacher. "It's a shift that is biologically determined." Sleep deprivation in teenagers is linked to mental health struggles, worse grades, traffic accidents, and more. That's why states including California and Florida have mandated later start times. Individual districts across the country — including some in Tennessee — have made the same change. But resistance to later starts is less about the science than it is about logistical and financial difficulties, especially with basics like busing. Melatonin makes people feel drowsy. The brain starts producing it when it gets dark outside, and its production peaks in the middle of the night. Adolescents' brains start releasing melatonin about three hours later than adults' and younger children's brains, according to the American Chemical Society. When teens wake up early, their brains are still producing melatonin. © 2023 npr

Keyword: Biological Rhythms; Sleep
Link ID: 28995 - Posted: 11.11.2023

Emily Waltz A highly experimental implant that delivers electrical stimulation to the spinal cord has substantially improved mobility for one man with advanced Parkinson’s disease, according to a report published today in Nature Medicine1. Stimulating spinal cord helps paralysed people to walk again The technology, developed by researchers at the Swiss Federal Institute of Technology in Lausanne (EPFL), enables the man to walk fluidly and to navigate terrain without falling — something he couldn’t do before the treatment. Parkinson’s causes uncontrollable movements and difficulty with coordination that worsens over time. The effects of the treatment have lasted for two years. “There are no therapies to address the severe gait problems that occur at a later stage of Parkinson’s, so it’s impressive to see him walking,” says Jocelyne Bloch, a neurosurgeon at the EPFL and a lead author of the paper. But with only one individual tested, it remains unclear whether the approach will work for other people with the disease. The next step “would be to do a randomized, controlled trial”, says Susan Harkema, a neuroscientist at the University of Louisville in Kentucky who works on stimulation therapy in people with spinal cord injuries. Spinal cord stimulation involves surgically implanting a neuroprosthetic device that delivers pulses of electricity to specific regions of the spinal cord in an effort to activate dysfunctional neural circuits. The technique has been used experimentally to enable people paralysed by spinal cord injury to stand on their own, and even to walk short distances. © 2023 Springer Nature Limited

Keyword: Parkinsons; Robotics
Link ID: 28994 - Posted: 11.08.2023

Ross Pomeroy Numerous hypotheses attempt to explain obesity‘s meteoric rise over the past few decades. There’s the energy balance hypothesis, which states that weight gain is due to consuming more calories than the amount expended. There’s the carbohydrate-insulin hypothesis, which argues that excess consumption of carbohydrates stimulates an insulin response that drives cells to accumulate fat. Then there’s the protein-leverage hypothesis, which suggests that we don’t eat enough protein, driving incessant hunger. Now, researchers have put forth a new hypothesis that places the blame on a sugar ubiquitous in modern food: fructose. Commonly known as “fruit sugar,” fructose is a simple, monosaccharide sugar found in many plants. But the compound that sweetens your watermelon, apples, and oranges can mess with your cells’ energy metabolism, Richard Johnson, a professor of medicine at the University of Colorado, and his co-authors Laura G. Sánchez-Lozada and Miguel A. Lanaspa explain in a paper published October 17 in the journal Obesity. “We suggest that obesity is not a disease of energy excess but rather a disease of energy crisis,” they wrote. The fructose hypothesis As studies in rodents have elucidated, fructose uniquely suppresses the function of mitochondria compared to other nutrients. When these cellular powerhouses are slowed, the cells get stuck in a low-energy state, triggering hunger and thirst. Eating nutrients including fats and protein eventually restores cellular energy levels, but not before we’ve eaten more calories than we need. This excess gets stored as fat. In the long term, frequent fructose exposure can damage mitochondria and reduce the amount of mitochondria in cells, the researchers say, locking people in a low-energy state which drives chronic overeating.

Keyword: Obesity
Link ID: 28993 - Posted: 11.08.2023

Saima Sidik When the scent of morning coffee wafts past the nose, the brain encodes which nostril it enters, new research shows1. Integrating information from both nostrils might help us to identify the odour. The results were published today in Current Biology. A region of the brain called the piriform cortex, which spans the brain’s two hemispheres, is known to receive and process information about scents. However, scientists were unsure whether the two sides of the piriform cortex react to smells in unison or independently. To investigate this question, researchers recruited people with epilepsy who were undergoing brain surgery to identify the areas of their brains responsible for their seizures. Participants were awake for the surgery, during which the scientists delivered scents to one or both nostrils through tiny tubes that reached roughly one centimetre into each nostril. The authors took advantage of electrodes placed in the study participants’ brains to take readings of activity in the piriform cortex. In reality, scents rarely hit only one nostril. Instead, they’re likely to enter one nostril slightly ahead of the other. “The question to ask is, well, can the brain exploit these potential differences?” says Naz Dikecligil, a neuroscientist at the University of Pennsylvania in Philadelphia and a co-author of the study. The findings suggest that the brain does make use of the different arrival times. When an odour was delivered to a single nostril, the side of the brain closest to that nostril reacted first, and a reaction then followed in the opposite side of the brain. “There seem to be actually two odour representations, corresponding to odour information coming from each nostril,” Dikecligil says. When the researchers provided a scent to both nostrils simultaneously, they saw that both sides of the brain recognized the scent faster than either did when it was delivered through only one nostril. This suggests that the two sides do synergize to some degree, even though one lags behind the other in encoding a scent, Dikecligil says. © 2023 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 28992 - Posted: 11.08.2023

By Claudia López Lloreda Genetic tweaks in kingfishers might help cushion the blow when the diving birds plunge beak first into the water to catch fish. Analysis of the genetic instruction book of some diving kingfishers identified changes in genes related to brain function as well as retina and blood vessel development, which might protect against damage during dives, researchers report October 24 in Communications Biology. The results suggest the different species of diving kingfishers may have adapted to survive their dives unscathed in some of the same ways, but it’s still unclear how the genetic changes protect the birds. Hitting speeds of up to 40 kilometers per hour, kingfisher dives put huge amounts of potentially damaging pressure on the birds’ heads, beaks and brains. The birds dive repeatedly, smacking their heads into the water in ways that could cause concussions in humans, says Shannon Hackett, an evolutionary biologist and curator at the Field Museum in Chicago. “So there has to be something that protects them from the terrible consequences of repeatedly hitting their heads against a hard substrate.” Hackett first became interested in how the birds protect their brains while she worked with her son’s hockey team and started worrying about the effect of repeated hits on the human brain. Around the same time, evolutionary biologist Chad Eliason joined the museum to study kingfishers and their plunge diving behavior. In the new study, Hackett, Eliason and colleagues analyzed the complete genome of 30 kingfisher species, some that plunge dive and others that don’t, from specimens frozen and stored at the museum. The preserved birds came from all over the world; some of the diving species came from mainland areas and others from islands and had evolved to dive independently rather than from the same plunge-diving ancestor. The team wanted to know if the different diving species had evolved similar genetic changes to arrive at the same behaviors. Many kingfisher species have developed this behavior, but it was unclear whether this was through genetic convergence, similar to how many species of birds have lost their flight or how bats and dolphins independently developed echolocation (SN: 9/6/2013). © Society for Science & the Public 2000–2023.

Keyword: Brain Injury/Concussion; Evolution
Link ID: 28991 - Posted: 11.08.2023

By Caren Chesler In 2019, Debra Halsch was diagnosed with smoldering multiple myeloma, a rare blood and bone marrow disorder that can develop into a type of blood cancer. Her doctors recommended chemotherapy, she said, but she feared the taxing side effects the drugs might wreak on her body. Instead, the life coach from Piermont, New York tried meditation. A friend had told Halsch, now 57, about Joe Dispenza, who holds week-long meditation retreats that regularly attract thousands of people and carry a $2,299 price tag. Halsch signed up for one in Cancun, Mexico and soon became a devotee. She now meditates for at least two hours a day and says her health has improved as a result. Goop, the health and lifestyle brand launched by actor and entrepreneur Gwyneth Paltrow in 2008, will have its own series on Netflix beginning January 24. Dispenza, a chiropractor who has written various self-help books, has said he believes the mind can heal the body. After all, he says he healed himself back in 1986, when a truck hit him while he was bicycling, breaking six vertebrae. Instead of surgery, Dispenza says he spent hours each day recreating his spine in his mind, visualizing it healthy and healed. After 11 weeks, the story goes, he was back on his feet. Halsch said she believes she can do the same for her illness. “If our thoughts and emotions can make our bodies sick, they can make us well, too,” she said. In an email to Undark, Rhadell Hovda, chief operating officer for Dispenza’s parent company, Encephalon, Inc., emphasized that Dispenza does not claim meditation can treat or cure cancer. However, he does “follow the evidence when it is presented,” and has encountered people at workshops and retreats “who claimed to have healed from many conditions.” For more than two decades, various studies have suggested that meditation and mindfulness — that is, being aware of the present moment — can help reduce and improve pain management, lending some credence to the notion that the brain can affect the body. Such results have helped the field grow into a multibillion-dollar industry, populated by meditation apps, guided workshops, and upscale retreats.

Keyword: Attention; Stress
Link ID: 28990 - Posted: 11.08.2023

By Catherine Offord Close your eyes and picture yourself running an errand across town. You can probably imagine the turns you’d need to take and the landmarks you’d encounter. This ability to conjure such scenarios in our minds is thought to be crucial to humans’ capacity to plan ahead. But it may not be uniquely human: Rats also seem to be able to “imagine” moving through mental environments, researchers report today in Science. Rodents trained to navigate within a virtual arena could, in return for a reward, activate the same neural patterns they’d shown while navigating—even when they were standing still. That suggests rodents can voluntarily access mental maps of places they’ve previously visited. “We know humans carry around inside their heads representations of all kinds of spaces: rooms in your house, your friends’ houses, shops, libraries, neighborhoods,” says Sean Polyn, a psychologist at Vanderbilt University who was not involved in the research. “Just by the simple act of reminiscing, we can place ourselves in these spaces—to think that we’ve got an animal analog of that very human imaginative act is very impressive.” Researchers think humans’ mental maps are encoded in the hippocampus, a brain region involved in memory. As we move through an environment, cells in this region fire in particular patterns depending on our location. When we later revisit—or simply think about visiting—those locations, the same hippocampal signatures are activated. Rats also encode spatial information in the hippocampus. But it’s been impossible to establish whether they have a similar capacity for voluntary mental navigation because of the practical challenges of getting a rodent to think about a particular place on cue, says study author Chongxi Lai, who conducted the work while a graduate student and later a postdoc at the Howard Hughes Medical Institute’s Janelia Research Campus. In their new study, Lai, along with Janelia neuroscientist Albert Lee and colleagues, found a way around this problem by developing a brain-machine interface that rewarded rats for navigating their surroundings using only their thoughts.

Keyword: Learning & Memory; Attention
Link ID: 28989 - Posted: 11.04.2023

By Laura Sanders Like tiny, hairy Yodas raising X-wings from a swamp, rats can lift digital cubes and drop them near a target. But these rats aren’t using the Force. Instead, they are using their imagination. This telekinetic trick, described in the Nov. 3 Science, provides hints about how brains imagine new scenarios and remember past ones. “This is fantastic research,” says Mayank Mehta, a neurophysicist at UCLA. “It opens up a lot of exciting possibilities.” A deeper scientific understanding of the brain area involved in the feat could, for instance, help researchers diagnose and treat memory disorders, he says. Neuroscientist Albert Lee and his colleagues study how brains can go back in time by revisiting memories and jump ahead to imagine future scenarios. Those processes, sometimes called “mental time travel,” are “part of what makes our inner mental lives quite rich and interesting,” says Lee, who did the new study while at Howard Hughes Medical Institute’s Janelia Research Campus in Ashburn, Va. To dip into these complex questions, the researchers began with a simpler one: “Can you be in one place and think about another place?” says Lee, who is now an HHMI investigator at Beth Israel Deaconess Medical Center in Boston. “The rat isn’t doing anything fancier than that. We’re not asking them to recall their summer vacation.” Neuroscientist and engineer Chongxi Lai, also now at Beth Israel Deaconess, Lee and colleagues trained rats to move on a spherical treadmill in the midst of a 3-D virtual world projected onto a surrounding screen. While the rats poked around their virtual world, electrodes recorded signals from nerve cells in the rats’ hippocampi, brain structures known to hold complex spatial information, among other things (SN: 10/6/14). In this way, researchers matched patterns of brain activity with spots in the virtual world. © Society for Science & the Public 2000–2023.

Keyword: Attention
Link ID: 28988 - Posted: 11.04.2023

By Dan Falk You’re thirsty so you reach for a glass of water. It’s either a freely chosen action or the inevitable result of the laws of nature, depending on who you ask. Do we have free will? The question is ancient—and vexing. Everyone seems to have pondered it, and many seem quite certain of the answer, which is typically either “yes” or “absolutely not.” One scientist in the “absolutely not” camp is Robert Sapolsky. In his new book, Determined: A Science of Life Without Free Will, the primatologist and Stanford professor of neurology spells out why we can’t possibly have free will. Why do we behave one way and not another? Why do we choose Brand A over Brand B, or vote for Candidate X over Candidate Y? Not because we have free will, but because every act and thought are the product of “cumulative biological and environmental luck.” Sapolsky tells readers that the “biology over which you had no control, interacting with the environment over which you had no control, made you you.” That is to say, “everything in your childhood, starting with how you were mothered within minutes of birth, was influenced by culture, which means as well by the centuries of ecological factors that influenced what kind of culture your ancestors invented, and by the evolutionary pressures that molded the species you belong to.” In Body ImageNO, WE DON’T: Robert Sapolsky on free will: “I have spent forever trying to understand where behavior comes from. And what you see is there’s absolutely no room for free will.” Photo courtesy of Christine Johnston. Sapolsky brings the same combination of earthy directness and literary flourish that marked his earlier books, including Why Zebras Don’t Get Ulcers, about the biology of stress, to this latest work. To summarize his point of view in Determined, he writes, “Or as Maria sings in The Sound of Music, ‘Nothing comes from nothing, nothing ever could.’” The affable, bushy-bearded Sapolsky is now in his mid 60s. During our recent interview over Zoom, I was on the lookout for any inconsistency; anything that might suggest that deep down he admits we really do make decisions, as many of us surely feel. But he was prepared and stuck to his guns. © 2023 NautilusNext Inc.,

Keyword: Consciousness
Link ID: 28987 - Posted: 11.04.2023

Sara Reardon Psychedelic drugs have been undergoing a major makeover in psychiatry, earning mainstream acceptance that has eluded them for decades. In 2019, a variant of ketamine — an animal tranquillizer well known as a club drug — was approved by the US Food and Drug Administration (FDA) for treating post-traumatic stress disorder (PTSD). In May, Oregon opened its first treatment centre for administering psilocybin — the hallucinogenic compound found in magic mushrooms — following the state’s decision to legalize it (psilocybin remains illegal at the federal level). And, after decades of effort, the Multidisciplinary Association for Psychedelic Studies, a non-profit research organization in San Jose, California, formally asked the FDA for approval to market MDMA — also known as molly or ecstasy — as a treatment for PTSD. Most specialists expect the MDMA approval to go through on the weight of clinical evidence and popular support. Two large trials have shown that the drug can reduce the symptoms of PTSD when administered in controlled therapy sessions1,2. And it seems to do so more quickly than other treatments. But how MDMA and other psychedelics work is still largely a mystery, both because the drugs have long been illegal and because psychiatric conditions are difficult to study in animals. Psychedelic drug MDMA moves closer to US approval following success in PTSD trial With the regulatory landscape shifting, legal psychedelic research is becoming easier — and potentially more profitable. Neuroscientists, psychiatrists, pharmacologists, biochemists and others are entering the field, bringing fresh ideas about what the drugs do at a cellular and molecular level and trying to unravel how these mechanisms might help to relieve symptoms of psychiatric conditions. From a clinical perspective, understanding how the drugs work might not matter. “You don’t need to know the mechanism of the drug to have a very effective therapy,” says David Olson, a biochemist at the University of California, Davis. But, understanding more about psychedelics could lead to the development of proprietary drugs that are safer, less hallucinogenic and ultimately more effective. It could also affect the way psychedelics are administered in the clinic — helping providers to tailor treatments to each person. Several key questions are driving the basic research that progresses in the background as MDMA and others march towards the market. © 2023 Springer Nature Limited

Keyword: Depression; Stress
Link ID: 28986 - Posted: 11.04.2023

By Regina G. Barber What your parents didn't tell you about pulling an all-nighter? It might just ease depression for several days. At least, that's what researchers found happened to mice in a study published in the journal Neuron Thursday. Most people who've stayed up all night know the "tired and wired" feeling they get the next day. The body might be exhausted, but the brain feels jittery, hyperactive or even giddy. Even after these changes wear off, sleep loss can have a strong antidepressant effect in people that lasts several days. But researchers hadn't figured out why sleeplessness might have this effect —until this study from neurobiologists at Northwestern University. To study all of this, the team looked at the effects of sleep loss in mice. They induced sleep loss in some of the mice, while the others got a typical night's rest. They found that after this sleepless night, the mice were more excitable, more aggressive, more sexual and less depressed than mice that got a regular amount of sleep. Of course, researchers can't just ask mice whether they feel "less depressed." Instead, they created a depression-like state in all the mice before either disrupting their sleep or allowing them to rest by repeatedly giving them small shocks. In response to these shocks, the mice entered a depressive-like state and eventually stopped trying to escape their cages. Then, they tested the mice's response to shocks again. The ones that had stayed up all night showed a reversed depressive state, indicated by more attempts to escape the shocks. Dopamine is responsible for the brain's reward response. Changes in the brain's dopamine system have also been implicated in conditions like depression and in sleep regulation. And so, to see how the mice's brains responded to their sleepless night, the researchers measured dopamine neuron activity. They saw that sleep-deprived mice showed higher dopamine activity in three regions: the prefrontal cortex, nucleus accumbens and hypothalamus. © 2023 npr

Keyword: Sleep; Depression
Link ID: 28985 - Posted: 11.04.2023

By Clay Risen William E. Pelham Jr., a child psychologist who challenged how his field approached attention deficit hyperactivity disorder in children, arguing for a therapy-based regimen that used drugs like Ritalin and Adderall as an optional supplement, died on Oct. 21 in Miami. He was 75. His son, William E. Pelham III, who is also a child psychologist, confirmed the death, in a hospital, but did not provide a cause. Dr. Pelham began his career in the mid-1970s, when the modern understanding of mental health was emerging and psychologists were only just beginning to understand A.D.H.D. — and with it a new generation of medication to treat it. Through the 1980s and ’90s, doctors and many parents embraced A.D.H.D. drugs like Ritalin and Adderall as miracle medications, though some, including Dr. Pelham, raised concerns about their efficacy and side effects. Dr. Pelham was not opposed to medication. He recognized that drugs were effective at rapidly addressing the symptoms of A.D.H.D., like fidgeting, impulsiveness and lack of concentration. But in a long string of studies and papers, he argued that for most children, behavioral therapy, combined with parental intervention techniques, should be the first line of attack, followed by low doses of drugs, if necessary. And yet, as he pointed out repeatedly, the reality was far different: The Centers for Disease Control and Prevention reported in 2016 that while six in 10 children diagnosed with A.D.H.D. were on medication, fewer than half received behavioral therapy. In one major study, which he published in 2016 along with Susan Murphy, a statistician at the University of Michigan, he demonstrated the importance of treatment sequencing — that behavioral therapy should come first, then medication. He and Dr. Murphy split a group of 146 children with A.D.H.D., from ages 5 to 12, into two groups. One group received a low dose of generic Ritalin; the other received nothing, but their parents were given instruction in behavioral-modification techniques. After two months, children from both groups who showed no improvement were arranged into four new groups: The children given generic Ritalin received either more medication or behavioral modification therapy, and the children given behavioral modification therapy received either more intense therapy or a dose of medication. © 2023 The New York Times Company

Keyword: ADHD; Drug Abuse
Link ID: 28984 - Posted: 11.04.2023

By Meghan Rosen In endurance athletes, some brain power may come from an unexpected source. Marathon runners appear to rely on myelin, the fatty tissue bundled around nerve fibers, for energy during a race, scientists report October 10 in a paper posted at bioRxiv.org. In the day or two following a marathon, this tissue seems to dwindle drastically, brain scans of runners reveal. Two weeks after the race, the brain fat bounces back to nearly prerace levels. The find suggests that the athletes burn so much energy running that they need to tap into a new fuel supply to keep the brain operating smoothly. “This is definitely an intriguing observation,” says Mustapha Bouhrara, a neuroimaging scientist at the National Institute on Aging in Baltimore. “It is quite plausible that myelin lipids are used as fuel in extended exercise.” If what the study authors are seeing is real, he says, the work could have therapeutic implications. Understanding how runners’ myelin recovers so rapidly might offer clues for developing potential treatments — like for people who’ve lost myelin due to aging or neurodegenerative disease. Much of the human brain contains myelin, tissue that sheathes nerve fibers and acts as an insulator, like rubber coating an electrical wire. That insulation lets electrical messages zip from nerve cell to nerve cell, allowing high-speed communication that’s crucial for brain function. The fatty tissue seems to be a straightforward material with a straightforward job, but there’s likely more to it than that, says Klaus-Armin Nave, a neurobiologist at the Max Planck Institute for Multidisciplinary Sciences in Göttingen, Germany. “For the longest time, it was thought that myelin sheathes were assembled, inert structures of insulation that don’t change much after they’re made,” he says. Today, there’s evidence that myelin is a dynamic structure, growing and shrinking in size and abundance depending on cellular conditions. The idea is called myelin plasticity. “It’s hotly researched,” Nave says. © Society for Science & the Public 2000–2023.

Keyword: Glia; Multiple Sclerosis
Link ID: 28983 - Posted: 11.01.2023

By Jake Buehler A fruit bat hanging in the corner of a cave stirs; it is ready to move. It scans the space to look for a free perch and then takes flight, adjusting its membranous wings to angle an approach to a spot next to one of its fuzzy fellows. As it does so, neurological data lifted from its brain is broadcast to sensors installed in the cave’s walls. This is no balmy cave along the Mediterranean Sea. The group of Egyptian fruit bats is in Berkeley, California, navigating an artificial cave in a laboratory that researchers have set up to study the inner workings of the animals’ minds. The researchers had an idea: that as a bat navigates its physical environment, it’s also navigating a network of social relationships. They wanted to know whether the bats use the same or different parts of their brain to map these intersecting realities. In a new study published in Nature in August, the scientists revealed that these maps overlap. The brain cells informing a bat of its own location also encode details about other bats nearby — not only their location, but also their identities. The findings raise the intriguing possibility that evolution can program those neurons for multiple purposes to serve the needs of different species. The neurons in question are located in the hippocampus, a structure deep within the mammalian brain that is involved in the creation of long-term memories. A special population of hippocampal neurons, known as place cells, are thought to create an internal navigation system. First identified in the rat hippocampus in 1971 by the neuroscientist John O’Keefe, place cells fire when an animal is in a particular location; different place cells encode different places. This system helps animals determine where they are, where they need to go and how to get from here to there. In 2014, O’Keefe was awarded the Nobel Prize for his discovery of place cells, and over the last several decades they have been identified in multiple primate species, including humans. However, moving from place to place isn’t the only way an animal can experience a change in its surroundings. In your home, the walls and furniture mostly stay the same from day to day, said Michael Yartsev, who studies the neural basis of natural behavior at the University of California, Berkeley and co-led the new work. But the social context of your living space could change quite regularly. © 2023 An editorially independent publication supported by the Simons Foundation.

Keyword: Learning & Memory
Link ID: 28982 - Posted: 11.01.2023

Michaeleen Doucleff For several months now, I've been studying how the new medications, Ozempic and Wegovy, cause dramatic weight loss. Both medications contain a compound, semaglutide, that squelches hunger like a fly swatter smashes a mosquito. People who take the medication say they no longer have constant cravings for food, so they eat less frequently. The drug seems to quiet what some people call "food noise," the constant internal chatter telling them to eat. While reading study after study about Wevgovy and Ozempic, I learned that the drug mimics a hormone that our bodies naturally make when we're eating food. It's called GLP-1. This made me wonder: Could we increase levels of this hormone by changing our diet? Turns out, the answer is yes – you can increase your body's production of GLP-1 with your diet, says Frank Duca, who studies metabolic diseases at the University of Arizona. One of the key foods that triggers its release is a food most Americans struggle to eat enough of, even though it comes with a cornucopia of health benefits. Yup, I'm talking about fiber. "Whenever my family finds out that I'm studying obesity or diabetes, they say, 'Oh, what's the wonder drug? What do I need to take? What do I need to do?'" Duca explains. "And I say, 'Eat more fiber.' " But here's the hitch. Not all fiber works the same way. Duca and other researchers are beginning to show that particular types of fibers are more potent at triggering GLP-1 release and at regulating hunger than others. "We're seeing now that companies are adding fiber to foods, but a lot of the time, they don't add the kind of fiber that's super beneficial for you," Duca says. To understand why fiber is so important for producing GLP-1, let's look at what happens when you don't eat much fiber. Let's say you wake up in the morning feeling hungry and you eat two slices of white bread and a fried egg. As the digested food moves into the small intestine, many of the nutrients, such as the carbohydrates, fats and amino acids, trigger an avalanche of activity in your blood and brain. "The food activates cells in your intestine, which then release a ton of hormones," says Sinju Sundaresan, who's a gut physiologist at Midwestern University. About 20 of these hormones, including GLP-1, are known as satiation hormones. © 2023 npr

Keyword: Obesity
Link ID: 28981 - Posted: 11.01.2023

by Giorgia Guglielmi / The ability to see inside the human brain has improved diagnostics and revealed how brain regions communicate, among other things. Yet questions remain about the replicability of neuroimaging studies that aim to connect structural or functional differences to complex traits or conditions, such as autism. Some neuroscientists call these studies ‘brain-wide association studies’ — a nod to the ‘genome-wide association studies,’ or GWAS, that link specific variants to particular traits. But unlike GWAS, which typically analyze hundreds of thousands of genomes at once, most published brain-wide association studies involve, on average, only about two dozen participants — far too few to yield reliable results, a March analysis suggests. Spectrum talked to Damien Fair, co-lead investigator on the study and director of the Masonic Institute for the Developing Brain at the University of Minnesota in Minneapolis, about solutions to the problem and reproducibility issues in neuroimaging studies in general. Spectrum: How have neuroimaging studies changed over time, and what are the consequences? Damien Fair: The realization that we could noninvasively peer inside the brain and look at how it’s reacting to certain types of stimuli blew open the doors on studies correlating imaging measurements with behaviors or phenotypes. But even though there was a shift in the type of question that was being asked, the study design stayed identical. That has caused a lot of the reproducibility issues we’re seeing today, because we didn’t change sample sizes. The opportunity is huge right now because we finally, as a community, are understanding how to use magnetic resonance imaging for highly reliable, highly reproducible, highly generalizable findings. S: Where did the reproducibility issues in neuroimaging studies begin? DF: The field got comfortable with a certain type of study that provided significant and exciting results, but without having the rigor to show how those findings reproduced. For brain-wide association studies, the importance of having large samples just wasn’t realized until more recently. It was the same problem in the early age of genome-wide association studies looking at common genetic variants and how they relate to complex traits. If you’re underpowered, highly significant results may not generalize to the population. © 2023 Simons Foundation

Keyword: Brain imaging
Link ID: 28980 - Posted: 11.01.2023

By Paula Span A year ago, the Food and Drug Administration announced new regulations allowing the sale of over-the-counter hearing aids and setting standards for their safety and effectiveness. That step — which was supposed to take three years but required five — portended cheaper, high-quality hearing aids that people with mild to moderate hearing loss could buy online or at local pharmacies and big stores. So how’s it going? It’s a mixed picture. Manufacturers and retailers have become serious about making hearing aids more accessible and affordable. Yet the O.T.C. market remains confusing, if not downright chaotic, for the mostly older consumers the new regulations were intended to help. The past year also brought renewed focus on the importance of treating hearing loss, which affects two-thirds of people over age 70. Researchers at Johns Hopkins University published the first randomized clinical trial showing that hearing aids could help reduce the pace of cognitive decline. Some background: In 2020, the influential Lancet Commission on Dementia Prevention, Intervention and Care identified hearing loss as the greatest potentially modifiable risk factor for dementia. Previous studies had demonstrated a link between hearing loss and cognitive decline, said Dr. Frank Lin, an otolaryngologist and epidemiologist at Johns Hopkins and lead author of the new research. “What remained unanswered was, If we treat hearing loss, does it actually reduce cognitive loss?” he said. The ACHIEVE study (for Aging and Cognitive Health Evaluation in Elders) showed that, at least for a particular group of older adults, it could. Of nearly 1,000 people ages 70 to 84 with untreated mild to moderate hearing loss, half received hearing assessments from audiologists, were fitted with midpriced hearing aids and were counseled on how to use them for several months. The control group participated in a health education program. Over three years, the study found that hearing-aid use had scant effect on healthy volunteers at low risk of cognitive loss. But among participants who were older and less affluent, hearing aids reduced the rate of cognitive decline by 48 percent, compared with the control group, a difference the researchers deemed “clinically meaningful.” © 2023 The New York Times Company

Keyword: Hearing; Alzheimers
Link ID: 28979 - Posted: 11.01.2023