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

By Carl Zimmer Why do we grow old and die? In the 19th century, the German biologist August Weismann argued that the machinery of life inevitably wore out with time. Death had evolved “for the need of the species,” he declared. It cleared away weak, old individuals so they wouldn’t compete with young ones. That explanation never made sense to George Williams, an American evolutionary biologist. Natural selection acts only on the genes that are passed down from one generation to the next. What happens at the end of an animal’s life can have no effect on the course of evolution. It occurred to Williams that growing old might instead be an inescapable side effect of natural selection. In 1957, he proposed a new theory: Genetic mutations that increased an animal’s fertility could also cause harm late in life. Over many generations, those mutations would create a burden that would lead eventually to death. A new study, published on Friday in the journal Science Advances, bolsters Williams’s theory using a trove of human DNA. Researchers found hundreds of mutations that could boost a young person’s fertility and that were linked to bodily damage later in life. Smaller studies in the past had already offered some support for Williams’s theory. In 2007, for example, a team of researchers studying a tiny worm found a pair of mutations that lengthened the creature’s life while cutting down its average number of offspring. But Jianzhi Zhang, an evolutionary biologist at the University of Michigan, was not satisfied with these experiments. “These are case studies,” he said. “We don’t know if in the entire genome there are lots of such mutations.” Dr. Zhang tapped into the UK Biobank, a database containing genetic material from half a million volunteers in Britain, along with information on their health and life experiences. The biobank has permitted scientists to uncover subtle links between genetic variations and thousands of traits such as high blood pressure, schizophrenia and a habit of smoking. Working with Dr. Erping Long, a medical researcher now at the Chinese Academy of Sciences, Dr. Zhang pored over the database for information about reproduction and longevity. The scientists found that the genetic variations linked to fertility, such as the number of children a volunteer had, were also linked to a shorter life span. © 2023 The New York Times Company

Keyword: Development of the Brain; Evolution
Link ID: 29048 - Posted: 12.16.2023

By Tosin Thompson Last month saw the first-ever approval of a gene therapy that uses the CRISPR–Cas9 gene-editing tool, a treatment for the blood conditions sickle-cell disease and β-thalassaemia that works by precisely cutting out a faulty gene in people’s stem cells. Now, researchers in search of new treatments for Alzheimer’s disease are hoping to deploy similar strategies against forms of the disease that are caused by genetic mutations. Although there are now some treatments that slow the progression of Alzheimer’s, these often don’t benefit people who are in the later stages or who have mutations that raise the risk of the disease. “CRISPR therapies could potentially be a one-and-done cure, which no other drug can match,” says Subhojit Roy, a neuroscientist at the University of California, San Diego. But he adds that there is a long way to go before these therapies could be deployed against such a complex condition. “Cutting and pasting a gene is much harder to do in the brain using current technology.” Alzheimer’s is the most common form of dementia, a health issue of global concern. More than 55 million people are affected by dementia, and this figure is projected to nearly triple by 2050. “We do not fully understand how the brain works, which makes the challenge of understanding and treating brain diseases like Alzheimer’s very difficult,” says Tara Spires-Jones, who studies neurodegeneration at the University of Edinburgh, UK. Much of Alzheimer’s research is driven by the amyloid hypothesis, the idea that the build-up of amyloid-β proteins in the brain, which eventually form clumps called plaques, is the main cause of the disease. Amyloid plaques trigger another brain protein, called tau, to clump together and spread inside neurons. It is usually well into this process that symptoms such as memory loss start to appear. Usually, the more tau is present, the more severe the symptoms are. © 2023 Springer Nature Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 29046 - Posted: 12.13.2023

By Sabrina Malhi Cannabis use is associated with a greater risk of an unhealthy pregnancy outcomes, especially low birth weight, according to a study funded by the National Institutes of Health. While the study did not identity why cannabis use might have these effects, it underscores the potentially damaging impact of the substance on fetal health, the authors say. Many pregnant people use cannabis to help manage symptoms, including nausea and pain. The prevalence of the drug has surged in the past decade as more states have legalized its use for medicine or recreation, and many people believe it is relatively safe. But the impact cannabis has on pregnancy has been understudied. For the new study, researchers analyzed urine samples from more than 9,000 pregnant people between 2010 and 2013 to determine whether cannabis was used at any point during pregnancy, at how many weeks of gestation it was used and the amount. The team measured THC, the psychoactive substance in cannabis, at three different periods roughly tracking with trimesters and used that data to calculate total cannabis exposure throughout the entire pregnancy. Their findings were published in JAMA on Tuesday. The authors determined that pregnant people who used cannabis experienced unfavorable birth outcomes at rates of 25.9 percent, compared with 17.4 percent among those who did not use cannabis. Low birth weight and cannabis use had the strongest association out of all the adverse outcomes, the study found. Low birth weight is defined as weighing less than 5 lbs., 8 ounces at birth. This can lead to a range of health complications and long-term risks, including an increased likelihood of chronic conditions later in life. Experts say the study adds to a growing body of evidence that no amount of cannabis is safe during pregnancy.

Keyword: Drug Abuse; Development of the Brain
Link ID: 29040 - Posted: 12.13.2023

By Esther Landhuis Dropping an ice crystal into a bottle of near-frozen water produces a dramatic effect: very quickly, the liquid crystallizes into a block of ice. At the molecular level, an ice crystal has a distinct shape—a lattice structure. As incoming water molecules reshape to join the lattice, the crystal grows. Some researchers think an analogous process underlies Alzheimer’s disease, Parkinson’s disease and other neurodegenerative illnesses. According to this theory, these diseases begin when a particular protein misfolds, or fails to assume the proper shape for its intended role. That misshapen molecule ensnares normal versions of the protein, causing them to similarly misfold, and over time, these rogue proteins clump into toxic clusters that spread through the brain. In mad cow disease—a brain disorder in cattle that can spread to people who eat meat from ill animals —the toxic proteins, called prions, ravage the mind quickly, leading to dementia and death within months. Prion diseases are rare. About 350 cases of the most common type, Creutzfeldt-Jakob disease, are reported each year in the U.S. By comparison, each year, nearly 500,000 people in the U.S. are diagnosed with Alzheimer’s, which develops more gradually. Plaques made up of abnormal beta-amyloid proteins can accumulate in the brain for years or even decades before a person notices signs of mental decline. While the time lines for toxicity differ, “the mechanism of misfolding is the same,” says Mathias Jucker, a neuroscientist at the Hertie Institute for Clinical Brain Research at the University of Tübingen in Germany. Just as all of the water in a bottle freezes after a “‘misfolded’ water molecule” slips into the vessel, if “you have one misfolded protein, all the other ones will take the same shape.” The idea that many diseases could arise from a common prionlike process raises an intriguing and troubling question: Under certain circumstances, could neurodegenerative disorders be transmitted from person to person? © 2023 SCIENTIFIC AMERICAN,

Keyword: Alzheimers; Prions
Link ID: 29032 - Posted: 12.06.2023

Claudia López Lloreda The idea that the nervous system passes messages from one nerve cell to another only through synapses — the points where the cells link up end to end — is changing. Two studies show how messages can pass between cells over longer distances, through a ‘wireless’ nerve network in the worm Caenorhabditis elegans. Researchers had not appreciated the extent of this wireless communication, which happens when a molecule called a neuropeptide is released by one neuron and intercepted by another some distance away. The new studies, published in Nature1 and in Neuron2, map out the entire network of neuropeptide communication in a model organism for the first time. “We knew that these chemical connections existed, but this is probably the most comprehensive study in an entire nervous system,” says Gáspár Jékely, a neuroscientist at Heidelberg University in Germany who was not involved in the work. And what the research shows, he adds, is that “it’s not all about the synapses”. Researchers had previously worked out anatomical wiring maps — connectomes — showing how all the neurons in the fruit fly (Drosophila melanogaster) and in C. elegans are linked by their synapses. However, William Schafer, a neuroscientist at the MRC Laboratory of Molecular Biology in Cambridge, UK, wondered about the role of neuropeptides, which had been considered merely helpers in nervous-system messaging. “When I first started talking about this,” he says, “some people wondered, ‘is it all just kind of a soup’” where neuropeptides randomly float from one neuron to the next, “or can you really think about it like a network?” He and his colleagues analysed which neurons in the C. elegans nervous system expressed genes for certain neuropeptides and which ones expressed genes for the receptors of those neuropeptides. Using this data, the team predicted which pairs of nerve cells might be communicating wirelessly. On the basis of these results, the researchers generated a potential map of wireless connections in the worm, finding dense connectivity that looks very different from the anatomical wiring diagram of C. elegans. They published their findings in Neuron2 last week. © 2023 Springer Nature Limited

Keyword: Hormones & Behavior
Link ID: 29017 - Posted: 11.22.2023

Lilly Tozer By analysing more than one million people’s genomes, researchers have identified stretches of DNA that could be linked to cannabis addiction. They also found that some of the same regions in the genome are associated with other health conditions, such as lung cancer and schizophrenia. The findings are evidence that cannabis addiction “could have substantial public-health risks if the usage increases”, says Daniel Levey, a medical neuroscientist at Yale University in New Haven, Connecticut, and a co-author of the study, published today in Nature Genetics1. Taking cannabis recreationally is legal in at least 8 countries, and 48 countries have legalized medicinal use of the drug for conditions including chronic pain, cancer and epilepsy. But one-third of people who take cannabis end up becoming addicted, or using the drug in a way that is damaging to their health. Previous studies have suggested that there is a genetic component, and have shown links between problematic cannabis use and some cancers and psychiatric disorders. Weighing the dangers of cannabis Drug taking and addiction can be influenced both by people’s genes and by their environment, which makes them extremely difficult to study, says Levey. But the team was able to build on data from previous work2 by including genetic information from additional sources, predominantly the Million Veteran Program — a US-based biobank with a large genetic database that aims to improve health care for former military service members. The analysis encompassed multiple ethnic groups, a first for a genetic study looking at cannabis misuse. As well as identifying regions of the genome that might be involved, the researchers saw a bi-directional link between excessive cannabis use and schizophrenia, meaning that the two conditions can influence each other. This finding is intriguing, says Marta Di Forti, a psychiatrist-scientist at King’s College London. Cannabis use “is the most preventable risk factor” for schizophrenia, she says, adding that the type of genetic data examined in the study could be used in future to identify and support people at increased risk of developing psychiatric disorders through cannabis use. © 2023 Springer Nature Limited

Keyword: Drug Abuse; Genes & Behavior
Link ID: 29015 - Posted: 11.22.2023

By Laura Sanders WASHINGTON — Brain scans could be used to predict how teenagers’ mental health will fare during a stressful time, an analysis that spanned the COVID-19 pandemic suggests. The findings, presented November 13 in a news briefing at the annual meeting of the Society for Neuroscience, may help explain why some people succumb to stress while others are more resilient. For a lot of research, “the study happens, and you report on the results, and that’s about it,” says Margot Wagner, a bioengineer at the University of California, San Diego who was not involved in the new work. But this research followed hundreds of teenagers over time, a study design that “means you can intervene and help way sooner than otherwise,” Wagner says. The pandemic was particularly tough for many teenagers, as isolation, worry and upheaval of daily routines affected them in ways that scientists are just now starting to see (SN: 1/3/23). A record number of young people are struggling with depression and anxiety, a mental health crisis that some scientists are calling “the second pandemic” (SN: 6/30/23). While many teenagers struggled during the pandemic, others did OK. Computational neuroscientist Caterina Stamoulis of Harvard Medical School and Boston Children’s Hospital investigated why responses differed using data collected as part of the Adolescent Brain Cognitive Development, or ABCD, study. That larger study — involving scientists at 21 research sites across the United States — aims to figure out how teenagers’ brains grow over the years. “This is the first time in history we’re looking at thousands of participants and getting these measures over time,” Wagner says. “It’s truly remarkable.” The ABCD study, begun in 2015, was well under way when COVID hit, so researchers possessed brain scans from before the pandemic. “Without the pandemic, we would not have been able to understand the impact of a long-lasting adverse event” that deeply affected the participants’ lives, changing their interactions with their family and friends, Stamoulis says. © Society for Science & the Public 2000–2023.

Keyword: Development of the Brain; Stress
Link ID: 29012 - Posted: 11.18.2023

Max Kozlov Researchers have sifted through genomes from thousands of individuals in an effort to identify genes linked to Alzheimer’s disease. But these scientists have faced a serious obstacle: it’s hard to know for certain which of those people have Alzheimer’s. There’s no foolproof blood test for the disease, and dementia, a key symptom of Alzheimer’s, is also caused by other disorders. Early-stage Alzheimer’s might cause no symptoms at all. Now, researchers have developed artificial intelligence (AI)-based approaches that could help. One algorithm efficiently sorts through large numbers of brain images and picks out those that include characteristics of Alzheimer’s. A second machine-learning method identifies important structural features of the brain — an effort that could eventually help scientists to spot new signs of Alzheimer’s in brain scans. The goal is to use people’s brain images as visual ‘biomarkers’ of Alzheimer’s. Applying the method to large databases that also include medical information and genetic data, such as the UK Biobank, could allow scientists to pinpoint genes that contribute to the disease. In turn, this work could aid the creation of treatments and of models that predict who’s at risk of developing the disease. Combining genomics, brain imaging and AI is allowing researchers to “find brain measures that are tightly linked to a genomic driver”, says Paul Thompson, a neuroscientist at the University of Southern California in Los Angeles, who is spearheading efforts to develop these algorithms. Thompson and others described the new AI techniques on 4 November at the annual conference of the American Society of Human Genetics in Washington DC. Overwhelmed with data © 2023 Springer Nature Limited

Keyword: Alzheimers; Robotics
Link ID: 29004 - Posted: 11.13.2023

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

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 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

By Carl Zimmer An international team of scientists has mapped the human brain in much finer resolution than ever before. The brain atlas, a $375 million effort started in 2017, has identified more than 3,300 types of brain cells, an order of magnitude more than was previously reported. The researchers have only a dim notion of what the newly discovered cells do. The results were described in 21 papers published on Thursday in Science and several other journals. Ed Lein, a neuroscientist at the Allen Institute for Brain Science in Seattle who led five of the studies, said that the findings were made possible by new technologies that allowed the researchers to probe millions of human brain cells collected from biopsied tissue or cadavers. “It really shows what can be done now,” Dr. Lein said. “It opens up a whole new era of human neuroscience.” Still, Dr. Lein said that the atlas was just a first draft. He and his colleagues have only sampled a tiny fraction of the 170 billion cells estimated to make up the human brain, and future surveys will certainly uncover more cell types, he said. Biologists first noticed in the 1800s that the brain was made up of different kinds of cells. In the 1830s, the Czech scientist Jan Purkinje discovered that some brain cells had remarkably dense explosions of branches. Purkinje cells, as they are now known, are essential for fine-tuning our muscle movements. Later generations developed techniques to make other cell types visible under a microscope. In the retina, for instance, researchers found cylindrical “cone cells” that capture light. By the early 2000s, researchers had found more than 60 types of neurons in the retina alone. They were left to wonder just how many kinds of cells were lurking in the deeper recesses of the brain, which are far harder to study. © 2023 The New York Times Company

Keyword: Brain imaging; Development of the Brain
Link ID: 28963 - Posted: 10.14.2023