By Elizabeth Pennisi Biologists have long known that new protein-coding genes can arise through the duplication and modification of existing ones. But some protein genes can also arise from stretches of the genome that once encoded aimless strands of RNA instead. How new protein genes surface this way has been a mystery, however. Now, a study identifies mutations that transform seemingly useless DNA sequences into potential genes by endowing their encoded RNA with the skill to escape the cell nucleus—a critical step toward becoming translated into a protein. The study’s authors highlight 74 human protein genes that appear to have arisen in this de novo way—more than half of which emerged after the human lineage branched off from chimpanzees. Some of these newcomer genes may have played a role in the evolution of our relatively large and complex brains. When added to mice, one made the rodent brains grow bigger and more humanlike, the authors report this week in Nature Ecology & Evolution. “This work is a big advance,” says Anne-Ruxandra Carvunis, an evolutionary biologist at the University of Pittsburgh, who was not involved with the research. It “suggests that de novo gene birth may have played a role in human brain evolution.” Although some genes encode RNAs that have structural or regulatory purposes themselves, those that encode proteins instead create an intermediary RNA. Made in the nucleus like other RNAs, these messenger RNAs (mRNAs) exit into the cytoplasm and travel to organelles called ribosomes to tell them how to build the gene’s proteins. A decade ago, Chuan-Yun Li, an evolutionary biologist at Peking University, and colleagues discovered that some human protein genes bore a striking resemblance to DNA sequences in rhesus monkeys that got transcribed into long noncoding RNAs (lncRNAs), which didn’t make proteins or have any other apparent purpose. Li couldn’t figure out what it had taken for those stretches of monkey DNA to become true protein-coding genes in humans. © 2023 American Association for the Advancement of Science.

Related chapters from BN: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28624 - Posted: 01.07.2023

By Freda Kreier Living through the COVID-19 pandemic may have matured teens’ brains beyond their years. From online schooling and social isolation to economic hardship and a mounting death count, the last few years have been rough on young people. For teens, the pandemic and its many side effects came during a crucial window in brain development. Now, a small study comparing brain scans of young people from before and after 2020 reveals that the brains of teens who lived through the pandemic look about three years older than expected, scientists say. This research, published December 1 in Biological Psychiatry: Global Open Science, is the first to look at the impact of the pandemic on brain aging. The finding reveals that “the pandemic hasn’t been bad just in terms of mental health for adolescents,” says Ian Gotlib, a clinical neuroscientist at Stanford University. “It seems to have altered their brains as well.” The study can’t link those brain changes to poor mental health during the pandemic. But “we know there is a relationship between adversity and the brain as it tries to adapt to what it’s been given,” says Beatriz Luna, a developmental cognitive neuroscientist at the University of Pittsburgh, who wasn’t involved in the research. “I think this is a very important study that sets the ball rolling for us to look at this.” The roots of this study date back to nearly a decade ago, when Gotlib and his colleagues launched a project in California’s Bay Area to study depression in adolescents. The researchers were collecting information on the mental health of the kids in the study, and did MRI scans of their brains. © Society for Science & the Public 2000–2023.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28620 - Posted: 01.04.2023

By Ellen Barry The effect of social media use on children is a fraught area of research, as parents and policymakers try to ascertain the results of a vast experiment already in full swing. Successive studies have added pieces to the puzzle, fleshing out the implications of a nearly constant stream of virtual interactions beginning in childhood. A new study by neuroscientists at the University of North Carolina tries something new, conducting successive brain scans of middle schoolers between the ages of 12 and 15, a period of especially rapid brain development. The researchers found that children who habitually checked their social media feeds at around age 12 showed a distinct trajectory, with their sensitivity to social rewards from peers heightening over time. Teenagers with less engagement in social media followed the opposite path, with a declining interest in social rewards. The study, published on Tuesday in JAMA Pediatrics, is among the first attempts to capture changes to brain function correlated with social media use over a period of years. The study has important limitations, the authors acknowledge. Because adolescence is a period of expanding social relationships, the brain differences could reflect a natural pivot toward peers, which could be driving more frequent social media use. “We can’t make causal claims that social media is changing the brain,” said Eva H. Telzer, an associate professor of psychology and neuroscience at the University of North Carolina, Chapel Hill, and one of the authors of the study. But, she added, “teens who are habitually checking their social media are showing these pretty dramatic changes in the way their brains are responding, which could potentially have long-term consequences well into adulthood, sort of setting the stage for brain development over time.” © 2023 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 28619 - Posted: 01.04.2023

Heidi Ledford Severe COVID-19 is linked to changes in the brain that mirror those seen in old age, according to an analysis of dozens of post-mortem brain samples1. The analysis revealed brain changes in gene activity that were more extensive in people who had severe SARS-CoV-2 infections than in uninfected people who had been in an intensive care unit (ICU) or had been put on ventilators to assist their breathing — treatments used in many people with serious COVID-19. The study, published on 5 December in Nature Aging, joins a bevy of publications cataloguing the effects of COVID-19 on the brain. “It opens a plethora of questions that are important, not only for understanding the disease, but to prepare society for what the consequences of the pandemic might be,” says neuropathologist Marianna Bugiani at Amsterdam University Medical Centers. “And these consequences might not be clear for years.” Maria Mavrikaki, a neurobiologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, embarked on the study about two years ago, after seeing a preprint, later published as a paper2, that described cognitive decline after COVID-19. She decided to follow up to see whether she could find changes in the brain that might trigger the effects. She and her colleagues studied samples taken from the frontal cortex — a region of the brain closely tied to cognition — of 21 people who had severe COVID-19 when they died and one person with an asymptomatic SARS-CoV-2 infection at death. The team compared these with samples from 22 people with no known history of SARS-CoV-2 infection. Another control group comprised nine people who had no known history of infection but had spent time on a ventilator or in an ICU — interventions that can cause serious side effects. The team found that genes associated with inflammation and stress were more active in the brains of people who had had severe COVID-19 than in the brains of people in the control group. Conversely, genes linked to cognition and the formation of connections between brain cells were less active. © 2022 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 28584 - Posted: 12.06.2022

Allison Whitten Our understanding of the inner workings of the human brain has long been held back by the practical and ethical difficulty of observing human neurons develop, connect and interact. Today, in a new study published in Nature, neuroscientists at Stanford University led by Sergiu Paşca report that they have found a new way to study human neurons — by transplanting human brainlike tissue into rats that are just days old, when their brains have not yet fully formed. The researchers show that human neurons and other brain cells can grow and integrate themselves into the rat’s brain, becoming part of the functional neural circuitry that processes sensations and controls aspects of behaviors. Using this technique, scientists should be able to create new living models for a wide range of neurodevelopmental disorders, including at least some forms of autism spectrum disorder. The models would be just as practical for neuroscientific lab studies as current animal models are but would be better stand-ins for human disorders because they would consist of real human cells in functional neural circuits. They could be ideal targets for modern neuroscience tools that are too invasive to use in real human brains. “This approach is a step forward for the field and offers a new way to understand disorders of neuronal functioning,” said Madeline Lancaster, a neuroscientist at the MRC Laboratory of Molecular Biology in Cambridge, U.K., who was not involved in the work. The work also marks an exciting new chapter in the use of neural organoids. Nearly 15 years ago, biologists discovered that human stem cells could self-organize and grow into small spheres that held different types of cells and resembled brain tissue. These organoids opened a new window into the activities of brain cells, but the view has its limits. While neurons in a dish can connect to each other and communicate electrically, they can’t form truly functional circuits or attain the full growth and computational prowess of healthy neurons in their natural habitat, the brain. Pioneering work by various research groups proved years ago that human brain organoids could be inserted into the brains of adult rats and survive. But the new study shows for the first time that the burgeoning brain of a newborn rat will accept human neurons and allow them to mature, while also integrating them into local circuits capable of driving the rat’s behavior. All Rights Reserved © 2022

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28512 - Posted: 10.13.2022

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

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Balance, Taste, and Smell
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 28493 - Posted: 09.28.2022

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.

Related chapters from BN: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
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

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 13: Memory and Learning
Link ID: 28466 - Posted: 09.07.2022

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.)

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
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

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28422 - Posted: 08.06.2022

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.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 15: Language and Lateralization
Link ID: 28404 - Posted: 07.22.2022

By Tim Vernimmen Developmental neuroscientist Eveline Crone, based at Erasmus University Rotterdam, has studied adolescents, defined by researchers as people aged 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 like 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 her colleague Andrew Fuligni of the University of California, Los Angeles, explore how adolescents feel and think about themselves and others, and stress that far from being either/or, both are inextricably intertwined. This conversation has been edited for length and clarity. How did you get interested in studying adolescents, and how have your views evolved over time? When I started to study psychology, I was interested in the way people think and make decisions, and I started to realize that you can answer these questions if you understand how they got there. That is how I got interested in development: I wanted to understand the pathways to becoming an adult. © 2022 Annual Reviews

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28396 - Posted: 07.14.2022

Viviane Callier Our human brains can seem like a crowning achievement of evolution, but the roots of that achievement run deep: The modern brain arose from hundreds of millions of years of incremental advances in complexity. Evolutionary biologists have traced that progress back through the branch of the animal family tree that includes all creatures with central nervous systems, the bilaterians, but it is clear that fundamental elements of the nervous system existed much earlier. How much earlier has now been made dramatically clear by a recent discovery by a team of researchers at the University of Exeter in the United Kingdom. They found that the chemical precursors of two important neurotransmitters, or signaling molecules used in nervous systems, appear in all the major animal groups that preceded creatures with central nervous systems. The big surprise, however, is that these molecules are also present in single-celled relatives of animals, called choanoflagellates. This finding shows that animal neuropeptides originated before the evolution of even the very first animals. The discovery “solves a long-standing question about when and how animal neuropeptides evolved,” said Pawel Burkhardt, who studies the evolutionary origin of neurons at the Sars International Center for Marine Molecular Biology in Norway. It also indicates that at least some of the signaling molecules fundamental to the operation of our brains first evolved for an entirely different purpose in organisms that consisted of only a single cell. Animal nervous systems are made of neurons that connect to each other, zipping information across synapses with a variety of small peptide neurotransmitters. These peptides are the language with which neurons speak to each other. All Rights Reserved © 2022

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 4: Development of the Brain
Link ID: 28354 - Posted: 06.04.2022

By Benjamin Mueller Five years ago, Tal Iram, a young neuroscientist at Stanford University, approached her supervisor with a daring proposal: She wanted to extract fluid from the brain cavities of young mice and to infuse it into the brains of older mice, testing whether the transfers could rejuvenate the aging rodents. Her supervisor, Tony Wyss-Coray, famously had shown that giving old animals blood from younger ones could counteract and even reverse some of the effects of aging. But the idea of testing that principle with cerebrospinal fluid, the hard-to-reach liquid that bathes the brain and spinal cord, struck him as such a daunting technical feat that trying it bordered on foolhardy. “When we discussed this initially, I said, ‘This is so difficult that I’m not sure this is going to work,’” Dr. Wyss-Coray said. Dr. Iram persevered, working for a year just to figure out how to collect the colorless liquid from mice. On Wednesday, she reported the tantalizing results in the journal Nature: A week of infusions of young cerebrospinal fluid improved the memories of older mice. The finding was the latest indication that making brains resistant to the unrelenting changes of older age might depend less on interfering with specific disease processes and more on trying to restore the brain’s environment to something closer to its youthful state. “It highlights this notion that cerebrospinal fluid could be used as a medium to manipulate the brain,” Dr. Iram said. Turning that insight into a treatment for humans, though, is a more formidable challenge, the authors of the study said. The earlier studies about how young blood can reverse some signs of aging have led to recent clinical trials in which blood donations from younger people were filtered and given to patients with Alzheimer’s or Parkinson’s disease. But exactly how successful those treatments might be, much less how widely they can be used, remains unclear, scientists said. And the difficulties of working with cerebrospinal fluid are steeper than those involved with blood. Infusing the fluid of a young human into an older patient is probably not possible; extracting the liquid generally requires a spinal tap, and scientists say that there are ethical questions about how to collect enough cerebrospinal fluid for infusions. © 2022 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 28327 - Posted: 05.14.2022

Grace Browne In early February 2016, after reading an article featuring a couple of scientists at the Massachusetts Institute of Technology who were studying how the brain reacts to music, a woman felt inclined to email them. “I have an interesting brain,” she told them. EG, who has requested to go by her initials to protect her privacy, is missing her left temporal lobe, a part of the brain thought to be involved in language processing. EG, however, wasn’t quite the right fit for what the scientists were studying, so they referred her to Evelina Fedorenko, a cognitive neuroscientist, also at MIT, who studies language. It was the beginning of a fruitful relationship. The first paper based on EG’s brain was recently published in the journal Neuropsychologia, and Fedorenko’s team expects to publish several more. For EG, who is in her fifties and grew up in Connecticut, missing a large chunk of her brain has had surprisingly little effect on her life. She has a graduate degree, has enjoyed an impressive career, and speaks Russian—a second language–so well that she has dreamed in it. She first learned her brain was atypical in the autumn of 1987, at George Washington University Hospital, when she had it scanned for an unrelated reason. The cause was likely a stroke that happened when she was a baby; today, there is only cerebro-spinal fluid in that brain area. For the first decade after she found out, EG didn't tell anyone other than her parents and her two closest friends. “It creeped me out,” she says. Since then, she has told more people, but it's still a very small circle that is aware of her unique brain anatomy. © Condé Nast Britain 2022.

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 13: Memory and Learning
Link ID: 28295 - Posted: 04.20.2022

Joan L. Luby, M.D., John N. Constantino, M.D., Deanna M. Barch, Ph.D. Numerous studies of children in the US across decades have shown striking correlations between poverty and less-than-optimal physical and mental health and developmental outcomes. Trauma, poor health care, inadequate nutrition, and increased exposures to psychosocial stress and environmental toxins—all of which have significant negative developmental impact—are likely to be involved. The effects of elevated stress on child-caregiver relationships appear to be particularly detrimental, unsurprising in that nurturing and supportive caregiver relationships are foundational for healthy development in early childhood. For adults whose job options are unconducive to their role as parents (such as working multiple jobs or night shift hours), or for whom family support is unavailable, or for those do not have the material resources they need, the resulting stress may result in sleep disruption, depression, and anxiety—all of which translate to poor developmental trajectories for their children. Other health and developmental risks often associated with poverty include lead and other pollutants in air and water, poor nutrition (often related to living in “food desert” areas where healthy foods such as fresh fruits and vegetables are scarce), neighborhood violence, and trauma. “Toxic stress” that exceeds a child’s ability to adapt can occur when the burden of stressful life experience overwhelms the brain’s regulatory capacity, or when the compensatory abilities of brain and body are compromised. A lack of cognitive stimulation (due to such factors as the absence of books and educational materials in the home, poor immersion in language, and a lack of after school or other enrichment activities) or disruption of sleep and circadian rhythms (by neighborhood noise or parents’ irregular work schedules) is likely to impact brain development and emotional and behavioral regulation when these systems are rapidly developing. © 2022 The Dana Foundation.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 13: Memory and Learning
Link ID: 28288 - Posted: 04.16.2022

Max Kozlov When neuroscientist Jakob Seidlitz took his 15-month-old son to the paediatrician for a check-up last week, he left feeling unsatisfied. There wasn’t anything wrong with his son — the youngster seemed to be developing at a typical pace, according to the height and weight charts the physician used. What Seidlitz felt was missing was an equivalent metric to gauge how his son’s brain was growing. “It is shocking how little biological information doctors have about this critical organ,” says Seidlitz, who is based at the University of Pennsylvania in Philadelphia. Soon, he might be able to change that. Working with colleagues, Seidlitz has amassed more than 120,000 brain scans — the largest collection of its kind — to create the first comprehensive growth charts for brain development. The charts show visually how human brains expand quickly early in life and then shrink slowly with age. The sheer magnitude of the study, published in Nature on 6 April1, has stunned neuroscientists, who have long had to contend with reproducibility issues in their research, in part because of small sample sizes. Magnetic resonance imaging (MRI) is expensive, meaning that scientists are often limited in the number of participants they can enrol in experiments. “The massive data set they assembled is extremely impressive and really sets a new standard for the field,” says Angela Laird, a cognitive neuroscientist at Florida International University in Miami. Even so, the authors caution that their database isn’t completely inclusive — they struggled to gather brain scans from all regions of the globe. The resulting charts, they say, are therefore just a first draft, and further tweaks would be needed to deploy them in clinical settings. If the charts are eventually rolled out to paediatricians, great care will be needed to ensure that they are not misinterpreted, says Hannah Tully, a paediatric neurologist at the University of Washington in Seattle. “A big brain is not necessarily a well-functioning brain,” she says. © 2022 Springer Nature Limited

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 28277 - Posted: 04.09.2022

Elena Renken Even when it’s not apparent, cells in our tissues and organs are constantly on the move. In fact, the ability of cells to get where they need to go is essential to our health and survival. Skin cells migrate to heal wounds. Immune system cells migrate to fight infections. “Every day, you look at your body and it’s not changing much,” said Peter Devreotes, a professor of cell biology at the Johns Hopkins University School of Medicine. “But the cells within it are migrating constantly.” It starts from the earliest stages of life. When we are embryos just a few weeks old, a special population of “neural crest” cells in our back suddenly spreads through the body to become a wide range of essential tissues — bones, cartilage and nerves in the face, tendons, pigment cells in the skin, parts of the heart and more. But how do these cells know where to go? Studies long suggested that they were following chemical trails to their routes. Biologists traditionally saw these chemical gradients as simple and the cells as mere followers: Like dogs trotting toward the scent of food, the cells sensed the gradient and followed the stream of signals back to the source. Countless examples of this have been found among bacteria and other cells navigating through the wild, as well as inside larger organisms. When you nick your skin, for instance, the tissue around the cut releases a cloud of molecules that attract immune cells nearby. The immune cells crawl toward it and stave off infection. Yet scientists also came to understand that this system can’t sustain many of the migrations that unfold in the body. The structure of simple passive gradients is too fragile and too easily disrupted. Simple gradients like these don’t always reach far enough to guide cells’ lengthier journeys, and they may dissipate too quickly to maintain migrations that take longer. Raising the sensitivity of the cells might seem like a way to offset those problems, but then cells might often be too flooded with signals to sense where they come from. For a simple gradient to work, it has to be perfect, and nothing can go awry. But in reality, cells must find a way to navigate under all kinds of conditions. All Rights Reserved © 2022

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28261 - Posted: 03.30.2022

by Angie Voyles Askham Mice chemically coaxed to produce high levels of an autism-linked gut molecule have anxiety-like behavior and unusual patterns of brain connectivity, according to a study published today in Nature. The findings present a direct mechanism by which the gut could send signals to the brain and alter development, the researchers say. “It’s a true mechanistic paper, [like] the field has been asking for,” says Jane Foster, professor of psychiatry and behavioral neurosciences at McMaster University in Hamilton, Canada, who was not involved in the study. Although it’s not clear that this exact signaling pathway is happening in people, she says, “this is the sort of work that’s going to get us that answer.” The molecule, 4-ethylphenol (4EP), is produced by gut microbes in mice and people. An enzyme in the colon and liver converts 4EP to 4-ethylphenyl sulfate (4EPS), which then circulates in the blood. Mice exposed to a maternal immune response in the womb have atypically high blood levels of 4EPS, as do some autistic people, previous research shows. And injecting mice with the molecule increases behaviors indicative of anxiety. But it wasn’t clear how the molecule could contribute to those traits. In the new work, researchers show that 4EPS can enter the brain and that its presence is associated with altered brain connectivity and a decrease in myelin — the insulation around axons that helps conduct electrical signals. Boosting the function of myelin-producing cells, the team found, eases the animals’ anxiety. “This is one of the first — maybe, arguably, the first — demonstrations of a specific microbe molecule that has such a profound impact on a complex behavior,” says lead researcher Sarkis Mazmanian, professor of microbiology at the California Institute of Technology in Pasadena. “How it’s doing it, we still need to understand.” without the engineered enzymes, they showed increased anxiety-like behaviors, © 2022 Simons Foundation

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory and Learning
Link ID: 28205 - Posted: 02.16.2022

by Laura Dattaro Early in her first postdoctoral position, Hollis Cline first showed her hallmark flair for creative problem-solving. Cline, who goes by Holly, and her adviser, neuroscientist Martha Constantine-Paton, wanted to study the brain’s ‘topographical maps’ — internal representations of sensory input from the external world. These maps are thought to shape a person’s ability to process sensory information — filtering that can go awry in autism and other neurodevelopmental conditions. No one knew just how these maps formed or what could potentially disrupt them. Cline and Constantine-Paton, who was then at Yale University and is now emerita professor of brain and cognitive sciences at the Massachusetts Institute of Technology, weren’t sure how to find out. But as a first step, the pair decided to take the plunge with an unusual animal model: the frog — specifically, a spotted greenish-brown species called Rana pipiens, or the northern leopard frog. The amphibians spend two to three months as tadpoles, a span during which their brains change rapidly and visibly — unlike in mammals, which undergo similar stages of development inside of the mother’s body. These traits made it possible for Cline and Constantine-Paton to introduce changes and repeatedly watch their effects in real time. “That’s an extended period when you can actually have access to the developing brain,” Cline says. The unorthodox approach paid off. Cline, 66, now professor of neuroscience at the Scripps Research Institute in La Jolla, California, worked out that a receptor for the neurotransmitter glutamate, which had been shown to be important for learning and memory, also mediated how visual experiences influence the developing topographical map. She later created a novel live imaging technique to visualize frog neurons’ development over time and, sticking with frogs over the ensuing decades, went on to make fundamental discoveries about how sensory experiences shape brain development and sensory processing. © 2022 Simons Foundation

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 28179 - Posted: 02.02.2022