Chapter 7. Life-Span Development of the Brain and Behavior

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By Tina Hesman Saey One particular retrovirus — embedded in the DNA of jawed vertebrates — helps turn on production of a protein needed to insulate nerve fibers, researchers report February 15 in Cell. Such insulation, called myelin, may have helped make speedy thoughts and complex brains possible. The retrovirus trick was so handy, in fact, that it showed up many times in the evolution of vertebrates with jaws, the team found. Retroviruses — also known as jumping genes or retrotransposons — are RNA viruses that make DNA copies of themselves to embed in a host’s DNA. Scientists once thought of remnants of ancient viruses as genetic garbage, but that impression is changing, says neuroscientist Jason Shepherd, who was not involved in the study. “We’re finding more and more that these retrotransposons and retroviruses have influenced the evolution of life on the planet,” says Shepherd, of the University of Utah Spencer Fox Eccles School of Medicine in Salt Lake City. Remains of retroviruses were already known to have aided the evolution of the placenta, the immune system and other important milestones in human evolution (SN: 5/16/17). Now, they’re implicated in helping to produce myelin. Myelin is a coating of fat and protein that encases long nerve fibers known as axons. The coating works a bit like the insulation around an electrical wire: Nerves sheathed in myelin can send electrical signals faster than uninsulated nerves can. © Society for Science & the Public 2000–2024.

Keyword: Glia; Evolution
Link ID: 29154 - Posted: 02.20.2024

By Matt Richtel Growing numbers of children and adolescents are being prescribed multiple psychiatric drugs to take simultaneously, according to a new study by researchers at the University of Maryland. The phenomenon is increasing despite warnings that psychotropic drug combinations in young people have not been tested for safety or studied for their impact on the developing brain. The study, published Friday in JAMA Open Network, looked at the prescribing patterns among patients 17 or younger enrolled in Medicaid from 2015 to 2020 in a single U.S. state that the researchers declined to name. In this group, there was a 9.5 percent increase in the prevalence of “polypharmacy,” which the study defined as taking three or more different classes of psychiatric medications, including antidepressants, mood-stabilizing anticonvulsants, sedatives and drugs for A.D.H.D. and anxiety drugs. The study looked at only one state, but state data have been used in the past to explore this issue, in part because of the relative ease of gathering data from Medicaid, the health insurance program administered by states. At the same time, some research using nationally weighted samples have revealed the increasing prevalence of polypharmacy among young people. One recent paper drew data from the National Ambulatory Medical Care Survey and found that in 2015, 40.7 percent of people aged 2 to 24 in the United States who took a medication for A.D.H.D. also took a second psychiatric drug. That figure had risen from 26 percent in 2006. The latest data from the University of Maryland researchers show that, at least in one state, the practice continues to grow and “was significantly more likely among youths who were disabled or in foster care,” the new study noted. Mental health experts said that psychotropic medications can prove very helpful and that doctors have discretion to prescribe what they see fit. A concern among some experts is that many drugs used in frequently prescribed cocktails have not been approved for use in young people. And it is unclear how the simultaneous use of multiple psychotropic medications affects brain development long-term. © 2024 The New York Times Company

Keyword: Depression; Development of the Brain
Link ID: 29152 - Posted: 02.20.2024

By Miryam Naddaf An analysis of around 1,500 blood proteins has identified biomarkers that can be used to predict the risk of developing dementia up to 15 years before diagnosis. The findings, reported today in Nature Aging1, are a step towards a tool that scientists have been in search of for decades: blood tests that can detect Alzheimer’s disease and other forms of dementia at a very early, pre-symptomatic stage. Researchers screened blood samples from more than 50,000 healthy adults in the UK Biobank, 1,417 of whom developed dementia in a 14-year period. They found that high blood levels of four proteins — GFAP, NEFL, GDF15 and LTBP2 — were strongly associated with dementia. “Studies such as this are required if we are to intervene with disease-modifying therapies at the very earliest stage of dementia,” said Amanda Heslegrave, a neuroscientist at University College London, in a statement to the Science Media Centre in London. According to the World Health Organization, more than 55 million people worldwide currently live with dementia. People are often diagnosed only when they notice memory problems or other symptoms. At that point, the disease might have been progressing for years. “Once we diagnose it, it’s almost too late,” says study co-author Jian-Feng Feng, a computational biologist at Fudan University in Shanghai, China. “And it’s impossible to reverse it.” By screening 1,463 proteins in blood samples from 52,645 people, the authors found that increased levels of GFAP, NEFL, GDF15 and LTBP2 were associated with dementia and Alzheimer’s disease. For some participants who developed dementia, blood levels of these proteins were outside normal ranges more than ten years before symptom onset. © 2024 Springer Nature Limited

Keyword: Alzheimers
Link ID: 29146 - Posted: 02.13.2024

By Claudia López Lloreda By squirting cells from a 3D printer, researchers have created tissue that looks—and acts—like a chunk of brain. In recent years, scientists have learned how to load up 3D printers with cells and other scaffolding ingredients to create living tissues, but making realistic brainlike constructs has been a challenge. Now, one team has shown that, by modifying its printing techniques, it can print and combine multiple subtypes of cells that better mimic signaling in the human brain. “It’s remarkable that [the researchers] can replicate” how brain cells work, says Riccardo Levato, a regenerative medicine researcher at Utrecht University who was not involved with the study. “It’s the first demonstration that, with some simple organization [of cells], you can start getting some interesting functional [responses].” The new technology, described last week in Cell Stem Cell, could offer advantages over existing techniques that neuroscientists use to create 3D brain tissues in the lab. One common approach involves using stem cells to grow miniature brainlike blobs called organoids. But researchers can’t control the types of cells or their precise location in these constructs. Each organoid “is unique,” making it difficult to reproduce research results, says neuroscientist Su-Chun Zhang of the University of Wisconsin–Madison, an author of the new study. With the right kind of 3D printing, however, “you can control where different cell types are placed,” says developmental biologist Francis Szele of the University of Oxford. Past studies have used 3D printers to construct brain tissues that allowed researchers to study how the cells matured and made connections, and even integrate printed tissue into mouse brains. But those constructs had limited functionality. And efforts that produced more functional printed tissue used rat cells, not human cells. © 2024 American Association for the Advancement of Science.

Keyword: Development of the Brain; Robotics
Link ID: 29145 - Posted: 02.10.2024

Ian Sample Science editor After a decades-long and largely fruitless hunt for drugs to combat Alzheimer’s disease, an unlikely candidate has raised its head: the erectile dysfunction pill Viagra. Researchers found that men who were prescribed Viagra and similar medications were 18% less likely to develop the most common form of dementia years later than those who went without the drugs. The effect was strongest in men with the most prescriptions, with scientists finding a 44% lower risk of Alzheimer’s in those who received 21 to 50 prescriptions of the erectile dysfunction pills over the course of their study. While the findings are striking, the observational study cannot determine whether Viagra and similar pills protect against Alzheimer’s or whether men who are already less prone to the condition are simply more likely to use the tablets. “We can’t say that the drugs are responsible, but this does give us food for thought on how we move into the future,” said the lead author Dr Ruth Brauer at University College London. “We now need a proper clinical trial to look at the effects of these drugs on Alzheimer’s in women as well as men.” Brauer and her colleagues analysed medical records for more than 260,000 men who were diagnosed with erectile dysfunction but had no evidence of memory or thinking problems. Just over half were taking PDE5 inhibitor drugs, including sildenafil (sold as Viagra), avanafil, vardenafil and tadalafil. The men were followed for an average of five years to record any new cases of Alzheimer’s. © 2024 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29138 - Posted: 02.08.2024

By Laura Sanders Under extremely rare circumstances, it appears that Alzheimer’s disease can be transmitted between people. Five people who received contaminated injections of a growth hormone as children went on to develop Alzheimer’s unusually early, researchers report January 29 in Nature Medicine. The findings represent “the first time iatrogenic Alzheimer’s disease has been described,” neurologist John Collinge said January 25 in a news briefing, referring to a disease caused by a medical procedure. That sounds alarming, but researchers are quick to emphasize that Alzheimer’s disease is not contagious in everyday life, including caretaking and most medical settings. Support Science Today. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. Donate Now “We are not suggesting for a moment that you can catch Alzheimer’s disease,” said Collinge, of the University College London’s Institute of Prion Diseases. “This is not transmissible in the sense of a viral or bacterial infection.” The reassurance is echoed by Carlo Condello, a neurobiologist at the University of California, San Francisco who wasn’t involved in the study. “In no way do we believe sporadic Alzheimer’s disease is a communicable disease,” he says. “Only under incredibly artificial, now out-of-date, medical practices is this appearing. It’s no longer an issue.” © Society for Science & the Public 2000–202

Keyword: Alzheimers
Link ID: 29126 - Posted: 01.31.2024

By Laurie McGinley ABINGTON, Pa. — Wrapped in a purple blanket, Robert Williford settles into a quiet corner of a bustling neurology clinic, an IV line delivering a colorless liquid into his left arm. The 67-year-old, who has early Alzheimer’s disease, is getting his initial dose of Leqembi. The drug is the first to clearly slow the fatal neurodegenerative ailment that afflicts 6.7 million older Americans, though the benefits may be modest. The retired social worker, one of the first African Americans to receive the treatment, hopes it will ease his forgetfulness so “I drive my wife less crazy.” But as Williford and his doctors embark on this treatment, they are doing so with scant scientific data about how the medication might work in people of color. In the pivotal clinical trial for the drug, Black patients globally accounted for only 47 of the 1,795 participants — about 2.6 percent. For U.S. trial sites, the percentage was 4.5 percent. The proportion of Black enrollees was similarly low for Eli Lilly Alzheimer’s drug, called donanemab, expected to be cleared by the Food and Drug Administration in coming months. Black people make up more than 13 percent of the U.S. population. The paltry data for the new class of groundbreaking drugs, which strip a sticky substance called amyloid beta from the brain, has ignited an intense debate among researchers and clinicians. Will the medications — the first glimmer of hope after years of failure — be as beneficial for African Americans as for White patients? “Are these drugs going to work in non-Whites? And particularly in Blacks? We just don’t have enough data, I don’t think,” said Suzanne E. Schindler, a clinical neurologist and dementia specialist at Washington University in St. Louis.

Keyword: Alzheimers
Link ID: 29122 - Posted: 01.31.2024

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 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

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 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 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

Jon Hamilton A new generation of blood tests is poised to change the way doctors determine whether patients with memory loss also have Alzheimer's disease. The tests detect substances in the blood that indicate the presence of sticky amyloid plaques in the brain — a hallmark of Alzheimer's. So these tests have the potential to replace current diagnostic procedures, like costly PET scans and uncomfortable spinal taps. Blood tests also promise to provide doctors with a quick way to identify patients who could benefit from new drugs that remove amyloid from the brain. But the accuracy of the tests still varies widely. "Some of them are really good, and some of them are really bad," says Dr. Suzanne Schindler, a dementia specialist at Washington University School of Medicine in St. Louis. Blood tests represent the latest advance in efforts to detect the buildup of amyloid plaques and fibrous tangles in the brain. "It used to be that the only way you could definitively diagnose someone with Alzheimer disease is by doing an autopsy," Schindler says. Then, starting in the early 2000s, scientists found ways to detect plaques and tangles using PET scans and tests of spinal fluid. There are now versions of both approaches that are approved by the Food and Drug Administration. But the scans are costly, and spinal taps are unpopular with many doctors and patients. Both also require expertise that is in short supply. So Schindler and her colleagues got a lot of attention in 2019 when they published a paper showing that amyloid plaques could be revealed by a blood test. © 2024 npr

Keyword: Alzheimers
Link ID: 29088 - Posted: 01.11.2024

By Mark Johnson In the first study of its kind in humans, researchers have discovered that it is safe to use sound waves fired into specific areas of the brain to open a protective barrier and clear the way for Alzheimer’s medications. The study, reported in the New England Journal of Medicine, involved just three patients, but it raises hope about the long-term potential of the treatment strategy known as focused ultrasound. “We want to be very cautious. This is the first three people in the world that have had this [treatment]. What we’ve learned from this, I think, can help us,” said Ali Rezai, lead author of the study and executive chair and director of the Rockefeller Neuroscience Institute at West Virginia University. Rezai stressed that the goal of the research is not to replace pharmaceutical treatments but to improve their benefits by helping more of the drug penetrate the brain. Nature has provided humans with a barrier made of tightly packed cells that blocks harmful toxins, such as viruses, bacteria and fungi, from reaching the brain. Known as the blood-brain barrier, this shield has for decades presented a major challenge to scientists trying to treat neurodegenerative diseases such as Alzheimer’s and Parkinson’s, which afflict at least 7 million Americans. The barrier is a locked door that stops about 98 percent of treatments from reaching the brain. With focused ultrasound, Rezai explained, “what we want to do is push individuals toward the milder stages of Alzheimer’s with less plaques to give them a fighting chance.” Two men and a woman suffering from mild loss of memory, learning, concentration and decision-making skills due to Alzheimer’s took part in the study. The patients, who ranged in age from 59 to 77, were given six monthly doses of the federally approved — if somewhat controversial — lab-made antibody aducanumab, sold under the brand name Aduhelm. The antibody, which is administered directly into a patient’s vein, reduces a sticky substance in the brain called amyloid beta, which clumps between neurons and disrupts their function.

Keyword: Alzheimers; Brain imaging
Link ID: 29085 - Posted: 01.09.2024

By Aimee Cunningham Ask thousands of teens whether frequent use of certain substances brings a high risk of harm, and they mostly nail it: a majority say yes for cigarettes, alcohol, cocaine and heroin. But there’s one substance that many skip over — cannabis. Only 35 percent of 12- to 17-year-olds perceive a “great risk of harm” from smoking marijuana once or twice a week, according to the National Survey on Drug Use and Health. It’s a sentiment that some of their parents may share. Parents often don’t understand that the products used today “are not what they knew when they were in high school,” says Kelly Young-Wolff, a licensed clinical psychologist and research scientist at Kaiser Permanente Northern California Division of Research in Oakland. If their children are using cannabis, parents may think, “‘it’s not that bad, at least they’re not using this other drug that’s worse.’” But the cannabis products available now are leaps and bounds more potent — which may increase the risks for addiction and psychosis — than in the past. Marijuana plants have been bred to contain more delta-9-tetrahydrocannabinol, or THC, the main psychoactive chemical. In 1995, the total percent of THC by weight of marijuana plant material was around 4 percent; now marijuana with a THC potency of 20 percent or more is available. Trouncing that are concentrated cannabis products, including wax, budder and shatter, which can have a THC potency as high as 95 percent. Cannabis is legal for adults to use recreationally in 24 states and Washington, D.C., and is allowed for medical use in 38 states and D.C. The widespread availability of cannabis “promotes the idea that it’s safe,” says pediatrician Beth Ebel of the University of Washington School of Medicine and Seattle Children’s Hospital. But that “is an incorrect assumption.” THC can impact brain chemistry “in a way that wasn’t intended,” Ebel says. “Some of the worst effects can have lifelong health consequences, especially for a young person.” © Society for Science & the Public 2000–2024.

Keyword: Drug Abuse; Development of the Brain
Link ID: 29083 - Posted: 01.06.2024

By Elizabeth Svoboda Esther Oladejo knew she'd crossed an invisible boundary when she started forgetting to eat for entire days at a time. A gifted rugby player, Oladejo had once thrived on her jam-packed school schedule. But after she entered her teenage years, her teachers started piling on assignments and quizzes to prepare students for high-stakes testing that would help them to qualify for university. As she devoted hours on hours to cram sessions, Oladejo's resolve began to fray. Every time she got a low grade, her mood tanked—and with it, her resolve to study hard for the next test. “Teachers [were] saying, ‘Oh, you can do much better than this,’” says Oladejo, now 18, who lives in Merseyside, England. “But you're thinking, ‘Can I? I tried my best on that. Can I do any more than what I've done before?’” One morning, as Oladejo steeled herself for another endless day, her homeroom teacher passed out a questionnaire to the students, explaining that it would help assess their moods and well-being. Oladejo filled it out, her mind ticking forward to her upcoming classes. Soon after that, someone called to tell her she'd been slotted into a new school course called the Blues Program. Developed by Oregon Research Institute psychologist Paul Rohde and his colleagues at Stanford University, the program—a six-week series of hour-long group sessions—teaches students skills for managing their emotions and stress. The goal is to head off depression in vulnerable teens. Although Oladejo didn't know it at the time, her course was one in an expanding series of depression prevention programs for young people, including Vanderbilt University's Teens Achieving Mastery Over Stress (TEAMS); the University of Pennsylvania's Penn Resiliency Program; Happy Lessons, developed by Dutch social scientists; and Spain's Smile Program. The growing global interest in depression prevention is helping to establish the efficacy of a range of programs in diverse settings. © 2023 SCIENTIFIC AMERICAN,

Keyword: Depression; Development of the Brain
Link ID: 29066 - Posted: 12.27.2023

By Cathleen O’Grady Why do some children learn to talk earlier than others? Linguists have pointed to everything from socioeconomic status to gender to the number of languages their parents speak. But a new study finds a simpler explanation. An analysis of nearly 40,000 hours of audio recordings from children around the world suggests kids speak more when the adults around them are more talkative, which may also give them a larger vocabulary early in life. Factors such as social class appear to make no difference, researchers report this month in the Proceedings of the National Academy of Sciences. The paper is a “wonderful, impactful, and much needed contribution to the literature,” says Ece Demir-Lira, a developmental scientist at the University of Iowa who was not involved in the work. By looking at real-life language samples from six different continents, she says, the study provides a global view of language development sorely lacking from the literature. Most studies on language learning have focused on children in Western, industrialized nations. To build a more representative data set, Harvard University developmental psychologist Elika Bergelson and her collaborators scoured the literature for studies that had used LENA devices: small audio recorders that babies can wear—tucked into a pocket on a specially made vest—for days at a time. These devices function as a kind of “talk pedometer,” with an algorithm that estimates how much its wearer speaks, as well as how much language they hear in their environment—from parents, other adults, and even siblings. The team asked 18 research groups across 12 countries whether they would share their data from the devices, leaving them with a whopping 2865 days of recordings from 1001 children. Many of the kids, who ranged from 2 months to 4 years old, were from English-speaking families, but the data also included speakers of Dutch, Spanish, Vietnamese, and Finnish, as well as Yélî Dnye (Papua New Guinea), Wolof (Senegal), and Tsimané (Bolivia). Combining these smaller data sets gave the researchers a more powerful, diverse sample.

Keyword: Language; Development of the Brain
Link ID: 29061 - Posted: 12.22.2023

Robin McKie, Science Editor People in Britain could benefit from a key medical breakthrough next year. They may be given access to the first drugs ever developed to slow the impact of Alzheimer’s disease. The first of these medicines – lecanemab – was recently approved in the US and Japan, where treatments using it have already been launched. A second drug, donanemab, is expected to follow soon, and next year it is anticipated that the UK medical authorities will consider both of them for approval in Britain. The prospect has raised hopes that, after years of effort, scientists may be closing in on ways to directly tackle the UK’s dementia crisis. About a million people are living with the condition in this country, and this is expected to rise to about 1.7 million by 2040 – with potentially grim consequences. Last year dementia took the lives of 66,000 people in England and Wales, and it is now the leading cause of death in Britain, with Alzheimer’s accounting for two-thirds of cases. Until now doctors have only been able to prescribe medicines that help patients manage their symptoms, so the arrival of the first drugs that treat the actual cause of the condition has been welcomed – although experts have warned that their use should be treated with some caution. “The new drugs slow down the development of Alzheimer’s by six months to a year and are useful only for those in the early stages of the condition, so they are certainly not miracle medicines,” said David Thomas, head of policy at Alzheimer’s Research UK. “However, after decades of research, they are the first to improve patients’ lives directly, and that is a justifiable cause for excitement. If nothing else, they suggest we are probably on the right road to tackling Alzheimer’s.” © 2023 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29056 - Posted: 12.19.2023

By Yasemin Saplakoglu In the 16th century, the Belgian cartographer Abraham Ortelius created the world’s first modern atlas — a collection of maps that he called “The Theater of the World.” The maps, drawn by Ortelius and others, detailed what was at the time the best knowledge of the world’s continents, cities, mountains, rivers, lakes and oceans and helped usher in a new understanding of global geography. Similarly, the creation of cell atlases — maps of organs and bodies constructed cell by cell — is heralding a new era in our understanding of biology. Powerful sequencing and imaging technologies invented in the last decade are revealing with unprecedented detail the composition of human organs and tissues, from the pancreas and liver to the placenta, as well as those of other animals like the mouse and fruit fly. With these new tools, researchers can fingerprint individual cells based on which genes they are expressing. That information has revealed subtle and unsuspected distinctions among cells and has begun to illuminate how the diversity of cell types can be essential to the healthy functioning of organs. “We’re at this amazing point in time in science where we’re now able to understand the composition of these cell types,” said Steve Quake, a bioengineer and biophysicist at Stanford University who helped develop the technologies that make cell atlases possible. “It’s changed the way we understand how human biology works.” Two cell atlas efforts, part of the National Institutes of Health’s $250 million brain cell census, that just released their findings illustrate the excitement bubbling up in the field. Today in Nature, a coalition of laboratories published nine studies that collectively form a detailed atlas of the mouse brain — the most comprehensive mammalian brain atlas to date. It describes more than 5,300 types of cells found throughout the organ. How these cells are distributed and are related to one another suggests many intriguing ideas about the evolution of the mammalian brain. All Rights Reserved © 2023

Keyword: Development of the Brain; Brain imaging
Link ID: 29053 - Posted: 12.16.2023