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

By Laura Sanders A new look at the human brain is beginning to reveal the inner lives of its cellular residents. The human brain holds a dizzying collection of diverse cells, and no two brains are the same, cellularly speaking. Those are the prevailing conclusions of an onslaught of 21 papers published online October 12 in Science, Science Advances and Science Translational Medicine. The results just start to scratch the surface of understanding the mysteries of the brain. Still, they provide the most intimate look yet at the cells that build the brain, and offer clues about how the brain enables thoughts, actions and memories. The collection of data may also guide researchers in their hunt for the causes of brain disorders such as schizophrenia, Alzheimer’s disease and depression. The new brain map is a result of a coordinated international research effort called the National Institutes of Health’s Brain Initiative Cell Census Network, or BICCN, which ramped up in 2017. Many of the studies in the collection are based on a powerful technology called single-cell genomics. The method reveals which genes are active inside of a single cell, information that provides clues about the cell’s identity and job. As part of the BICCN, researchers examined all sorts of brains. One project detailed the cells in small pieces of live brain tissue taken from 75 people undergoing surgery for tumors or epilepsy, an approach that’s been used on smaller scales before (SN: 8/7/19). Another looked at samples taken from the brains of 17 deceased children. Still another looked at brain tissue from seven people, seven chimpanzees, four gorillas, three rhesus macaques and three marmosets. © Society for Science & the Public 2000–2023.

Keyword: Development of the Brain; Brain imaging
Link ID: 28962 - Posted: 10.14.2023

By Mark Johnson Using a host of high-tech tools to simulate brain development in a lab dish, Stanford University researchers have discovered several dozen genes that interfere with crucial steps in the process and may lead to autism, a spectrum of disorders that affects about one in every 36 Americans, impairing their ability to communicate and interact with others. The results of a decade of work, the findings published in the journal Nature may one day pave the way for scientists to design treatments that allow these phases of brain development to proceed unimpaired. The study delves into a 20-year-old theory that suggests one cause of autism may be a disruption of the delicate balance between two types of nerve cells found in the brain’s cerebral cortex, the area responsible for higher-level processes such as thought, emotion, decision-making and language. Some nerve cells in this region of the brain excite other nerve cells, encouraging them to fire; other cells, called interneurons, do the opposite. Too much excitation can impair focus in the brain and cause epilepsy, a seizure disorder that is more common in people with autism than in the general population. Scientists therefore believe a proper balance requires more of the inhibiting interneurons. In the developing fetus, these nerve cells start out deep in the brain in a region called the subpallium, then migrate slowly to the cerebral cortex. The process begins mid-gestation and ends in the infant’s second year of life, said Sergiu Pasca, a Stanford University professor of psychiatry and behavioral sciences who led the study. Pasca’s team, which included researchers from the University of California at San Francisco and the Icahn School of Medicine at Mount Sinai, tested 425 genes that have been linked to neurodevelopmental disorders to determine which ones interfere with the generation and migration of interneurons. Genes linked to autism were among those identified in the study. “What’s really cool about this paper is that autism is a collection of different behaviors, but we don’t have [an] understanding of how those behaviors are connected to differences in the brain,” said James McPartland, a professor of child psychiatry and psychology at the Yale School of Medicine, who was not involved in the study. The new work advances research into autism by “beginning to create a fundamental understanding of the building blocks of brain development,” he said.

Keyword: Autism; Genes & Behavior
Link ID: 28947 - Posted: 10.07.2023

Jon Hamilton A team of researchers has developed a new way to study how genes may cause autism and other neurodevelopmental disorders: by growing tiny brain-like structures in the lab and tweaking their DNA. These "assembloids," described in the journal Nature, could one day help researchers develop targeted treatments for autism spectrum disorder, intellectual disability, schizophrenia, and epilepsy. "This really accelerates our effort to try to understand the biology of psychiatric disorders," says Dr. Sergiu Pașca, a professor of psychiatry and behavioral sciences at Stanford University and an author of the study. The research suggests that someday "we'll be able to predict which pathways we can target to intervene" and prevent these disorders, adds Kristen Brennand, a professor of psychiatry at Yale who was not involved in the work. The study comes after decades of work identifying hundreds of genes that are associated with autism and other neurodevelopmental disorders. But scientists still don't know how problems with these genes alter the brain. "The challenge now is to figure out what they're actually doing, how disruptions in these genes are actually causing disease," Pașca says. "And that has been really difficult." For ethical reasons, scientists can't just edit a person's genes to see what happens. They can experiment on animal brains, but lab animals like rodents don't really develop anything that looks like autism or schizophrenia. So Pașca and a team of scientists tried a different approach, which they detailed in their new paper. The team did a series of experiments using tiny clumps of human brain cells called brain organoids. These clumps will grow for a year or more in the lab, gradually organizing their cells much the way a developing brain would. And by exposing an organoid to certain growth factors, scientists can coax it into resembling tissue found in brain areas including the cortex and hippocampus. © 2023 npr

Keyword: Epilepsy; Autism
Link ID: 28940 - Posted: 10.03.2023

Sara Reardon Scientists have identified two types of brain cell linked to a reduced risk of dementia in older people — even those who have brain abnormalities that are hallmarks of Alzheimer’s disease1. The finding could eventually lead to new ways to protect these cells before they die. The results were published in Cell on 28 September. The most widely held theory about Alzheimer’s attributes the disease to a build-up of sticky amyloid proteins in the brain. This leads to clump-like ‘plaques’ of amyloid that slowly kill neurons and eventually destroy memory and cognitive ability. But not everyone who develops cognitive impairment late in life has amyloid clumps in their brain, and not everyone with amyloid accumulation develops Alzheimer’s. Neurobiologist Hansruedi Mathys at the University of Pittsburgh School of Medicine in Pennsylvania and neuroscientist Li-Huei Tsai and computer scientist Manolis Kellis at the Massachusetts Institute of Technology in Cambridge and their colleagues decided to investigate this disconnect. To do so, they used data from a massive study that tracks cognitive and motor skills in thousands of people throughout old age. The researchers examined tissue samples from 427 brains from participants who had died. Some of those participants had dementia typical of advanced Alzheimer’s disease, some had mild cognitive impairment and the remainder had no sign of impairment. The researchers isolated cells from each participant’s prefrontal cortex, the region involved in higher brain function. To classify the cells, they sequenced all the active genes in each one. This allowed them to create an atlas of the brain showing where the different cell types occur. The scientists identified two key cell types that had a specific genetic marker. One had active genes coding for reelin, a protein associated with brain disorders such as schizophrenia, and the other had active genes that code for somatostatin, a hormone that regulates processes throughout the body. © 2023 Springer Nature Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 28938 - Posted: 09.29.2023

COMIC: When, why and how did neurons first evolve? Scientists are piecing together the ancient story. By Tim Vernimmen Illustrated by Maki Naro 09.14.2023 © 2023 Annual Reviews

Keyword: Evolution; Development of the Brain
Link ID: 28920 - Posted: 09.21.2023

By Janet Lee Doing puzzles, playing memory-boosting games, taking classes and reading are activities that we often turn to for help keeping our brains sharp. But research is showing that what you eat, how often you exercise and the type of exercise you do can help lower your risk of dementia to a greater extent than previously thought. Live well every day with tips and guidance on food, fitness and mental health, delivered to your inbox every Thursday. Although more studies are needed, “there’s a lot of data that suggests exercise and diet are good for the brain and can prevent or help slow down” cognitive changes, says Jeffrey Burns, co-director of the University of Kansas Alzheimer’s Disease Research Center in Fairway. And living a healthy lifestyle can produce brain benefits no matter what your age. The big diet picture If you’re already eating in a way that protects your heart — plenty of whole grains, vegetables, and fruit, and little saturated fat, sodium and ultra-processed “junk” foods — there’s good news: You’re also protecting your brain. A healthy cardiovascular system keeps blood vessels open, allowing good blood flow to the brain and reducing the risk of high blood pressure, stroke and dementia. Research suggests that two specific dietary approaches — the Mediterranean diet and the MIND diet (the Mediterranean-DASH Intervention for Neurodegenerative Delay, essentially a combo of two heart-healthy eating plans) — may help stave off cognitive decline. Both diets rely on eating mostly plant foods (fruits, vegetables, whole grains, beans, nuts), olive oil, fish and poultry. The main difference between the two is that the MIND diet emphasizes specific fruits and vegetables, such as berries and leafy greens. Studies show that people who most closely follow either diet have a reduced risk of dementia compared with those who don’t. For example, people eating the Mediterranean way had a 23 percent lower risk of dementia in a nine-year study of more than 60,000 men and women published this year in BMC Medicine.

Keyword: Alzheimers
Link ID: 28915 - Posted: 09.21.2023

By Jacqueline Howard and Deidre McPhillips, Most families of children with autism may face long wait times to diagnose their child with the disorder, and once a diagnosis is made, it sometimes may not be definitive. But now, two studies released Tuesday suggest that a recently developed eye-tracking tool could help clinicians diagnose children as young as 16 months with autism – and with more certainty. Kids’ developmental disability diagnoses became more common during pandemic, but autism rates held steady, CDC report says “This is not a tool to replace expert clinicians,” said Warren Jones, director of research at the Marcus Autism Center at Children’s Healthcare of Atlanta and Nien Distinguished Chair in Autism at Emory University School of Medicine, who was an author on both studies. Rather, he said, the hope with this eye-tracking technology is that “by providing objective measurements that objectively measure the same thing in each child,” it can help inform the diagnostic process. The tool, called EarliPoint Evaluation, is cleared by the US Food and Drug Administration to help clinicians diagnose and assess autism, according to the researchers. Traditionally, children are diagnosed with autism based on a clinician’s assessment of their developmental history, behaviors and parents’ reports. Evaluations can take hours, and some subtle behaviors associated with autism may be missed, especially among younger children. “Typically, the way we diagnose autism is by rating our impressions,” said Whitney Guthrie, a clinical psychologist and scientist at the Children’s Hospital of Philadelphia’s Center for Autism Research. She was not involved in the new studies, but her research focuses on early diagnosis of autism.

Keyword: Autism; Schizophrenia
Link ID: 28904 - Posted: 09.13.2023

By Claudia López Lloreda Cells hidden in the skull may point to a way to detect, diagnose and treat inflamed brains. A detailed look at the skull reveals that bone marrow cells there change and are recruited to the brain after injury, possibly traveling through tiny channels connecting the skull and the outer protective layer of the brain. Paired with the discovery that inflammation in the skull is disease-specific, these new findings collectively suggest the skull’s marrow could serve as a target to track and potentially treat neurological disorders involving brain inflammation, researchers report August 9 in Cell. Immune cells that infiltrate the central nervous system during many diseases and neuronal injury can wreak havoc by flooding the brain with damaging molecules. This influx of immune cells causes inflammation in the brain and spinal cord and can contribute to diseases like multiple sclerosis (SN: 11/26/19). Detecting and dampening this reaction has been an extensive field of research. With this new work, the skull, “something that has been considered as just protective, suddenly becomes a very active site of interaction with the brain, not only responding to brain diseases, but also changing itself in response to brain diseases,” says Gerd Meyer zu Hörste, a neurologist at University of Münster in Germany who was not involved in the study. Ali Ertürk of the Helmholtz Center in Munich and colleagues discovered this potential role for the skull while probing the idea that the cells in skull marrow might behave differently from those in other bones. Ertürk’s team compared the genetic activity of cells in mice skull marrow, and the proteins those cells made, with those in the rodent’s humerus, femur and four other bones, along with the meninges, the protective membranes between the skull and the brain. © Society for Science & the Public 2000–2023.

Keyword: Alzheimers; Multiple Sclerosis
Link ID: 28898 - Posted: 09.07.2023

Diana Kwon Santiago Ramón y Cajal revolutionized neurobiology in the late nineteenth century with his exquisitely detailed illustrations of neural tissues. Created through years of meticulous microscopy work, the Spanish physician-scientist’s drawings revealed the unique cellular morphology of the brain. “With Cajal’s work, we saw that the cells of the brain don’t look like the cells of every other part of the body — they have incredible morphologies that you just don’t see elsewhere,” says Evan Macosko, a neuroscientist at the Broad Institute of MIT and Harvard in Cambridge, Massachusetts. Ramón y Cajal’s drawings provided one of the first clues that the keys to understanding how the brain governs its many functions, from regulating blood pressure and sleep to controlling cognition and mood, might lie at the cellular level. Still, when it comes it comes to the brain, crucial information remained — and indeed, remains — missing. “In order to have a fundamental understanding of the brain, we really need to know how many different types of cells there are, how are they organized, and how they interact with each other,” says Xiaowei Zhuang, a biophysicist at Harvard University in Cambridge. What neuroscientists require, Zhuang explains, is a way to systematically identify and map the many categories of brain cells. Now researchers are closing in on such a resource, at least in mice. By combining high-throughput single-cell RNA sequencing with spatial transcriptomics — methods for determining which genes are expressed in individual cells, and where those cells are located — they are creating some of the most comprehensive atlases of the mouse brain so far. The crucial next steps will be working out what these molecularly defined cell types do, and bringing the various brain maps together to create a unified resource that the broader neuroscience community can use. © 2023 Springer Nature Limited

Keyword: Brain imaging; Development of the Brain
Link ID: 28880 - Posted: 08.24.2023

By Lauren Leffer When a nematode wriggles around a petri dish, what’s going on inside a tiny roundworm’s even tinier brain? Neuroscientists now have a more detailed answer to that question than ever before. As with any experimental animal, from a mouse to a monkey, the answers may hold clues about the contents of more complex creatures’ noggin, including what resides in the neural circuitry of our own head. A new brain “atlas” and computer model, published in Cell on Monday, lays out the connections between the actions of the nematode species Caenorhabditis elegans and this model organism’s individual brain cells. With the findings, researchers can now observe a C. elegans worm feeding or moving in a particular way and infer activity patterns for many of the animal’s behaviors in its specific neurons. Through establishing those brain-behavior links in a humble roundworm, neuroscientists are one step closer to understanding how all sorts of animal brains, even potentially human ones, encode action. “I think this is really nice work,” says Andrew Leifer, a neuroscientist and physicist who studies nematode brains at Princeton University and was not involved in the new research. “One of the most exciting reasons to study how a worm brain works is because it holds the promise of being able to understand how any brain generates behavior,” he says. “What we find in the worm forms hypotheses to look for in other organisms.” Biologists have been drawn to the elegant simplicity of nematode biology for many decades. South African biologist Sydney Brenner received a Nobel Prize in Physiology or Medicine in 2002 for pioneering work that enabled C. elegans to become an experimental animal for the study of cell maturation and organ development. C. elegans was the first multicellular organism to have its entire genome and nervous system mapped. The first neural map, or “connectome,” of a C. elegans brain was published in 1986. In that research, scientists hand drew connections using colored pencils and charted each of the 302 neurons and approximately 5,000 synapses inside the one-millimeter-long animal’s transparent body. Since then a subdiscipline of neuroscience has emerged—one dedicated to plotting out the brains of increasingly complex organisms. Scientists have compiled many more nematode connectomes, as well as brain maps of a marine annelid worm, a tadpole, a maggot and an adult fruit fly. Yet these maps simply serve as a snapshot in time of a single animal. They can tell us a lot about brain structure but little about how behaviors relate to that structure. © 2023 Scientific American

Keyword: Brain imaging; Development of the Brain
Link ID: 28879 - Posted: 08.24.2023

by Calli McMurray One of the co-directors of a now-shuttered Maryland psychology clinic implicated in 18 paper retractions has retired, Spectrum has learned. Prior to her retirement, Clara Hill was professor of psychology at the University of Maryland in College Park. Headshot of Clara Hill. Recent retirement: Clara Hill retired from the University of Maryland in the midst of 18 paper retractions after a 49-year career. Starting on 1 June, the American Psychological Association (APA) retracted 11 papers by Hill and her university colleagues Dennis Kivlighan, Jr. and Charles Gelso over issues with obtaining participant consent. The publisher plans to retract six more papers by the end of the year, according to an APA representative. On 13 August, Taylor & Francis retracted an additional paper led solely by Hill. The research was conducted at the Maryland Psychotherapy Clinic and Research Lab, where Hill, Kivlighan and Gelso were co-directors. The clinic had shut down as of 1 June. When asked about the circumstances surrounding Hill’s retirement, a university spokesperson told Spectrum in an email, “Dr. Clara Hill retired from UMD effective July 1, 2023.” After Spectrum asked again about the circumstances, a spokesperson replied, “This is all we’ll have for you on the faculty member’s retirement — thanks!” Hill worked at the university for 49 years. As of 1 August, Hill’s faculty page did not mention her retirement. By 14 August, her position had been amended to “Professor (Retired),” and a notice of her retirement had been added to the beginning of her biography. Spectrum left two voicemails on Hill’s university office phone and emailed her university address with requests for comment but did not hear back. The 11 papers retracted by the APA appeared in the Journal of Counseling Psychology, Dreaming and Psychotherapy. The additional retractions will come from the same titles, according to an APA representative. Hill conducted all 11 studies, whereas Kivlighan and Gelso conducted 10 and 6, respectively. © 2023 Simons Foundation

Keyword: Autism
Link ID: 28877 - Posted: 08.24.2023

Saima May Sidik A protein involved in wound healing can improve learning and memory in ageing mice1. Platelet factor 4 (PF4) has long been known for its role in promoting blood clotting and sealing broken blood vessels. Now, researchers are wondering whether this signalling molecule could be used to treat age-related cognitive disorders such as Alzheimer’s disease. “The therapeutic possibilities are very exciting,” says geneticist and anti-ageing scientist David Sinclair at Harvard University in Boston, Massachusetts, who was not involved in the research. The study was published on 16 August in Nature. Young blood, old brains About a decade ago, scientists discovered that blood from young mice could restore youthful properties, including learning abilities, in older mice2,3. The idea captivated Saul Villeda, a neuroscientist at the University of California, San Francisco, and a co-author of the new study. He and his colleagues have since been trying to identify the components of blood that cause this rejuvenation. Several lines of evidence suggested that PF4 might be one of these components, including the fact that young mice have higher levels of this molecule in their blood than do older mice. Villeda and his colleagues tried injecting PF4 into aged mice without including other blood components. The researchers found that the ratios of various types of immune cell shifted to become more similar to what is typically seen in younger mice. Some immune cells also reverted to a more youthful pattern of gene expression. Although PF4 was not able to cross the blood–brain barrier, its effects on the immune system also led to changes in the brain, probably through indirect mechanisms. Old mice that received doses of PF4 showed decreases in damaging inflammation in the hippocampus — a part of the brain that’s particularly vulnerable to the effects of ageing. They also showed increases in the levels of molecules that promote synaptic plasticity (the capacity to alter the strength of connections between nerve cells). © 2023 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 28874 - Posted: 08.19.2023