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

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 5815

Nicola Davis Science correspondent If the taste of kale makes you screw up your face, you are not alone: researchers have observed foetuses pull a crying expression when exposed to the greens in the womb. While previous studies have suggested our food preferences may begin before birth and can be influenced by the mother’s diet, the team says the new research is the first to look directly at the response of unborn babies to different flavours. “[Previously researchers] just looked at what happens after birth in terms of what do [offspring] prefer, but actually seeing facial expressions of the foetus when they are getting hit by the bitter or by the non-bitter taste, that is something which is completely new,” said Prof Nadja Reissland, from Durham University, co-author of the research. Writing in the journal Psychological Science, the team noted that aromas from the mother’s diet were present in the amniotic fluid. Taste buds can detect taste-related chemicals from 14 weeks’ gestation, and odour molecules can be sensed from 24 weeks’ gestation. To delve into whether foetuses differentiate specific flavours, the team looked at ultrasound scans from almost 70 pregnant women, aged 18 to 40 from the north-east of England, who were split into two groups. One group was asked to take a capsule of powdered kale 20 minutes before an ultrasound scan, and the other was asked to take a capsule of powdered carrot. Vegetable consumption by the mothers did not differ between the kale and carrot group. The team also examined scans from 30 women, taken from an archive, who were not given any capsules. All the women were asked to refrain from eating anything else in the hour before their scans. The team then carried out a frame-by-frame analysis of the frequency of a host of different facial movements of the foetuses, including combinations that resembled laughing or crying. Overall, the researchers examined 180 scans from 99 foetuses, scanned at either 32 weeks, 36 weeks, or at both time points. © 2022 Guardian News & Media Limited

Keyword: Development of the Brain; Chemical Senses (Smell & Taste)
Link ID: 28493 - Posted: 09.28.2022

Terriline Porelle is puzzling over two mysteries. The first is: what’s plaguing her? For the past two years, the formerly healthy, active, 34-year-old resident of Cocagne, N.B. has been experiencing many strange and alarming symptoms, including muscle twitches and blurred vision, auditory hallucinations, brain fog and loss of balance and co-ordination. The second mystery is why health authorities no longer seem interested in finding out why she’s ill. “It’s like nobody’s really looking to see what’s going on and it doesn’t make any sense,” she said. Ms. Porelle is one of 48 people who were initially identified between late 2020 and May, 2021, as being part of a cluster of patients in New Brunswick who all had a mysterious brain illness, which the province referred to as a “potential neurological syndrome of unknown cause.” Doctors and researchers puzzled over the cases for months. Then, in a February report, the province announced that there was no mystery illness, and that its investigation into the matter had concluded. An independent oversight committee had found that the 48 patients were likely suffering from various previously known diseases that had simply been misdiagnosed, the report said. But some of the patients and their families say their suffering remains very real – and that it’s made worse by the fact that they’re no closer to getting answers about what’s causing it. The province’s report said neurologists on the oversight committee had provided potential alternative diagnoses for 41 of the 48 patients, including Alzheimer’s disease and other types of dementia, post-concussion syndrome, chronic severe anxiety disorder and cancer. It recommended that patients contact their primary caregivers for referrals to further treatment, or that they seek help from a specialized clinic in Moncton called the Moncton Interdisciplinary Neurodegenerative Diseases (MIND) Clinic.

Keyword: Alzheimers
Link ID: 28491 - Posted: 09.28.2022

by Angie Voyles Askham / Brain connectivity patterns in people with autism and other neuropsychiatric conditions are more closely related to genetics than to phenotypic traits, according to two new studies. The findings highlight why a single brain biomarker for autism has remained elusive, the researchers say. The condition’s genetic heterogeneity has hampered the search for a shared brain signature: More than 100 genes have been identified as strongly linked to autism, and multiple copy number variations (CNVs) — deleted or duplicated stretches of genetic code — can increase a person’s likelihood of the condition. Autism also often overlaps with other conditions, such as schizophrenia and attention-deficit/hyperactivity disorder (ADHD), making autism-specific markers difficult to disentangle. Common variants tied to autism overlap strongly with those linked to schizophrenia and high IQ, for example, whereas rare autism-linked variants track with low IQ. According to the new papers, however, autism’s genetic heterogeneity corresponds to similarly disparate maps of ‘functional connectivity’ — a measure of which brain areas activate in sync while the brain is at rest. “What we’re seeing is that these groups of variants have specific functional connectivity signatures,” says lead investigator Sébastien Jacquemont, associate professor of pediatrics at the University of Montreal in Canada. The findings need to be replicated, says Aaron Alexander-Bloch, assistant professor of psychiatry at the University of Pennsylvania and the Children’s Hospital of Philadelphia, who was not involved in the work, but they point to the importance of subgrouping study participants based on their underlying genetics. © 2022 Simons Foundation

Keyword: Autism; Brain imaging
Link ID: 28490 - Posted: 09.28.2022

by Charles Q. Choi Infection during pregnancy may be associated with having an autistic child simply because mothers of autistic children are prone to infections, a new study finds. The results suggest that “common infections during pregnancy do not seem increase their children’s risk of autism,” says study investigator Martin Brynge, a psychiatrist and doctoral student of global public health at the Karolinska Institutet in Stockholm, Sweden. “Prevention of maternal infections would likely not affect the prevalence of autism in the population.” A great deal of previous research has linked maternal infection during pregnancy with autism and intellectual disability in children. Whether the former causes the latter, however, has remained uncertain. For instance, both autism and intellectual disability are linked with gene variants that may influence the immune system, so mothers of children with either condition may also just be more vulnerable to serious infections. The new study analyzed data from 549,967 children, including 267,995 girls, living in Stockholm County who were born between 1987 and 2010; about 34,000 of the children had been exposed to a maternal infection requiring specialized health care, according to data from Sweden’s National Patient Register and National Medical Birth Register. Of the exposed children, 3.3 percent have autism, compared with 2.5 percent of unexposed children — a 16 percent increase in the chance of autism. But maternal infection in the year before pregnancy was also linked with a 25 percent greater chance of autism. “Mothers who had an infection during pregnancy may not be comparable to those mothers without infections,” Brynge says. “There may be systematic differences at the group level.” © 2022 Simons Foundation

Keyword: Autism; Neuroimmunology
Link ID: 28488 - Posted: 09.24.2022

By Mark Johnson A study using the electronic health records of more than 6 million Americans over age 65 found those who had covid-19 ran a greater risk of receiving a new diagnosis of Alzheimer’s disease within a year. The study, led by researchers at Case Western Reserve University School of Medicine and published in the Journal of Alzheimer’s Disease, does not show that covid-19 causes Alzheimer’s, but adds to a growing body of work suggesting links between the two. The results suggest researchers should be tracking older patients who recover from covid to see if they go on to show signs of memory loss, declining brain function or Alzheimer’s disease. The study found that for every 1,000 seniors with covid-19, seven will be diagnosed with Alzheimer’s within a year, slightly above the five-in-a-thousand diagnosis rate for seniors who did not have covid. “We know that covid can affect the brain, but I don’t think anyone had looked at new diagnoses of Alzheimer’s,” said Pamela Davis, one of the study’s co-authors and a research professor at Case Western Reserve University School of Medicine. Colleague Rong Xu said she had expected to see some increase among seniors sickened by covid, but was surprised “by the extent of the increase and how rapidly it occurred.” The study, though “important and useful” was “limited,” said Gabriel de Erausquin, director of the Laboratory of Brain Development, Modulation and Repair at University of Texas Health San Antonio, who was not involved in the research. He cautioned that a diagnosis of Alzheimer’s disease is not necessarily confirmation of the disease. Doctors sometimes diagnose Alzheimer’s based on changes in behavior, or responses to a memory test. These are considered less accurate than imaging or spinal fluid tests that measure two types of proteins, beta-amyloid and phosphorylated tau, which accumulate abnormally in the brains of people with Alzheimer’s. Brain scans that look for structural changes, such as the shrinking of certain regions, are another more accurate indicator. © 1996-2022 The Washington Post

Keyword: Alzheimers
Link ID: 28479 - Posted: 09.17.2022

by Nora Bradford A well-studied brain response to sound, called the M100, appears earlier in life in autistic children than in their non-autistic peers, according to a new longitudinal study. The finding suggests that the auditory cortex in children with autism matures unusually quickly, a growth pattern seen previously in other brain regions. “It’s a demonstration that when we look for autism markers in the brain, they can be very age-specific,” says lead investigator J. Christopher Edgar, associate professor of radiology at the Children’s Hospital of Philadelphia in Pennsylvania. For that reason, longitudinal studies such as this one — in which Edgar and his colleagues assessed children at up to three different ages — are essential, he adds. “If the two populations being studied have different rates of brain maturation, then the pattern of findings changes across time.” At the time of the first magnetoencephalography (MEG) scan, when the children were 6 to 9 years old, those with autism were more likely to have an M100 response to a barely audible tone in the right hemisphere than non-autistic children were. But this difference disappeared in the next two visits, presumably because the M100 response typically appears during early adolescence. By contrast, the M50 response, which occurs throughout life, beginning in utero, showed no significant difference between the two groups at any visit. The team also evaluated ‘phase locking,’ a measure of how similar a participant’s neural activity is from scan to scan within a certain frequency band. Autistic participants demonstrated more mature phase-locking patterns at the first visit, which then diminished at the later two visits. © 2022 Simons Foundation

Keyword: Autism; Hearing
Link ID: 28478 - Posted: 09.17.2022

Sara Reardon More than 500,000 years ago, the ancestors of Neanderthals and modern humans were migrating around the world when a pivotal genetic mutation caused some of their brains to improve suddenly. This mutation, researchers report in Science1, drastically increased the number of brain cells in the hominins that preceded modern humans, probably giving them a cognitive advantage over their Neanderthal cousins. “This is a surprisingly important gene,” says Arnold Kriegstein, a neurologist at the University of California, San Francisco. However, he expects that it will turn out to be one of many genetic tweaks that gave humans an evolutionary advantage over other hominins. “I think it sheds a whole new light on human evolution.” When researchers first reported the sequence of a complete Neanderthal genome in 20142, they identified 96 amino acids — the building blocks that make up proteins — that differ between Neanderthals and modern humans, as well as some other genetic tweaks. Scientists have been studying this list to learn which of these changes helped modern humans to outcompete Neanderthals and other hominins. Cognitive advantage To neuroscientists Anneline Pinson and Wieland Huttner at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany, one gene stood out. TKTL1 encodes a protein that is made when a fetus’s brain is first developing. A mutation in the human version changed one amino acid, resulting in a protein that is different from those found in hominin ancestors, Neanderthals and non-human primates. The researchers suspected that this protein could increase the proliferation of neural progenitor cells, which become neurons, as the brain develops, specifically in an area called the neocortex — a region involved in cognitive function. This, they reasoned, could contribute to modern humans’ cognitive advantage. © 2022 Springer Nature Limited

Keyword: Evolution; Genes & Behavior
Link ID: 28477 - Posted: 09.14.2022

Jon Hamilton In some families, Alzheimer's disease seems inevitable. "Your grandmother has it, your mom has it, your uncle has it, your aunts have it, your cousin has it. I always assumed that I would have it," says Karen Douthitt, 57. "It was always in our peripheral vision," says Karen's sister June Ward, 61. "Our own mother started having symptoms at age 62, so it has been a part of our life." Nearly a decade ago, Karen, June, and an older sister, Susie Gilliam, 64, set out to learn why Alzheimer's was affecting so many family members. Since then, each sister has found out whether she carries a rare gene mutation that makes Alzheimer's inescapable. And all three have found ways to help scientists trying to develop treatments for the disease. I met Karen and June in 2015, at the first-ever conference for families with a particular type of genetic mutation in which Alzheimer's often appears in middle age. The annual conference is sponsored by the Alzheimer's Association and the Dominantly Inherited Alzheimer's Network Trials Unit, a research program run by Washington University School of Medicine in St. Louis. Karen and June had come to Washington, D.C., for the family conference because of something they had just learned about a cousin on their mother's side. The cousin had developed Alzheimer's in her 50s. And genetic tests showed that she carried a rare, inherited gene mutation called presenilin 1. It's one of three mutations that typically cause Alzheimer's to appear in middle age. The three gene mutations responsible for early Alzheimer's are unlike a better known gene called APOE4, which merely increases the likelihood somewhat that a person will develop Alzheimer's – and usually at age 65 or older. In contrast, the early-onset mutations, including presenilin 1, make it almost certain an individual will develop the disease, and usually before age 60. Each child of a parent who has the presenilin 1 mutation has a 50% chance of inheriting it. © 2022 npr

Keyword: Alzheimers; Genes & Behavior
Link ID: 28474 - Posted: 09.14.2022

ByRodrigo Pérez Ortega We humans are proud of our big brains, which are responsible for our ability to plan ahead, communicate, and create. Inside our skulls, we pack, on average, 86 billion neurons—up to three times more than those of our primate cousins. For years, researchers have tried to figure out how we manage to develop so many brain cells. Now, they’ve come a step closer: A new study shows a single amino acid change in a metabolic gene helps our brains develop more neurons than other mammals—and more than our extinct cousins, the Neanderthals. The finding “is really a breakthrough,” says Brigitte Malgrange, a developmental neurobiologist at the University of Liège who was not involved in the study. “A single amino acid change is really, really important and gives rise to incredible consequences regarding the brain.” What makes our brain human has been the interest of neurobiologist Wieland Huttner at the Max Planck Institute of Molecular Cell Biology and Genetics for years. In 2016, his team found that a mutation in the ARHGAP11B gene, found in humans, Neanderthals, and Denisovans but not other primates, caused more production of cells that develop into neurons. Although our brains are roughly the same size as those of Neanderthals, our brain shapes differ and we created complex technologies they never developed. So, Huttner and his team set out to find genetic differences between Neanderthals and modern humans, especially in cells that give rise to neurons of the neocortex. This region behind the forehead is the largest and most recently evolved part of our brain, where major cognitive processes happen. The team focused on TKTL1, a gene that in modern humans has a single amino acid change—from lysine to arginine—from the version in Neanderthals and other mammals. By analyzing previously published data, researchers found that TKTL1 was mainly expressed in progenitor cells called basal radial glia, which give rise to most of the cortical neurons during development. © 2022 American Association for the Advancement of Science.

Keyword: Development of the Brain; Evolution
Link ID: 28472 - Posted: 09.10.2022

By Helen Santoro I barreled into the world — a precipitous birth, the doctors called it — at a New York City hospital in the dead of night. In my first few hours of life, after six bouts of halted breathing, the doctors rushed me to the neonatal intensive care unit. A medical intern stuck his pinky into my mouth to test the newborn reflex to suck. I didn’t suck hard enough. So they rolled my pink, 7-pound-11-ounce body into a brain scanner. Lo and behold, there was a huge hole on the left side, just above my ear. I was missing the left temporal lobe, a region of the brain involved in a wide variety of behaviors, from memory to the recognition of emotions, and considered especially crucial for language. My mother, exhausted from the labor, remembers waking up after sunrise to a neurologist, pediatrician and midwife standing at the foot of her bed. They explained that my brain had bled in her uterus, a condition called a perinatal stroke. They told her I would never speak and would need to be institutionalized. The neurologist brought her arms up to her chest and contorted her wrists to illustrate the physical disability I would be likely to develop. In those early days of my life, my parents wrung their hands wondering what my life, and theirs, would look like. Eager to find answers, they enrolled me in a research project at New York University tracking the developmental effects of perinatal strokes. But month after month, I surprised the experts, meeting all of the typical milestones of children my age. I enrolled in regular schools, excelled in sports and academics. The language skills the doctors were most worried about at my birth — speaking, reading and writing — turned out to be my professional passions. My case is highly unusual but not unique. Scientists estimate that thousands of people are, like me, living normal lives despite missing large chunks of our brains. Our myriad networks of neurons have managed to rewire themselves over time. But how? © 2022 The New York Times Company

Keyword: Development of the Brain; Language
Link ID: 28466 - Posted: 09.07.2022

Nicola Davis Regular doses of a hormone may help to boost cognitive skills in people with Down’s syndrome, a pilot study has suggested. Researchers fitted seven men who have Down’s syndrome with a pump that provided a dose of GnRH, a gonadotropin-releasing hormone, every two hours for six months. Six out of the seven men showed moderate cognitive improvements after the treatment, including in attention and being able to understand instructions, compared with a control group who were not given the hormone. However, experts raised concerns about the methods used in the study, urging caution over the findings. The team behind the work said brain scans of the participants, who were aged between 20 and 37, given the hormone suggest they underwent changes in neural connectivity in areas involved in cognition. “[People] with Down’s syndrome have cognitive decline which starts in the 30s,” said Prof Nelly Pitteloud, co-author of the study from the University of Lausanne. “I think if we can delay that, this would be great, if the therapy is well tolerated [and] without side effects.” Writing in the journal Science, Pitteloud and colleagues said they previously found mice with an extra copy of chromosome 16 experienced an age-related decline in cognition and sense of smell, similar to that seen in people with Down’s syndrome – who have an extra copy of chromosome 21. In a series of experiments, the team found regular doses of gonadotropin-releasing hormone boosted both the sense of smell and cognitive performance of these mice. Pitteloud said no side effects were seen in the participants and that the hormone is already used to induce puberty in patients with certain disorders. “I think these data are of course very exciting, but we have to remain cautious,” said Pitteloud. She said larger, randomised control studies are now needed to confirm that the improvements were not driven by patients becoming less stressed during assessments and thus performing better. Prof Michael Thomas of Birkbeck, University of London, who studies cognitive development across the lifespan in Down’s syndrome, said the results were exciting. “For parents, this is good news: interventions can still yield benefits across the lifespan,” he said, although he noted it is not clear how applicable the hormone therapy would be for children. © 2022 Guardian News & Media Limited

Keyword: Hormones & Behavior; Development of the Brain
Link ID: 28462 - Posted: 09.03.2022

By Diana Kwon During an embryo's development, a piece of the still-growing brain branches off to form the retina, a sliver of tissue in the back of the eye. This makes the retina, which is composed of several layers of neurons, a piece of the central nervous system. As evidence builds that changes in the brain can manifest in this region, scientists are turning to retinas as a potential screening target for early signs of Alzheimer's, an incurable neurodegenerative disease that affects an estimated six million people in the U.S. alone. Initially clinicians could diagnose Alzheimer's only through brain autopsies after patients died. Since the early 2000s, however, research advances have made it possible to pinpoint signs of the disease—and to begin to investigate treatment—years before symptoms first appear. Today positron emission tomography (PET) brain imaging and tests of cerebrospinal fluid (CSF), the clear liquid surrounding the brain and spinal cord, aid Alzheimer's diagnosis at its early stages. “There have been tremendous improvements in our ability to detect early disease,” says Peter J. Snyder, a neuropsychologist and neuroscientist at the University of Rhode Island. But these diagnostic methods are not always readily available, and they can be expensive and invasive. PET imaging requires injecting a radioactive tracer molecule into the bloodstream, and spinal fluid must be extracted with a needle inserted between vertebrae in the back. “We need ways of funneling the right high-risk individuals into the diagnostic process with low-cost screening tools that are noninvasive and simple to administer,” Snyder says. The retina is a particularly attractive target, he adds, because it is closely related to brain tissue and can be examined noninvasively through the pupil, including with methods routinely used to check for eye diseases. © 2022 Scientific American,

Keyword: Alzheimers; Vision
Link ID: 28442 - Posted: 08.24.2022

By Frances Stead Sellers A study published this week in the journal Lancet Psychiatry showed increased risks of some brain disorders two years after infection with the coronavirus, shedding new light on the long-term neurological and psychiatric aspects of the virus. The analysis, conducted by researchers at the University of Oxford and drawing on health records data from more than 1 million people around the world, found that while the risks of many common psychiatric disorders returned to normal within a couple of months, people remained at increased risk for dementia, epilepsy, psychosis and cognitive deficit (or brain fog) two years after contracting covid. Adults appeared to be at particular risk of lasting brain fog, a common complaint among coronavirus survivors. The study’s findings were a mix of good and bad news, said Paul Harrison, a professor of psychiatry at the University of Oxford and the senior author of the study. Among the reassuring aspects was the quick resolution of symptoms such as depression and anxiety. “I was surprised and relieved by how quickly the psychiatric sequelae subsided,” Harrison said. David Putrino, director of rehabilitation innovation at Mount Sinai Health System in New York, who has been studying the lasting impacts of the coronavirus since early in the pandemic, said the study revealed some very troubling outcomes. “It allows us to see without a doubt the emergence of significant neuropsychiatric sequelae in individuals that had covid and far more frequently than those who did not,” he said. Because it focused only on the neurological and psychiatric effects of the coronavirus, the study authors and others emphasized that it is not strictly long-covid research.

Keyword: Alzheimers; Learning & Memory
Link ID: 28438 - Posted: 08.20.2022

By Tim Vernimmen August 9, 2022 at 6:39 a.m. EDT Adolescence is often portrayed as a period of struggle and friction, filled to the brim with exhilarating ups and depressing downs. Young people’s behavior tends to be stereotyped as self-absorbed and impulsive. But how accurate is this picture, and what might explain it? Developmental neuroscientist Eveline Crone, based at Erasmus University Rotterdam, has studied adolescents, defined by researchers as people ages 10 to 24, for more than 20 years. She has gradually expanded her interest from the study of the many changes happening in adolescent brains to include her study subjects’ own views and experiences. This has helped to enrich her earlier findings on how young brains learn, produce emotions, process rewards and account for the perspectives of other people. It also provides new inspiration for adults trying to help them. To study adolescents, Crone visualizes their brain activity while they are engaged in various tasks and games on computer screens: ones designed to assess behaviors and attitudes toward things such as risk and reward, how they think about and are influenced by others, and more. She supplements these studies with other methods such as surveys and youth panels — and, these days, consults young people for their input from the moment the study is designed. In an article in the 2020 Annual Review of Psychology, Crone and colleague Andrew Fuligni of the University of California at Los Angeles, explored how adolescents feel and think about themselves and others, and stress that far from being either/or, both are inextricably intertwined. Recently, she discussed what she has learned about the adolescent brain. (This conversation has been edited for length and clarity.)

Keyword: Development of the Brain
Link ID: 28425 - Posted: 08.11.2022

By Siobhan Roberts In June, 100 fruit fly scientists gathered on the Greek island of Crete for their biennial meeting. Among them was Cassandra Extavour, a Canadian geneticist at Harvard University. Her lab works with fruit flies to study evolution and development — “evo devo.” Most often, such scientists choose as their “model organism” the species Drosophila melanogaster — a winged workhorse that has served as an insect collaborator on at least a few Nobel Prizes in physiology and medicine. But Dr. Extavour is also known for cultivating alternative species as model organisms. She is especially keen on the cricket, particularly Gryllus bimaculatus, the two-spotted field cricket, even though it does not yet enjoy anything near the fruit fly’s following. (Some 250 principal investigators had applied to attend the meeting in Crete.) “It’s crazy,” she said during a video interview from her hotel room, as she swatted away a beetle. “If we tried to have a meeting with all the heads of labs working on that cricket species, there might be five of us, or 10.” Crickets have already been enlisted in studies on circadian clocks, limb regeneration, learning, memory; they have served as disease models and pharmaceutical factories. Veritable polymaths, crickets! They are also increasingly popular as food, chocolate-covered or not. From an evolutionary perspective, crickets offer more opportunities to learn about the last common insect ancestor; they hold more traits in common with other insects than fruit flies do. (Notably, insects make up more than 85 percent of animal species.) Dr. Extavour’s research aims at the fundamentals: How do embryos work? And what might that reveal about how the first animal came to be? Every animal embryo follows a similar journey: One cell becomes many, then they arrange themselves in a layer at the egg’s surface, providing an early blueprint for all adult body parts. But how do embryo cells — cells that have the same genome but aren’t all doing the same thing with that information — know where to go and what to do? © 2022 The New York Times Company

Keyword: Development of the Brain
Link ID: 28422 - Posted: 08.06.2022

Scientists know both a lot and very little about the brain. With billions of neurons and trillions of connections among them, and the experimental limitations of examining the seat of consciousness and bodily function, studying the human brain is a technical, theoretical and ethical challenge. And one of the biggest challenges is perhaps one of the most fundamental – seeing what it looks like in action. The U.S. Brain Research Through Advancing Innovative Neurotechnologies (BRAIN) Initiative is a collaboration among the National Institutes of Health, Defense Advanced Research Projects Agency, National Science Foundation, Food and Drug Administration and Intelligence Advanced Research Projects Activity and others. Since its inception in 2013, its goal has been to develop and use new technologies to examine how each neuron and neural circuit comes together to “record, process, utilize, store, and retrieve vast quantities of information, all at the speed of thought.” Just as genomic sequencing enabled the creation of a comprehensive map of the human genome, tools that elucidate the connection between brain structure and function could help researchers answer long-standing questions about how the brain works, both in sickness and in health. These five stories from our archives cover research that has been funded by or advances the goals of the BRAIN Initiative, detailing a slice of what’s next in neuroscience. Attempts to map the structure of the brain date back to antiquity, when philosophers and scholars had only the unaided eye to map anatomy to function. New visualization techniques in the 20th century led to the discovery that, just like all the other organs of the body, the brain is composed of individual cells – neurons. © 2010–2022, The Conversation US, Inc.

Keyword: Brain imaging; Development of the Brain
Link ID: 28421 - Posted: 08.06.2022

By Lesley Evans Ogden Hana aced her memory test. After viewing the contents of three identical boxes arrayed in an arc on the back deck of her home, the 3-year-old Cavalier King Charles spaniel had to remember which box held a treat — a task she quickly learned after just a few trials. Hana is part of a pack that has grown to nearly 40,000 pet dogs enrolled in a citizen science initiative known as the Dog Aging Project, founded in 2014. Understanding the biology of aging in companion dogs is one of two main goals of the project, says cofounder and codirector Matt Kaeberlein, a pathologist at the University of Washington in Seattle who focuses on aging. “The other is to do something about it.” Through veterinary records, DNA samples, health questionnaires and cognitive tests like Hana’s treat-finding challenge, the initiative of the University of Washington and Texas A&M University will track many aspects of dogs’ lives over time. Smaller subsets of the dogs, including Hana, will participate in more focused studies and more extensive evaluations. From all of this, scientists hope to spot patterns and find links between lifestyles and health from puppyhood through the golden years. The effort joins that of an earlier one: the Family Dog Project, spearheaded in the 1990s at Eötvös Loránd University (ELTE) in Budapest to study “the behavioral and cognitive aspects of the dog-human relationship,” with tens of thousands of canines participating through the decades. The two projects have begun collaborating across continents, and the scientists hope that such a large combined group of dogs can help them tease out genetic and environmental factors that affect how long dogs live, and how much of that time is spent in good health. © 2022 Annual Reviews

Keyword: Alzheimers; Development of the Brain
Link ID: 28411 - Posted: 07.30.2022

ByCharles Piller In August 2021, Matthew Schrag, a neuroscientist and physician at Vanderbilt University, got a call that would plunge him into a maelstrom of possible scientific misconduct. A colleague wanted to connect him with an attorney investigating an experimental drug for Alzheimer’s disease called Simufilam. The drug’s developer, Cassava Sciences, claimed it improved cognition, partly by repairing a protein that can block sticky brain deposits of the protein amyloid beta (Aβ), a hallmark of Alzheimer’s. The attorney’s clients—two prominent neuroscientists who are also short sellers who profit if the company’s stock falls—believed some research related to Simufilam may have been “fraudulent,” according to a petition later filed on their behalf with the U.S. Food and Drug Administration (FDA). Schrag, 37, a softspoken, nonchalantly rumpled junior professor, had already gained some notoriety by publicly criticizing the controversial FDA approval of the anti-Aβ drug Aduhelm. His own research also contradicted some of Cassava’s claims. He feared volunteers in ongoing Simufilam trials faced risks of side effects with no chance of benefit. So he applied his technical and medical knowledge to interrogate published images about the drug and its underlying science—for which the attorney paid him $18,000. He identified apparently altered or duplicated images in dozens of journal articles. The attorney reported many of the discoveries in the FDA petition, and Schrag sent all of them to the National Institutes of Health (NIH), which had invested tens of millions of dollars in the work. (Cassava denies any misconduct [see sidebar, below].) But Schrag’s sleuthing drew him into a different episode of possible misconduct, leading to findings that threaten one of the most cited Alzheimer’s studies of this century and numerous related experiments. The first author of that influential study, published in Nature in 2006, was an ascending neuroscientist: Sylvain Lesné of the University of Minnesota (UMN), Twin Cities. His work underpins a key element of the dominant yet controversial amyloid hypothesis of Alzheimer’s, which holds that Aβ clumps, known as plaques, in brain tissue are a primary cause of the devastating illness, which afflicts tens of millions globally. In what looked like a smoking gun for the theory and a lead to possible therapies, Lesné and his colleagues discovered an Aβ subtype and seemed to prove it caused dementia in rats. If Schrag’s doubts are correct, Lesné’s findings were an elaborate mirage. © 2022 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 28409 - Posted: 07.23.2022

Anthony Hannan In a recent interview, Game of Thrones star Emilia Clarke spoke about being able to live “completely normally” after two aneurysms – one in 2011 and one in 2013 – that caused brain injury. She went on to have two brain surgeries. An aneurysm is a bulge or ballooning in the wall of a blood vessel, often accompanied by severe headache or pain. So how can people survive and thrive despite having, as Clarke put it, “quite a bit missing” from their brain? The key to understanding how brains can recover from trauma is that they are fantastically plastic – meaning our body’s supercomputer can reshape and remodel itself. Brains can adapt and change in incredible ways. Yours is doing it right now as you form new memories. It’s not that the brain has evolved to deal with brain trauma or stroke or aneurysms; our ancestors normally died when that happened and may not have gone on to reproduce. In fact, we evolved very thick skulls to try to prevent brain trauma happening at all. No, this neural plasticity is a result of our brains evolving to be learning machines. They allow us to adapt to changing environments, to facilitate learning, memory and flexibility. This functionality also means the brain can adapt after certain injuries, finding new pathways to function. A lot of organs wouldn’t recover at all after serious damage. But the brain keeps developing through life. At a microscopic level, you’re changing the brain to make new memories every day.

Keyword: Development of the Brain; Regeneration
Link ID: 28404 - Posted: 07.22.2022

by Charles Q. Choi Children with autism show atypical development of brain regions connected to the amygdala, an almond-size brain structure involved in processing fear and other emotions, a new study finds. The brain regions most affected vary between autistic boys and girls, the study also shows, adding to the growing body of evidence for sex differences in autism, researchers say. “Better understanding of amygdala development and its connectivity can aid in the development of novel biomarkers to study brain and social health,” says Emma Duerden, assistant professor of applied psychology at Western University in London, Canada, who was not involved in the study. The amygdala is a central hub for brain circuits involved in social function. Previous studies have found it to be enlarged in some autistic children compared with non-autistic children, a difference that may be linked with anxiety and depression. In the new study, researchers used structural magnetic resonance imaging to track the growth of 32 brain regions with direct connections to the amygdala. The study participants included 282 autistic children, 93 of whom are female, and 128 non-autistic children, 61 of whom are female. The researchers scanned each child up to four times — when the children were 39, 52, 64 and 137 months old, on average. They also measured the children’s autism traits and social difficulties using a questionnaire filled out by parents, called the Social Responsiveness Scale-2. Autistic children had larger amygdala-connected brain regions than non-autistic children at all ages. The differences grew over time and were most apparent among the autistic children with prominent social difficulties. The researchers found no differences in the size of brain areas not directly connected to the amygdala between children with and without autism. © 2022 Simons Foundation

Keyword: Autism; Emotions
Link ID: 28398 - Posted: 07.14.2022