By James Gorman Dogs go through stages in their life, just as people do, as is obvious to anyone who has watched their stiff-legged, white-muzzled companion rouse themselves to go for one more walk. Poets from Homer to Pablo Neruda have taken notice. As have folk singers and story tellers. Now science is taking a turn, in the hope that research on how dogs grow and age will help us understand how humans age. And, like the poets before them, scientists are finding parallels between the two species. Their research so far shows that dogs are similar to us in important ways, like how they act during adolescence and old age, and what happens in their DNA as they get older. They may be what scientists call a “model” for human aging, a species that we can study to learn more about how we age and perhaps how to age better. Most recently, researchers in Vienna have found that dogs’ personalities change over time. They seem to mellow in the same way that most humans do. The most intriguing part of this study is that like people, some dogs are just born old, which is to say, relatively steady and mature, the kind of pup that just seems ready for a Mr. Rogers cardigan. “That’s professor Spot, to you, thank you, and could we be a little neater when we pour kibble into my dish?” Mind you, the Vienna study dogs were all Border collies, so I’m a little surprised that any of them were mature. That would suggest a certain calm, a willingness to tilt the head and muse that doesn’t seem to fit the breed, with its desperate desire to be constantly chasing sheep, geese, children or Frisbees. Another recent paper came to the disturbing conclusion that the calculus of seven dog years for every human year isn’t accurate. To calculate dog years, you must now multiply the natural logarithm of a dog’s age in human years by 16 and then add 31. Is that clear? It’s actually not as hard as it sounds, as long as you have a calculator or internet access. For example the natural log of 6 is 1.8, roughly, which, multiplied by 16 is about 29, which, plus 31, is 60. OK, it’s not that easy, even with the internet. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory and Learning
Link ID: 27574 - Posted: 11.10.2020

By Laura Sanders Nearly 2,000 years ago, a cloud of scorching ash from Mount Vesuvius buried a young man as he lay on a wooden bed. That burning ash quickly cooled, turning some of his brain to glass. This confluence of events in A.D. 79 in the town of Herculaneum, which lay at the western base of the volcano, preserved the usually delicate neural tissue in a durable, glassy form. New scrutiny of this tissue has revealed signs of nerve cells with elaborate tendrils for sending and receiving messages, scientists report October 6 in PLOS ONE. That the young man once possessed these nerve cells, or neurons, is no surprise; human brains are packed with roughly 86 billion neurons (SN: 8/7/19). But samples from ancient brains are sparse. Those that do exist have become a soaplike substance or mummified, says Pier Paolo Petrone, a biologist and forensic anthropologist at the University of Naples Federico II in Italy. But while studying the Herculaneum site, Petrone noticed something dark and shiny inside this man’s skull. He realized that those glassy, black fragments “had to be the remains of the brain.” Petrone and colleagues used scanning electron microscopy to study glassy remains from both the man’s brain and spinal cord. The researchers saw tubular structures as well as cell bodies that were the right sizes and shapes to be neurons. In further analyses, the team found layers of tissue wrapped around tendrils in the brain tissue. This layering appears to be myelin, a fatty substance that speeds signals along nerve fibers. The preserved tissue was “something really astonishing and incredible,” Petrone says, because the conversion of objects to glass, a process called vitrification, is relatively rare in nature. “This is the first ever discovery of ancient human brain remains vitrified by hot ash during a volcanic eruption.” © Society for Science & the Public 2000–2020.

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: 27558 - Posted: 10.31.2020

The plant compound apigenin improved the cognitive and memory deficits usually seen in a mouse model of Down syndrome, according to a study by researchers at the National Institutes of Health and other institutions. Apigenin is found in chamomile flowers, parsley, celery, peppermint and citrus fruits. The researchers fed the compound to pregnant mice carrying fetuses with Down syndrome characteristics and then to the animals after they were born and as they matured. The findings raise the possibility that a treatment to lessen the cognitive deficits seen in Down syndrome could one day be offered to pregnant women whose fetuses have been diagnosed with Down syndrome through prenatal testing. The study appears in the American Journal of Human Genetics. Down syndrome is a set of symptoms resulting from an extra copy or piece of chromosome 21. The intellectual and developmental disabilities accompanying the condition are believed to result from decreased brain growth caused by increased inflammation in the fetal brain. Apigenin is not known to have any toxic effects, and previous studies have indicated that it is an antioxidant that reduces inflammation. Unlike many compounds, it is absorbed through the placenta and the blood brain barrier, the cellular layer that prevents potentially harmful substances from entering the brain. Compared to mice with Down symptoms whose mothers were not fed apigenin, those exposed to the compound showed improvements in tests of developmental milestones and had improvements in spatial and olfactory memory. Tests of gene activity and protein levels showed the apigenin-treated mice had less inflammation and increased blood vessel and nervous system growth. Guedj, F. et al. Apigenin as a candidate prenatal treatment for Trisomy 21: effects in human amniocytes and the Ts1Cje mouse model. American Journal of Human Genetics. 2020.

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: 27546 - Posted: 10.24.2020

Catherine Offord Overactivation of the brain’s immune cells, called microglia, may play a role in cognitive impairments associated with Down syndrome, according to research published today (October 6) in Neuron. Researchers in Italy identified elevated numbers of the cells in an inflammation-promoting state in the brains of mice with a murine version of the syndrome as well as in postmortem brain tissue from people with the condition. The team additionally showed that drugs that reduce the number of activated microglia in juvenile mice could boost the animals’ performance on cognitive tests. “This is a fabulous study that gives a lot of proof of principle to pursuing some clinical trials in people,” says Elizabeth Head, a neuroscientist at the University of California, Irvine, who was not involved in the work. “The focus on microglial activation, I thought, was very novel and exciting,” she adds, noting that more research will be needed to see how the effects of drugs used in the study might translate from mice to humans. Down syndrome is caused by an extra copy of part or all of human chromosome 21, and is the most commonly occurring chromosomal condition in the US. Children with Down syndrome often experience cognitive delays compared to typically developing children, although there’s substantial variation and the effects are usually mild or moderate. People with the syndrome also have a higher risk of certain medical conditions, including Alzheimer’s disease. © 1986–2020 The Scientist.

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: 27537 - Posted: 10.21.2020

By Elizabeth Svoboda After a 3-year-old named Matthew started having one seizure after another, his worried parents learned he had a chronic brain condition that was causing the convulsions. They faced an impossible decision: allow the damaging seizures to continue indefinitely, or allow surgeons to remove half of their son’s brain. They chose the latter. When Matthew emerged from surgery, he couldn’t walk or speak. But bit by bit, he remastered speech and recaptured his lost milestones. The moment one side of his brain was removed, the remainder set itself to the colossal task of re-forging lost neural connections. This gut-level renovation was so successful that no one who meets Matthew today would guess that half his brain is gone. Stanford neuroscientist David Eagleman is obsessed with probing the outer limits of this kind of neural transformation — and harnessing it to useful ends. We’ve all heard that our brains are more plastic than we think, that they can adapt ingeniously to changed conditions, but in “Livewired: The Inside Story of the Ever-Changing Brain,” Eagleman tackles this topic with fresh élan and rigor. He shows not just how we can direct our own neural remodeling on a cellular level, but how such remodeling — a process he calls “livewiring” — alters the core of who we are. “Our machinery isn’t fully preprogrammed, but instead shapes itself by interacting with the world,” Eagleman writes. “You are a different person than you were at this time last year, because the gargantuan tapestry of your brain has woven itself into something new.”

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: 27515 - Posted: 10.10.2020

By Macarena Carrizosa, Sophie Bushwick A new system called PiVR creates working artificial environments for small animals such as zebra fish larvae and fruit flies. Developers say the system’s affordability could help expand research into animal behavior. © 2020 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 27505 - Posted: 10.07.2020

In an article published in Nature Genetics, researchers confirm that about 14% of all cases of cerebral palsy, a disabling brain disorder for which there are no cures, may be linked to a patient’s genes and suggest that many of those genes control how brain circuits become wired during early development. This conclusion is based on the largest genetic study of cerebral palsy ever conducted. The results led to recommended changes in the treatment of at least three patients, highlighting the importance of understanding the role genes play in the disorder. The work was largely funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our results provide the strongest evidence to date that a significant portion of cerebral palsy cases can be linked to rare genetic mutations, and in doing so identified several key genetic pathways involved,” said Michael Kruer, M.D., a neurogeneticist at Phoenix Children’s Hospital and the University of Arizona College of Medicine - Phoenix and a senior author of the article. “We hope this will give patients living with cerebral palsy and their loved ones a better understanding of the disorder and doctors a clearer roadmap for diagnosing and treating them.” Cerebral palsy affects approximately one in 323 children(link is external) in the United States. Signs of the disorder appear early in childhood resulting in a wide range of permanently disabling problems with movement and posture, including spasticity, muscle weakness, and abnormal gait. Nearly 40% of patients need some assistance with walking. In addition, many patients may also suffer epileptic seizures, blindness, hearing and speech problems, scoliosis, and intellectual disabilities.

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: 27494 - Posted: 09.28.2020

By Lisa Friedman WASHINGTON — The Trump administration has rejected scientific evidence linking the pesticide chlorpyrifos to serious health problems, directly contradicting federal scientists’ conclusions five years ago that it can stunt brain development in children. The Environmental Protection Agency’s assessment of the pesticide, which is widely used on soybeans, almonds, grapes and other crops, is a fresh victory for chemical makers and the agricultural industry, as well as the latest in a long list of Trump administration regulatory rollbacks. In announcing its decision, the E.P.A. said on Tuesday that “despite several years of study, the science addressing neurodevelopmental effects remains unresolved.” However, in making its finding, the agency excluded several epidemiological studies, most prominently one conducted at Columbia University, that found a correlation between prenatal exposure to chlorpyrifos and developmental disorders in toddlers. As a result, the assessment may be the first major test of the Trump administration’s intention, often referred to as its “secret science” proposal, to bar or give less weight to scientific studies that can’t or don’t publicly release their underlying data. This controversial policy would eliminate many studies that track the effects of exposure to substances on people’s health over long periods of time, because the data often includes confidential medical records of the subjects, scientists have said. © 2020 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: 27485 - Posted: 09.25.2020

By Carolyn Wilke New findings in mice suggest yet another role for gut microbes, even before birth. The microbes residing in a female mouse’s gut help shape the wiring of her offspring’s brain, researchers report September 23 in Nature. While mouse and human development are worlds apart, the study hints at how a mother’s microbiome may have long-term consequences for her offspring. Scientists have previously found links between a mouse mother’s microbiome and her young’s brain and behavior, but many of those studies worked with animals that were stressed (SN: 7/9/18) or sick. Instead, Helen Vuong, a neurobiologist at UCLA, and her colleagues looked at what a mother’s microbial mix normally does for her pups’ brains. The new results point to the influence of specific microbes and the small molecules they produce, called metabolites. “Metabolites from the microbiome of the mother can influence the developing brain of the fetus,” says Cathryn Nagler, an immunologist at the University of Chicago who was not involved with the study. The metabolites do this by reaching a developing pup’s brain where they affect the growth of axons, she says. Axons are the threadlike signal-transmitters of nerve cells. Vuong and her team looked at the brains of fetuses from pregnant mice — some with their usual gut bugs, some raised without microbes and others ridded of their gut bacteria with antibiotics. When a mother’s microbes were missing, fetuses had shorter and fewer axons extending from the brain’s “relay station” to the cortex, Vuong says. These connections are important for processing sensory information. © Society for Science & the Public 2000–2020.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 27483 - Posted: 09.25.2020

by Angie Voyles Askham . Many problems associated with fragile X syndrome stem from a leak in mitochondria, organelles that act as the power stations of the cell, a new study suggests1. Stopping this leak eases some of the autism-like traits of mice that model the syndrome. “The paper is very solid,” says John Jay Gargus, director of the Center for Autism Research and Translation at the University of California, Irvine, who was not involved in the study. And because mitochondrial energy deficiency is seen in other forms of autism, the findings may be relevant beyond fragile X syndrome, Gargus says. Fragile X syndrome results from mutations in the FMR1 gene, which lead to a loss of the protein FMRP. Without FMRP, cells have immature dendritic spines — the bumps along a neuron’s arms that receive input from other neurons — and produce other proteins in excess. These differences are thought to contribute to the syndrome’s characteristic traits, such as developmental delay, intellectual disability and, often, autism. The new study shows that a leak in the mitochondrial membrane, possibly caused by the lack of FMRP, may drive the affected cells’ immaturity and excess protein production. The leak affects a cell’s metabolism, causing it to produce energy quickly but not efficiently, says lead researcher Elizabeth Jonas, professor of internal medicine and neuroscience at Yale University. All cells start out with mitochondrial leaks; the rapid energy production these leaks allow may be useful in early development. As typical cells mature and efficiency becomes more important than speed, however, they seem to close the leaks, Jonas says. Because cells with a fragile X mutation cannot close their leaks, they remain in an immature state. © 2020 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: 27466 - Posted: 09.12.2020

When it comes to brain cells, one size does not fit all. Neurons come in a wide variety of shapes, sizes, and contain different types of brain chemicals. But how did they get that way? A new study in Nature suggests that the identities of all the neurons in a worm are linked to unique members of a single gene family that control the process of converting DNA instructions into proteins, known as gene expression. The results of this study could provide a foundation for understanding how nervous systems have evolved in many other animals, including humans. The study was funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “The central nervous systems of all animals, from worms to humans, are incredibly intricate and highly ordered. The generation and diversity of a plethora of neuronal cell types is driven by gene expression,” said Robert Riddle, Ph.D., program director at NINDS. “So, it is surprising and exciting to consider that the cell diversity we see in the entire nervous system could come from a just a single group of genes.” Researchers led by Oliver Hobert, Ph.D., professor of biochemistry and molecular biophysics at Columbia University in New York City and graduate student Molly B. Reilly, wanted to know how brain cells in the C. elegans worm got their various shapes and functions. For these experiments, the researchers used a genetically engineered worm in which individual neurons were color coded. In addition, coding sequences for green fluorescence protein were inserted into homeobox genes, a highly conserved set of genes known to play fundamental roles in development. Homeobox gene expression patterns were determined by examining the patterns of the glowing fluorescent marker.

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 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 27428 - Posted: 08.20.2020

By Simon Makin New research could let scientists co-opt biology's basic building block—the cell—to construct materials and structures within organisms. A study, published in March in Science and led by Stanford University psychiatrist and bioengineer Karl Deisseroth, shows how to make specific cells produce electricity-carrying (or blocking) polymers on their surfaces. The work could someday allow researchers to build large-scale structures within the body or improve brain interfaces for prosthetic limbs. In the medium term, the technique may be useful in bioelectric medicine, which involves delivering therapeutic electrical pulses. Researchers in this area have long been interested in incorporating polymers that conduct or inhibit electricity without damaging surrounding tissues. Stimulating specific cells—to intervene in a seizure, for instance—is much more precise than flooding the whole organism with drugs, which can cause broad side effects. But current bioelectric methods, such as those using electrodes, still affect large numbers of cells indiscriminately. The new technique uses a virus to deliver genes to desired cell types, instructing them to produce an enzyme (Apex2) on their surface. The enzyme sparks a chemical reaction between precursor molecules and hydrogen peroxide, infused in the space between cells; this reaction causes the precursors to fuse into a polymer on the targeted cells. “What's new here is the intertwining of various emerging fields in one application,” says University of Florida biomedical engineer Kevin Otto, who was not involved in the research but co-authored an accompanying commentary in Science. “The use of conductive polymers assembled [inside living tissue] through synthetic biology, to enable cell-specific interfacing, is very novel.” © 2020 Scientific American

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 27411 - Posted: 08.11.2020

by Chloe Williams A new atlas lays bare how neuronal connections, or synapses, change from birth to old age in mice1. The ‘synaptome’ may help researchers investigate how mutations linked to autism affect these connections at different stages of life. Synapses are the junctions where information is transferred between cells, and they are integral to functions such as learning, behavior and movement. Autism is linked to several mutations that alter synaptic proteins. In 2018, researchers created the first synaptome of the mouse brain, mapping billions of synapses and sorting them into types based on their size, shape and composition2. The map revealed that synapse subtypes have distinct distributions in the brain, suggesting they have specific functions. This synaptome mapped the mouse brain only at one point in time, however. In the new work, the team charted five billion synapses in mice at 10 different ages, revealing how synapses change in number, structure and molecular makeup throughout life. “It’s the first time anybody’s ever done that in any species,” says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland, who led the research. To create the atlas, the team engineered mice to express fluorescent markers of different colors on two proteins — PSD95 and SAP102 — that frequently line the signal-receiving end of excitatory synapses, which make up the preponderance of synapses in the brain. Mutations in these proteins have been linked to autism, schizophrenia and intellectual disability. © 2020 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: 27402 - Posted: 08.06.2020

Ian Sample Science editor Doctors in France have reported what they believe to be the first proven case of Covid-19 being passed on from a pregnant woman to her baby in the womb. The newborn boy developed inflammation in the brain within days of being born, a condition brought on after the virus crossed the placenta and established an infection prior to birth. He has since made a good recovery. The case study, published in Nature Communications, follows the birth of a number of babies with Covid-19 who doctors suspect contracted the virus in the womb. Until now, they have not been able to rule out the possibility that the babies were infected during or soon after delivery. “Unfortunately there is no doubt about the transmission in this case,” said Daniele De Luca, medical director of paediatrics and neonatal critical care at the Antoine Béclère hospital in Paris. “Clinicians must be aware that this may happen. It’s not common, that’s for sure, but it may happen and it must be considered in the clinical workout.” The 23-year-old mother was admitted to the hospital on 24 March with a fever and severe cough after contracting coronavirus late in the third trimester. She tested positive for Covid-19 shortly her arrival. Three days after the woman was admitted, monitoring of the baby revealed signs of distress and doctors performed an emergency caesarean with the mother under general anaesthetic. The baby was immediately isolated in a neonatal intensive care unit and intubated because he was affected by the general anaesthetic. © 2020 Guardian News & Media Limited

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: 27366 - Posted: 07.15.2020

by Angie Voyles Askham An experimental drug prevents seizures and improves memory in a mouse model of fragile X syndrome, according to a new study1. The drug selectively blocks an enzyme that is overactive in the brains of people with fragile X and could offer a potential treatment for the condition. “It’s truly a novel target,” says co-lead investigator Mark Bear, professor of neuroscience at the Massachusetts Institute of Technology. Fragile X syndrome is characterized by intellectual disability, seizures, hyperactivity and, in one out of three people, autism. It results from mutations that diminish the gene FMR1’s production of FMRP, a protein that limits the synthesis of other proteins at synapses, where neurons exchange chemical messages. Without FMRP, according to one leading theory, proteins build up at synapses and disrupt this signaling, leading to fragile X’s outward signs. The new drug helps put the brakes on protein buildup by blocking a specific form of an enzyme called glycogen synthase kinase 3 (GSK3), which plays an important role during brain development. Previous trials have prevented protein buildup by blocking a different target, the mGluR5 receptor, which helps control protein production in neurons. But those drugs have failed in clinical trials because people have experienced adverse side effects and built up a tolerance to chronic dosing. The drug to block GSK3, called BRD0705, may result in fewer side effects because it is highly selective. The enzyme comes in two forms, known as alpha and beta, and BRD0705 blocks only the former. The findings should stimulate more research on GSK3 alpha, which has not been studied as well as its counterpart, researchers say. © 2020 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: 27355 - Posted: 07.11.2020

By Veronique Greenwood Planarians have unusual talents, to say the least. If you slice one of the tiny flatworms in half, the halves will grow back, giving you two identical worms. Cut a flatworm’s head in two, and it will grow two heads. Cut an eye off a flatworm — it will grow back. Stick an eye on a flatworm that lacks eyes — it’ll take root. Pieces as small as one-279th of a flatworm will turn into new, whole flatworms, given the time. This process of regeneration has fascinated scientists for more than 200 years, prompting myriad zany, if somewhat macabre, experiments to understand how it is possible for a complex organism to rebuild itself from scratch, over and over and over again. In a paper published Friday in Science, researchers revealed a tantalizing glimpse into how the worms’ nervous systems manage this feat. Specialized cells, the scientists report, point the way for neurons stretching from newly grown eyes to the brain of the worm, helping them connect correctly. The research suggests that cellular guides hidden throughout the planarian body may make it possible for the worm’s newly grown neurons to retrace their steps. Gathering these and other insights from the study of flatworms may someday help scientists interested in helping humans regenerate injured neurons. María Lucila Scimone, a researcher at M.I.T.’s Whitehead Institute for Biomedical Research, first noticed these cells while studying Schmidtea mediterranea, a planarian common to bodies of freshwater in Southern Europe and North Africa. During another experiment, she noted that they were expressing a gene involved in regeneration. The team looked more closely and realized that some of the regeneration-related cells were positioned at key branching points in the network of nerves between the worms’ eyes and their brains. When the researchers transplanted an eye from one animal to another, the neurons growing from the new eye always grew toward these cells. When the nerve cells reached their target, they kept growing along the route that would take them to the brain. Removing those cells meant the neurons got lost and did not reach the brain. © 2020 The New York Times Company

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 10: Vision: From Eye to Brain
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 7: Vision: From Eye to Brain
Link ID: 27340 - Posted: 07.01.2020

Amber Dance They told Marcelle Girard her baby was dead. Back in 1992, Girard, a dentist in Gatineau, Canada, was 26 weeks pregnant and on her honeymoon in the Dominican Republic. When she started bleeding, physicians at the local clinic assumed the baby had died. But Girard and her husband felt a kick. Only then did the doctors check for a fetal heartbeat and realize the baby was alive. The couple was medically evacuated by air to Montreal, Canada, then taken to the Sainte-Justine University Hospital Center. Five hours later, Camille Girard-Bock was born, weighing just 920 grams (2 pounds). Babies born so early are fragile and underdeveloped. Their lungs are particularly delicate: the organs lack the slippery substance, called surfactant, that prevents the airways from collapsing upon exhalation. Fortunately for Girard and her family, Sainte-Justine had recently started giving surfactant, a new treatment at the time, to premature babies. After three months of intensive care, Girard took her baby home. Today, Camille Girard-Bock is 27 years old and studying for a PhD in biomedical sciences at the University of Montreal. Working with researchers at Sainte-Justine, she’s addressing the long-term consequences of being born extremely premature — defined, variously, as less than 25–28 weeks in gestational age. Families often assume they will have grasped the major issues arising from a premature birth once the child reaches school age, by which time any neurodevelopmental problems will have appeared, Girard-Bock says. But that’s not necessarily the case. Her PhD advisers have found that young adults of this population exhibit risk factors for cardiovascular disease — and it may be that more chronic health conditions will show up with time.

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: 27279 - Posted: 06.04.2020

By Laura Sanders The heart has its own “brain.” Now, scientists have drawn a detailed map of this little brain, called the intracardiac nervous system, in rat hearts. The heart’s big boss is the brain, but nerve cells in the heart have a say, too. These neurons are thought to play a crucial role in heart health, helping to fine-tune heart rhythms and perhaps protecting people against certain kinds of heart disease. But so far, this local control system hasn’t been mapped in great detail. To make their map, systems biologist James Schwaber at Thomas Jefferson University in Philadelphia and colleagues imaged male and female rat hearts with a method called knife-edge scanning microscopy, creating detailed pictures of heart anatomy. Those images could then be built into a 3-D model of the heart. The scientists also plucked out individual neurons and measured the amount of gene activity within each cell. These measurements helped sort the heart’s neurons into discrete groups. Most of these neuron clusters dot the top of the heart, where blood vessels come in and out. Some of these clusters spread down the back of the heart, and were particularly abundant on the left side. With this new view of the individual clusters, scientists can begin to study whether these groups have distinct jobs. The comprehensive, 3-D map of the heart’s little brain could ultimately lead to targeted therapies that could treat or prevent heart diseases, the authors write online May 26 in iScience. © Society for Science & the Public 2000–2020.

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: 27274 - Posted: 06.03.2020

Jordana Cepelewicz In the 1990s, an army of clones invaded Germany. Within a decade, they had spread to Italy, Croatia, Slovakia, Hungary, Sweden, France, Japan and Madagascar — wreaking havoc in rivers and lakes, rice paddies and swamps; in waters warm and cold, acidic and basic. The culprits: six-inch-long, lobster-like creatures called marbled crayfish. Scientists suspect that sometime around 1995, a genetic mutation allowed a pet crayfish to reproduce asexually, giving rise to a new, all-female species that could make clones of itself from its unfertilized eggs. Deliberately or accidentally, some of these mutants were released from aquariums into the wild, where they rapidly multiplied into the millions, threatening native waterways species and ecosystems. But their success is strange. “All marbled crayfish which exist today derive from a single animal,” said Günter Vogt, a biologist at Heidelberg University. “They are all genetically identical.” Ordinarily, the absence of genetic diversity makes a population exceedingly vulnerable to the vagaries of its environment. Yet the marbled crayfish have managed to thrive around the globe. A closer look reveals that the crayfishes’ uniformity is only genome-deep. According to studies conducted by Vogt and others in the mid-2000s, these aquatic clones actually vary quite a bit in their color, size, behavior and longevity. Which means that something other than their genes is inspiring that diversity. Common sense tells us that if it’s not nature, it’s nurture: environmental influences that interact with an animal’s genome to generate different outcomes for various traits. But that’s not the whole story. New research on crayfish and scores of other organisms is revealing an important role for a third, often-overlooked source of variation and diversity — a surprising foundation for what makes us unique that begins in the first days of an embryo’s development: random, intrinsic noise. All Rights Reserved © 2020

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: 27139 - Posted: 03.24.2020

By Perri Klass, M.D. When you talk about sibling issues, everyone takes it personally. Whether it’s birth order and the supposed advantages of being the oldest (or youngest, or middle), or the question of having (or being) the favorite child, people tend to respond immediately with their own sometimes very individual and emotional stories. What I want to talk about today are sibling sex ratios — having a sibling of the other sex versus growing up in all-boy or all-girl sibling configurations. The most evocative phrase I’ve seen for this is “family constellations,” which I like because it suggests that there are lots of interesting — and even beautiful — arrangements, but that differences are real. But let’s take one step further back: Are there actually parents, or parent pairs, who are more likely to conceive boys or girls? Does the five-daughter family (from “Pride and Prejudice” or “Fiddler on the Roof”) or the seven-son setup (“Seven Brides for Seven Brothers”) just reflect five (or seven) random rolls of the dice, or is there actually something going on from an evolutionary point of view? The evolutionary theory, which has been advanced to explain sex ratio, goes back to Darwin, but was fully formulated in 1930 by a British scientist named Ronald Fisher, who made the argument that if individuals vary in the sex ratio among their offspring (that is, some are more likely to produce more males or more females), the reproductive advantage in a population will always lie with the rarer sex, and thus the sex ratio will equilibrate toward 1:1. After all, Fisher argued, half of the genetic material of the next generation must come by way of those who tend to produce males, and half from those who tend to produce females. But are there such tendencies? I’ve heard people say that having boys “runs in the family,” or that their cousins are almost all girls, that’s the “family pattern.” But a very large study of 4.7 million births in Sweden published in February in the journal Proceedings of the Royal Society argues that there is no evidence of a genetic tendency toward one sex or the other, or a family tendency. © 2020 The New York Times Company

Related chapters from BN: Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 13: Memory and Learning
Link ID: 27108 - Posted: 03.10.2020