By Evelyn Lake Functional MRI (fMRI), though expensive, has many properties of an ideal clinical tool. It’s safe and noninvasive. It is widely available in some countries, and increasingly so on a global scale. Its “blood oxygen level dependent,” or BOLD, signal is altered in people with almost any neurological condition and is rich enough to contain information specific to each person, offering the potential for a personalized approach to medical care across a wide spectrum of neurological conditions. But despite enormous interest and investment in fMRI — and its wide use in basic neuroscience research — it still lacks broad clinical utility; it is mainly employed for surgical planning. For fMRI to inform a wider range of clinical decision-making, we need better ways of deciphering what underlying changes in the brain drive changes to the BOLD signal. If someone with Alzheimer’s disease has an increase in functional connectivity (a measure of synchrony between brain regions), for example, does this indicate that synapses are being lost? Or does it suggest that the brain is forming compensatory pathways to help the person avoid further cognitive decline? Or something else entirely? Depending on the answer, one can imagine different courses of treatment. Put simply, we cannot extract sufficient information from fMRI and patient outcomes alone to determine which scenarios are playing out and therefore what we should do when we observe changes in our fMRI readouts. To better understand what fMRI actually shows, we need to use complementary methodologies, such as the emerging optical imaging tool of wide-field fluorescence calcium imaging. Combining modalities presents significant technical challenges but offers the potential for deeper insights: observing the BOLD signal alongside other signals that report more directly on what is occurring in brain tissue. Using these more direct measurements instead of fMRI in clinical practice is not an option — they are unethical to use in people or invasive, requiring physical or optical access to the brain. © 2023 Simons Foundation.

Keyword: Brain imaging
Link ID: 29109 - Posted: 01.23.2024

Karla Kaun Many people are wired to seek and respond to rewards. Your brain interprets food as rewarding when you are hungry and water as rewarding when you are thirsty. But addictive substances like alcohol and drugs of abuse can overwhelm the natural reward pathways in your brain, resulting in intolerable cravings and reduced impulse control. A popular misconception is that addiction is a result of low willpower. But an explosion of knowledge and technology in the field of molecular genetics has changed our basic understanding of addiction drastically over the past decade. The general consensus among scientists and health care professionals is that there is a strong neurobiological and genetic basis for addiction. As a behavioral neurogeneticist leading a team investigating the molecular mechanisms of addiction, I combine neuroscience with genetics to understand how alcohol and drugs influence the brain. In the past decade, I have seen changes in our understanding of the molecular mechanisms of addiction, largely due to a better understanding of how genes are dynamically regulated in the brain. New ways of thinking about how addictions form have the potential to change how we approach treatment. Each of your brain cells has your genetic code stored in long strands of DNA. For all that DNA to fit into a cell, it needs to be packed tightly. This is achieved by winding the DNA around “spools” of protein called histones. Areas where DNA is unwound contain active genes coding for proteins that serve important functions within the cell. When gene activity changes, the proteins your cells produce also change. Such changes can range from a single neuronal connection in your brain to how you behave. This genetic choreography suggests that while your genes affect how your brain develops, which genes are turned on or off when you are learning new things is dynamic and adapts to suit your daily needs. © 2010–2024, The Conversation US, Inc.

Keyword: Drug Abuse; Epigenetics
Link ID: 29108 - Posted: 01.23.2024

By Mark Johnson There had been early clues, but it was a family game of dominoes around Christmas 2021 that convinced Susan Stewart that something was wrong with her husband. Charlie Stewart, then 75 and retired, struggled to match the dots on different domino tiles. Susan assumed it was a vision problem. Charlie’s memory was fine, and he had no family history of dementia. But months later the Marin County, Calif., couple were shocked to learn that his domino confusion was a sign he had a lesser-known variant of Alzheimer’s disease. For patients with this variant, called posterior cortical atrophy, the disease begins with problems affecting vision rather than memory. The unusual early symptoms mean that thousands of people may go years before receiving the correct diagnosis, experts said. That may change with the first large-scale international study of the condition, published Monday in the journal Lancet Neurology. An international team led by researchers at the University of California at San Francisco studied records of 1,092 PCA patients from 16 countries and found that, on average, the syndrome begins affecting patients at age 59 ― about five to six years earlier than most patients with the more common form of Alzheimer’s. Although the number of patients with PCA has not been established, researchers say that the variant may account for as many as 10 percent of all Alzheimer’s cases; that would put the number of Americans with the condition close to 700,000. “We have a lot of work to do to raise awareness about the syndrome,” said Gil D. Rabinovici, one of the study’s authors and director of the UCSF Alzheimer’s Disease Research Center. “One thing that we found in our large study is that by the time people are diagnosed, they’ve had [the disease] for quite a few years.” The study authors said they hope greater awareness of the syndrome will help doctors diagnose it earlier and will encourage researchers to include patients with PCA in future Alzheimer’s clinical trials. Unusual symptoms delay diagnosis

Keyword: Alzheimers; Vision
Link ID: 29107 - Posted: 01.23.2024

By Mariana Lenharo Neuroscientist Lucia Melloni didn’t expect to be reminded of her parents’ divorce when she attended a meeting about consciousness research in 2018. But, much like her parents, the assembled academics couldn’t agree on anything. The group of neuroscientists and philosophers had convened at the Allen Institute for Brain Science in Seattle, Washington, to devise a way to empirically test competing theories of consciousness against each other: a process called adversarial collaboration. Devising a killer experiment was fraught. “Of course, each of them was proposing experiments for which they already knew the expected results,” says Melloni, who led the collaboration and is based at the Max Planck Institute for Empirical Aesthetics in Frankfurt, Germany. Melloni, falling back on her childhood role, became the go-between. The collaboration Melloni is leading is one of five launched by the Templeton World Charity Foundation, a philanthropic organization based in Nassau, the Bahamas. The charity funds research into topics such as spirituality, polarization and religion; in 2019, it committed US$20 million to the five projects. The aim of each collaboration is to move consciousness research forward by getting scientists to produce evidence that supports one theory and falsifies the predictions of another. Melloni’s group is testing two prominent ideas: integrated information theory (IIT), which claims that consciousness amounts to the degree of ‘integrated information’ generated by a system such as the human brain; and global neuronal workspace theory (GNWT), which claims that mental content, such as perceptions and thoughts, becomes conscious when the information is broadcast across the brain through a specialized network, or workspace. She and her co-leaders had to mediate between the main theorists, and seldom invited them into the same room. Their struggle to get the collaboration off the ground is mirrored in wider fractures in the field. © 2024 Springer Nature Limited

Keyword: Consciousness
Link ID: 29106 - Posted: 01.18.2024

By Holly Barker Sensory issues associated with autism may be caused by fluctuating neuronal noise — the background hum of electrical activity in the brain — according to a new mouse study. Up to 90 percent of autistic people report sensory problems, including heightened sensitivity to sounds or an aversion to certain smells. Yet others barely register sensory cues and may seek out sensations by making loud noises or rocking back and forth. But thinking in terms of hyper- or hyposensitivity may be an oversimplification, says Andreas Frick, lead investigator and research director at INSERM. “It’s becoming clear now that things are a lot more nuanced.” For instance, the brain’s response to visual patterns — measured using electroencephalography (EEG) recordings — varies more between viewings in autistic people than in those without the condition, one study found. And functional MRI has detected similar variability among autistic people, suggesting sensory problems may arise from inconsistent brain responses. In the new study, Frick and his colleagues found variability in the activity of individual neurons in a mouse model of fragile X syndrome, one of the leading causes of autism. That variability in neuronal response maps to fluctuations in the levels of noise in the brain, the study found. Noise within the brain isn’t necessarily a bad thing. In fact, an optimum amount is ideal: a little can give neurons the ‘push’ they might need to fire an action potential, while too much can make it difficult for the brain to distinguish between different stimuli. But in animals modeling fragile X syndrome, noise fluctuates such that they process sensory information less reliably, Frick says. © 2023 Simons Foundation.

Keyword: Autism
Link ID: 29105 - Posted: 01.18.2024

Nicola Davis Science correspondent Breaking up is hard to do, but it seems the brain may have a mechanism to help get over an ex. Researchers studying prairie voles say the rodents, which form monogamous relationships, experience a burst of the pleasure hormone dopamine in their brain when seeking and reuniting with their partner. However, after being separated for a lengthy period, they no longer experience such a surge. “We tend to think of it as ‘getting over a breakup’ because these voles can actually form a new bond after this change in dopamine dynamics – something they can’t do while the bond is still intact,” said Dr Zoe Donaldson, a behavioural neuroscientist at CU Boulder and senior author of the work. Writing in the journal Current Biology, the team describe how they carried out a series of experiments in which voles had to press levers to access either their mate or an unknown vole located on the other side of a see-through door. The team found the voles had a greater release of dopamine in their brain when pressing levers and opening doors to meet their mate than when meeting the novel vole. They also huddled more with their mate on meeting, and experienced a greater rise in dopamine while doing so. Donaldson said: “We think the difference is tied to knowing you are about to reunite with a partner and reflects that it is more rewarding to reunite with a partner than go hang out with a vole they don’t know.” However, these differences in dopamine levels were no longer present after they separated pairs of voles for four weeks – a considerable period in the lifetime of the rodents. Differences in huddling behaviour also decreased. The researchers say the findings suggest a devaluation of the bond between pairs of voles, rather than that they have forgotten each other. © 2024 Guardian News & Media Limited

Keyword: Sexual Behavior; Evolution
Link ID: 29104 - Posted: 01.18.2024

By Jude Coleman When it comes to tail wagging among dogs, some questions still hound researchers. We know that domesticated dogs (Canis familiaris) use their tails to communicate — with other dogs as well as humans — and even what various types of wags mean, researchers note in a new review of the scientific literature. But we don’t know why dogs seem to wag more than other canines or even how much of it is under their control, ethologist Silvia Leonetti and colleagues report January 17 in Biology Letters. “Among all possible animal behavior that humans experience in everyday life, domestic dog tail wagging is one of the most common,” says Leonetti, who is now at the University of Turin in Italy. “But a lot of dog behavior remains a scientific enigma.” So Leonetti and her colleagues pored through previous studies to figure out what elements of tail wagging are understood and which remain mysterious. They also hypothesized about the behavior’s origins: Perhaps tail wagging placates some human need for rhythm, the researchers suggest, or maybe the behavior is a genetic tagalong, a trait tied to others that humans bred into domesticated dogs. “People think wagging tail equals happy dog. But it’s actually a lot more complicated than that,” says Emily Bray, an expert in canine cognition at the University of Arizona in Tucson who was not involved with the work. Understanding why dogs wag their tails is important partly from an animal welfare perspective, she says, as it could help dog owners read their pups’ cues better. One main thing that researchers know about tail wagging is that it’s used predominantly for communication instead of locomotion, like a whale, or swatting away bugs, like a horse. Wagging also means different things depending on how the tail is wagged, such as its height or side-to-side movement. © Society for Science & the Public 2000–2024.

Keyword: Animal Communication; Emotions
Link ID: 29103 - Posted: 01.18.2024

By Lauren Peace Tampa Bay Times Nina Shand couldn’t stay awake. She had taken afternoon naps since she was a teenager to accommodate her “work hard, play hard” attitude, but when she was in her mid-20s the sleepiness became more severe. Menial computer tasks put her to sleep, and a 20-minute drive across her city, St. Petersburg, Florida, brought on a drowsiness so intense that her eyelids would flutter, forcing her to pull over. She knew something was really wrong when she no longer felt safe behind the wheel. In 2021, she received a diagnosis: narcolepsy, a rare disorder that causes excessive daytime sleepiness. Her doctor prescribed her Adderall, the brand-name version of the amphetamine-powered medication commonly known for treating attention-deficit/hyperactivity disorder. It worked. For the first time in years, Shand, now 28, felt energized. She was no longer struggling at work, sneaking naps, or downing coffees to trick her body into staying awake. She felt hope. But by 2022, a national Adderall shortage meant pharmacies were no longer able to fill her prescription. Shand and countless others across the country were being turned away, left to piece together a new — and often less effective — treatment plan with doctors scrambling to meet their needs. More than a year later, the shortage continues. In October, Democrats in the U.S. House of Representatives implored the FDA and Drug Enforcement Administration to work with drug manufacturers to ensure better supply. “We cannot allow this to be the continuing reality for Americans,” read their letter, led by Rep. Abigail Spanberger (D-Va.). But for now, it is.

Keyword: Sleep; Drug Abuse
Link ID: 29102 - Posted: 01.16.2024

Ian Sample Science editor From Cain and Abel and the Brothers Karamazov to Cinderella, the warmth and support provided by siblings has hardly been taken for granted. Now, researchers have found that children who moan about their brothers and sisters may have good reason to complain: the more siblings teenagers have, the more it hits their happiness, they claim. A study of secondary schoolchildren in the US and China found that those from larger families had slightly poorer mental health than those from smaller families. The greatest impact was seen in families with multiple children born less than a year apart. Doug Downey, a professor of sociology at Ohio State University, said previous work in the field had revealed a mixed picture of positives and negatives for children with more siblings, adding that the latest results “were not a given”. The researchers asked 9,100 eighth graders in the US and 9,400 in China, with an average age of 14, a range of questions about their mental health, though the specific questions varied between the countries. In China, the teenagers with no siblings fared best for mental health. In the US, children who had no siblings or only one were found to have similar mental health. Overall, mental health was worse the more siblings the teenagers had, with greater impacts seen for teenagers with older siblings, and when brothers and sisters were closely spaced in age. Writing in the Journal of Family Issues, Downey and his colleagues argue that the findings are in line with the “resource dilution” explanation, the driving force behind the unwritten formula that states that the number of balls dropped rises, sometimes dramatically, with the number of siblings born. © 2024 Guardian News & Media Limited

Keyword: Depression; Development of the Brain
Link ID: 29101 - Posted: 01.16.2024

By Meryl Davids Landau When Brian Meyer received a Stage 4 prostate cancer diagnosis three years ago at age 62, he was determined to make the most of his remaining years. He immediately retired from a decades-long career in the grocery business and took every opportunity to hike, camp and — his all-time favorite — fish for salmon. Brian and his wife, Cheryl, regularly visited their two grown children and three grandsons and spent time with their many friends. But it was sometimes hard to keep his mind off his pain and the reality that life was nearing an end. “It tugs at the heart all the time,” Meyer, from Vancouver Island, British Columbia, said in August. A calm person by nature, he found his anxiety skyrocketing. By November, though, despite a new, highly aggressive liver cancer that shrank his prognosis to months or weeks, Meyer felt calm much of the time. The prime reason: a 25-milligram dose of the psychedelic drug psilocybin he had taken several months earlier, due to a Canadian program being watched elsewhere for the emotional benefits it may offer people nearing death. In mid-August, Meyer and nine other people with terminal cancers had gathered in two rooms, and there, lying on plush floor mats with blankets covering their bodies, their eyes covered by sleeping masks and music piped in over headphones, they swallowed the psilocybin capsules. The consciousness-altering drug, administered by the nonprofit Vancouver Island wellness center Roots to Thrive, set Meyer and the others on a six-hour journey of fantastical images and thoughts. The hope was that this “trip” would lead to lasting improvements in mood and lessen their angst around death. It was accompanied by weeks of Zoom group therapy sessions before and after, along with an in-person gathering the evening before for a medical clearance and the opportunity for participants and their spouses to meet in person.

Keyword: Drug Abuse; Stress
Link ID: 29100 - Posted: 01.16.2024

By Carissa Wong Researchers have identified some of the earliest known cases of sex-chromosome syndromes — in five ancient humans. “It’s quite interesting to think that these people existed throughout human history and how they seem to have been part of their societies,” says Kyriaki Anastasiadou, who studies ancient genomics at the Francis Crick Institute in London and is a co-author of the study, which was published on 11 January in Communications Biology1. People with extra or missing chromosomes often have differences in appearance and behaviour compared with others in the population. By identifying individuals who had these genetic syndromes, the researchers could illuminate how past societies viewed and treated people with differences. Through sequencing ancient DNA, researchers have previously found2 ancient people with an atypical number of chromosomes, including an infant with Down syndrome — caused by an extra copy of chromosome 21 — who lived around 5,000 years ago. Anastasiadou and her colleagues have now discovered the first prehistoric person known to have had Turner syndrome, which occurs in females and is characterized by having only one complete copy of the X chromosome, instead of the two copies usually found in females (males have one X and one Y). The person lived in Somerset, UK, roughly 2,500 years ago, during the Iron Age. People with Turner syndrome tend to be shorter than average and experience fertility problems. The other people the researchers identified with sex-chromosome syndromes were male. Among them was the earliest known person to have an extra Y chromosome, known as Jacob’s syndrome, which is linked to being taller than average. The man lived around 1,100 years ago, during the Early Medieval Period. The team also found three ancient males from different points in time who had an extra X chromosome, a condition known as Klinefelter syndrome, which is linked to growing taller than average and having broader hips and larger breasts. © 2024 Springer Nature Limited

Keyword: Sexual Behavior
Link ID: 29099 - Posted: 01.16.2024

By David Levin It can start small: a peculiar numbness; a subtle facial tic; an inexplicably stiff muscle. But then time goes by — and eventually, the tremors set in. Roughly a million people in the United States (and roughly 10 million people worldwide) live with Parkinson’s disease, a potent neurological disorder that progressively kills neurons in the brain. As it does so, it can trigger a host of crippling symptoms, from violent tremors to excruciating muscle cramps, terrifying nightmares and constant brain fog. While medical treatments can alleviate some of these effects, researchers still don’t know exactly what causes the disease to occur in the first place. A growing number of studies, however, are suggesting that it may be tied to an unlikely culprit: bacteria living inside our guts. Every one of us has hundreds or thousands of microbial species in our stomach, small intestine and colon. These bacteria, collectively called our gut microbiome, are usually considerate guests: Although they survive largely on food that passes through our insides, they also give back, cranking out essential nutrients like niacin (which helps our body convert food into energy) and breaking down otherwise indigestible plant fiber into substances our bodies can use. As Parkinson’s advances in the brain, researchers have reported that the species of bacteria present in the gut also shift dramatically, hinting at a possible cause for the disease. A 2022 paper published in the journal Nature Communications recorded those differences in detail. After sequencing the mixed-together genomes of fecal bacteria from 724 people — a group with Parkinson’s and another without — the authors saw a number of distinct changes in the guts of people who suffered from the disease. The Parkinson’s group had dramatically lower amounts of certain species of Prevotella, a type of bacterium that helps the body break down plant-based fiber (changes like this in gut flora could explain why people with Parkinson’s disease often experience constipation). At the same time, the study found, two harmful species of Enterobacteriaceae, a family of microbes that includes Salmonella, E. coli and other bugs, proliferated. Those bacteria may be involved in a chain of biochemical events that eventually kill brain cells in Parkinson’s patients, says Tim Sampson, a biologist at Emory University School of Medicine and coauthor of the study.

Keyword: Parkinsons
Link ID: 29098 - Posted: 01.13.2024

By Christina Jewett and Noah Weiland Marijuana is neither as risky nor as prone to abuse as other tightly controlled substances and has potential medical benefits, and therefore should be removed from the nation’s most restrictive category of drugs, federal scientists have concluded. The recommendations are contained in a 250-page scientific review provided to Matthew Zorn, a Texas lawyer who sued Health and Human Services officials for its release and published it online on Friday night. An H.H.S. official confirmed the authenticity of the document. The records shed light for the first time on the thinking of federal health officials who are pondering a momentous change. The agencies involved have not publicly commented on their debates over what amounts to a reconsideration of marijuana at the federal level. Since 1970, marijuana has been considered a so-called Schedule I drug, a category that also includes heroin. Schedule I drugs have no medical use and a high potential for abuse, and they carry severe criminal penalties under federal trafficking laws. The documents show that scientists at the Food and Drug Administration and the National Institute on Drug Abuse have recommended that the Drug Enforcement Administration make marijuana a Schedule III drug, alongside the likes of ketamine and testosterone, which are available by prescription. The review by federal scientists found that even though marijuana is the most frequently abused illicit drug, “it does not produce serious outcomes compared to drugs in Schedules I or II.” Marijuana abuse does lead to physical dependence, the analysis noted, and some people develop a psychological dependence. “But the likelihood of serious outcomes is low,” the review concluded. The review also said there is some “scientific support” for therapeutic uses of marijuana, including treatment of anorexia, pain, and nausea and vomiting related to chemotherapy. © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29097 - Posted: 01.13.2024

By Elissa Welle Many of the physicians who worked on the current diagnostic and treatment guidelines for psychiatric conditions in the United States have financial ties to pharmaceutical companies, according to a study published today in The BMJ. Nearly 60 percent of the 92 U.S.-based physicians who shepherded the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, text revision (DSM-5-TR) accepted industry payments totaling $14.2 million during the three years prior to working on the manual, the study shows. The results raise questions about systemic “economies of influence” over a document used by public health officials, health insurance plans and drug regulators, says lead investigator Lisa Cosgrove, professor of counseling and school psychology and a faculty fellow at the Applied Ethics Center at the University of Massachusetts, Boston. “Financial conflicts of interest, industry ties don’t point to wrongdoing — we’re not saying that people did anything wrong consciously,” Cosgrove says. “It’s just implicit bias.” DSM-5-TR decision-makers were not allowed to receive more than $5,000 from industry, according to a statement to The Transmitter by a spokesperson for the American Psychiatric Association (APA), which published the DSM-5-TR in March 2022. And an independent committee reviewed financial and non-financial disclosures for all other contributors to the revision. The text revision centered on literature searches to incorporate new scientific findings since the publication of the DSM-5 in 2013, the spokesperson wrote. “Any rare, minor instances of content that connected a diagnosis to a therapy were omitted from DSM-5-TR,” the spokesperson wrote. “No content was found in the submitted text that related to a specific treatment for which industry funding may have been provided for related research.” © 2023 Simons Foundation.

Keyword: Depression; Schizophrenia
Link ID: 29096 - Posted: 01.13.2024

Diana Fleischman Because of the flaming culture wars, feminists and others who disagree about the nature of sex or sex differences often ascribe significant harms to researchers who claim that sex is binary or who acknowledge biological sex differences. These perceived harms include oppression, inequality, and even murder and suicide. As a result, many influential voices in the sex difference debate rarely engage in dialogue. This context made “The Big Conversation”—an October conference that brought together a diverse group of feminists, evolutionary psychologists, biologists, and neuroscientists—such a remarkable event. The rarity of such a meeting was highlighted by the cancellation of a panel on sex differences at an annual anthropological conference just a few days before. People who had sniped at each other for years through academic papers and social media not only shared stages and panels, they broke bread together. Attendees on all sides of the issue held my baby, whom I brought along. The fear of meeting ideological opponents often leads to the expectation of hostility in person, but what’s worse is that you often will come to like them! The Big Conversation took years to come together. It was organized by sex difference expert Marco Del Giudice and Paul Golding of the Santa Fe Boys Foundation. This foundation is dedicated to exploring how to help boys and young men and was the event’s sponsor. The conference featured 16 talks and 5 discussion sections. The entire conference is available for viewing (for free!) on the Santa Fe Boys Foundation website. A central questions in sex difference research concerns the origins of differences between men and women. Are these differences primarily the result of socialization, culture, and stereotype effects, or are these differences largely innate or biological? We can call these perspectives, as Carole Hooven did during her talk, the strong socialization view and the strong biology view, respectively. Many of the conference attendees, like Gina Rippon, Cordelia Fine and Daphna Joel, endorse the strong socialization view of sex differences, arguing that men and women are innately psychologically similar but are driven into different roles by cultural forces and socialization. This perspective sparks controversy surrounding discussions on biological sex differences because its proponents argue that legitimizing and publicizing sex differences creates them where they did not exist before. © 2024 Colin Wright

Keyword: Sexual Behavior; Evolution
Link ID: 29095 - Posted: 01.13.2024

By Conor Feehly A decade ago, when I was starting my first year of university in New Zealand, I attended a stage hypnosis. It was one of a number of events the university offered to incoming students during orientation week. From the stage of a campus auditorium, the hypnotist-for-hire asked an audience of some 200 students to close their eyes and listen to his voice. Then he directed us to clasp our hands tightly together, and to imagine an invisible thread wrapping around them—over and under, over and under—until it was impossible to pull them apart. After a few minutes of this, he told us to try to separate our hands. Those who could not, he said, should come on down to the stage. I instantly pulled my hands apart, but to my surprise, a close friend sitting next to me made his way to the front of the auditorium with roughly 20 others from the audience. Once on stage, the hypnotist tried to bring them deeper into a hypnotic trance, directing them to focus on his calm, authoritative voice. He then asked a few of them to role-play scenarios for our entertainment: a supermarket checkout clerk ringing up shopping items, a lifeguard scanning for lives to save. After a short time, I saw the hypnotist whisper something into the ear of my friend. He sheepishly made his way back to the seat next to me. “What did he say to you?” I asked. He replied, “I can tell you’re acting, mate, get off the stage.” In the more than 200 years since the practice of contemporary hypnosis was described by German physician Franz Mesmer, public perception of it has see-sawed between skepticism and credulity. Today hypnotherapy is used to provide therapeutic remedy for depression, pain, substance use disorders, and certain traumas, uses that are supported to a certain extent by research evidence. But many still consider hypnosis more of a cheap magician’s trick than legitimate clinical medicine. © 2024 NautilusNext Inc.,

Keyword: Attention
Link ID: 29094 - Posted: 01.13.2024

By Carl Zimmer Multiple sclerosis, an autoimmune disease that affects 2.9 million people, presents a biological puzzle. Many researchers suspect that the disease is triggered by a virus, known as Epstein-Barr, which causes the immune system to attack the nerves and can leave patients struggling to walk or talk. But the virus can’t be the whole story, since nearly everyone is infected with it at some point in life. A new study found a possible solution to this paradox in the skeletal remains of a lost tribe of nomads who herded cattle across the steppes of western Asia 5,000 years ago. It turns out that the nomads carried genetic mutations that most likely protected them from pathogens carried by their animals, but that also made their immune systems more sensitive. These genes, the study suggests, made the nomads’ descendants prone to a runaway immune response. The finding is part of a larger, unprecedented effort to understand how the evolutionary past has shaped the health of living people. Researchers are analyzing thousands of genomes of people who lived between Portugal and Siberia and between Norway and Iran roughly 3,000 to 11,000 years ago. They hope to trace the genetic roots of not only multiple sclerosis, but also diabetes, schizophrenia and many other modern illnesses. “We are taking ancient human genomics to a whole new level,” said Eske Willerslev, a geneticist at the University of Copenhagen who led the effort. The researchers published the multiple sclerosis study as well as three other papers on the genetics and health of ancient peoples on Wednesday in the journal Nature. For more than a decade, Dr. Willerslev and other researchers have been pulling DNA from ancient human bones. By comparing the surviving genetic material with that of living people, the scientists have been able to track some of the most significant migrations of people across the world. © 2024 The New York Times Company

Keyword: Multiple Sclerosis; Evolution
Link ID: 29093 - Posted: 01.11.2024

By Viviane Callier Aging can seem like an unregulated process: As time marches along, our cells and bodies inevitably accumulate dings and dents that cause dysfunctions, failures and ultimately death. However, in 1993 a discovery upended that interpretation of events. Researchers found a mutation in a single gene that doubled a worm’s life span; subsequent work showed that related genes, all involved in the response to insulin, are key regulators of aging in a host of animals, from worms and flies to humans. The discovery suggested that aging is not a random process — indeed, specific genes regulate it — and opened the door to further research into how aging proceeds at a molecular level. Recently, a set of papers documented a new biochemical pathway that regulates aging, one based on signals passed between mitochondria, the organelles best known as the powerhouse of the cell. Working with worms, the researchers found that damage to mitochondria in brain cells triggered a repair response that was then amplified, setting off similar reactions in mitochondria throughout the worm’s body. The effect of this repair activity was to extend the organism’s life span: The worms with repaired mitochondrial damage lived 50% longer. What’s more, cells in the germline — the cells that produce eggs and sperm — were central to this anti-aging communication system. It’s a finding that adds new dimensions to the fertility concerns implied when people talk about aging and their “biological clock.” Some of the findings were reported in Science Advances and others were posted on the scientific preprint server biorxiv.org in the fall. All Rights Reserved © 2024

Keyword: Development of the Brain
Link ID: 29092 - Posted: 01.11.2024

By Tim Vernimmen It is increasingly well understood that the countless microbes in our guts help us to digest our food, to absorb and produce essential nutrients, and to prevent harmful organisms from settling in. Less intuitive — perhaps even outlandish — is the idea that those microbes may also affect our mood, our mental health and how we perform on cognitive tests. But there is mounting evidence that they do. For nearly two decades, neuroscientist John Cryan of University College Cork in Ireland has been uncovering ways in which intestinal microbes affect the brain and behavior of humans and other animals. To his surprise, many of the effects he’s seen in rodents appear to be mirrored in our own species. Most remarkably, research by Cryan and others has shown that transplanting microbes from the guts of people with psychiatric disorders like depression to the guts of rodents can cause comparable symptoms in the animals. These effects may occur in several ways — through the vagus nerve connecting the gut to the brain, through the influence of gut bacteria on our immune systems, or by microbes synthesizing molecules that our nerve cells use to communicate. Cryan and coauthors summarize the science in a set of articles including “Man and the Microbiome: A New Theory of Everything?,” published in the Annual Review of Clinical Psychology. Cryan told Knowable Magazine that even though it will take much more research to pin down the mechanisms and figure out how to apply the insights, there are some things we can do already. This conversation has been edited for length and clarity.

Keyword: Depression; Stress
Link ID: 29091 - Posted: 01.11.2024

By Sara Reardon At birth, a human baby’s brain contains the most neurons it will ever have. How this complex brain develops in the womb has been hard to study in humans. But a new and potentially controversial method, growing tiny, brainlike structures called organoids in a dish from human fetal brain tissue, could provide a realistic model and improve the study of developmental disorders or brain cancers. The team that achieved this first, reported yesterday in Cell, has also shown it can genetically engineer the blobs of tissue, which could help the fetal brain organoids (FeBOs) mimic certain diseases. The researchers have “demonstrated some interesting and creative uses,” for the new organoids, says Arnold Kriegstein, a neurologist at the University of California (UC), San Francisco. He thinks FeBOs might help researchers tackle previously unexplored questions about how neurons take on specific identities in the maturing brain, for example. Researchers have already created organoids that mimic multiple parts of the brain and nervous system using stem cells that have the capacity to turn into many or all known cell types with the right stimulation and environment. To study genetic conditions that affect brain development, scientists can also “reprogram” mature cells from affected patients into stem cells to make organoids. Some stem cell–derived brain organoids, which are usually about the size of a grain of rice, have even produced electrical activity reminiscent of that in the brain of a fetus. But although these organoids can be useful representations of the brain, the starting stem cells must be “pushed” into a brainlike state through an introduced cocktail of signaling molecules—a complex process that may not fully replicate normal development, says stem cell biologist Benedetta Artegiani of the Princess Máxima Center for Pediatric Oncology. Using natural fetal brain tissue might reveal more about what the human brain really looks like at this stage of development. (Previous studies have made organoids from human fetal intestine, liver, and lung tissue, but not brain.) © 2024 American Association for the Advancement of Science.

Keyword: Development of the Brain
Link ID: 29090 - Posted: 01.11.2024