Jon Hamilton For years, public health officials have been trying to dispel the myth that people who get a flu shot are more likely to get Alzheimer's disease. They are not. And now there is evidence that vaccines that protect against the flu and pneumonia may actually protect people from Alzheimer's, too. The evidence comes from two studies presented Monday at this year's Alzheimer's Association International Conference, which is being held as a virtual event. "We've always known that vaccines are very important to our overall health," says Maria Carrillo, chief science officer of the Alzheimer's Association. "And maybe they even contribute to protecting our memory, our cognition, our brain." The first study came from a team at the University of Texas that combed through millions of medical records in a national database. The goal was to find factors that affected a person's risk of getting certain diseases, including Alzheimer's. "And one of the things that came back was flu shots," says Albert Amran, a medical student of the McGovern Medical School at the University of Texas Health Science Center in Houston and an author of the study. That seemed odd. So Amran and a team of researchers took a closer look at the medical records of about 9,000 people who were at least 60 years old. Some had received a seasonal flu shot. Some hadn't. "We [tried] to make sure that both groups had an equal amount of, say, smoking status, obesity, diabetes, cardiovascular disease," Amran says. Those are known risk factors for Alzheimer's. The team also looked at factors like education and income, and indicators like the number of prescriptions a person had received, to make sure that people who got vaccines weren't just healthier overall. They weren't. © 2020 npr

Keyword: Alzheimers; Neuroimmunology
Link ID: 27385 - Posted: 07.27.2020

Can a video game help children struggling with ADHD? That question inspired hopeful headlines last month after the Food and Drug Administration permitted marketing of the first digital game that may be prescribed to treat children ages 8 to 12 who have been diagnosed with attention-deficit/hyperactivity disorder. In EndeavorRx, designed for iPhones and iPads, children guide an avatar surfing through molten lava and an icy river, dodging fires and icebergs while grabbing flying objects. The game is not yet available for purchase, nor has a price been released, but its Boston-based developer, Akili Interactive Labs, may now feature its unique status in ads and pursue coverage by insurance plans. No trip to the pharmacy is needed: Doctors and nurses will be able to prescribe the game by giving parents a code to download an app. Akili’s website touts its digital approach as “the future of medicine.” But some critics say: Not so fast. “It’s a marketing ploy,” said clinical psychologist and researcher Russell Barkley, author of several books on ADHD. Barkley and three other ADHD experts who reviewed Akili’s research said the firm was overpromising by implying that EndeavorRx can provide meaningful help for children struggling in school and at home with the sometimes-debilitating neurodevelopmental disorder, whose symptoms include distraction, forgetfulness and impulsivity. “I’m a little shocked and more perplexed about why the FDA would approve this and allow it to be paid for by insurance,” said Mark Rapport, head of the Children’s Learning Clinic at the University of Central Florida, who has published extensive research on other brain-training programs making similar claims. “I abhor seeing desperate parents spend money based on empty promises. . . . On moral grounds, I think it’s wrong to tell people to get their doctors to prescribe this when it does nothing of real-world importance.”

Keyword: ADHD
Link ID: 27384 - Posted: 07.27.2020

Masakazu (Mark) Konishi, the Bing Professor of Behavioral Biology, Emeritus, passed away on July 23. He was 87 years old. Renowned for his work on the neuroscience underlying the behavior of owls and songbirds, Konishi joined the Caltech faculty as a professor of biology in 1975, becoming the Bing Professor of Behavioral Biology in 1980. Since the early 1960s, Konishi was a leader in the field of avian neuroethology—the neurobiological study of natural behavior, such as prey capture by owls and singing in songbirds. In his laboratory at Caltech, Konishi advised dozens of graduate students and postdoctoral scholars. His team worked extensively on the auditory systems of barn owls, which use their acute hearing to home in on prey on the ground, even in total darkness. Konishi was the first to theorize that young birds initially remember a tutor song and use the memory as a template to guide the development of their own song. Konishi was born in Kyoto, Japan, on February 17, 1933. He attended Hokkaido University in Sapporo, Japan, for his bachelor and master of science degrees, after which he attended the UC Berkeley for his PhD. Under Berkeley professor Peter Marler, Konishi focused his doctoral research on the idea of central coordination. Konishi began a full professorship at Caltech in 1975. He was the Bing Professor of Behavioral Biology until his retirement in 2013. From 1977 to 1980, Konishi served as the division's executive officer for biology.

Keyword: Animal Communication; Language
Link ID: 27383 - Posted: 07.27.2020

Ewen Callaway Despite their rough and tumble existence, Neanderthals had a biological predisposition to a heightened sense of pain, finds a first-of-its kind genome study published in Current Biology on 23 July1. Evolutionary geneticists found that the ancient human relatives carried three mutations in a gene encoding the protein NaV1.7, which conveys painful sensations to the spinal cord and brain. They also showed that in a sample of British people, those who had inherited the Neanderthal version of NaV1.7 tend to experience more pain than others. “It’s a first example, to me, about how we begin to perhaps get an idea about Neanderthal physiology by using present-day people as transgenic models,” says Svante Pääbo at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, who led the work with Hugo Zeberg at the Karolinska Institute in Stockholm. Pain-sensing protein Researchers have access to only a few Neanderthal genomes, and most of those have been sequenced at a low resolution. This has made it hard to identify mutations that evolved after their lineage split from that of humans some 500,000–750,000 years ago. But in the past few years, Pääbo and his team have generated three high-quality Neanderthal genomes from DNA found in caves in Croatia and Russia. This allows them to confidently identify mutations that were probably common in Neanderthals, yet very rare in humans. Mutations in a gene called SCN9A — which encodes the NaV1.7 protein — stood out because all of the Neanderthals had three mutations that alter the shape of the protein. The mutated version of the gene was found on both sets of chromosomes in all three Neanderthals, hinting that it was common across their populations. © 2020 Springer Nature Limited

Keyword: Pain & Touch; Evolution
Link ID: 27382 - Posted: 07.25.2020

By Karen Kwon, Liz Tormes In 1968 an exhibit entitled Cybernetic Serendipity: The Computer and the Arts was held at the Institute of Contemporary Arts in London. The first major event of its kind, Cybernetic Serendipity’s aim was to “present an area of activity which manifests artists’ involvement with science, and the scientists’ involvement with the arts,” wrote British art critic Jasia Reichardt, who curated the exhibit. Even though it was an art show, “most of the participants in the exhibition were scientists,” Reichardt said in a 2014 video. “Artists didn’t have computers in the 1960s.” A lot has changed since then, however. Computers, no longer the commodity of a select few, help artists to deviate from more traditional mediums. The changes since the 1960s are well-reflected in the entries for the 2020 Art of Neuroscience competition, held by the Netherlands Institute for Neuroscience. Now marking its 10th year, the contest features some highly technological pieces and others grounded in classical methods, such as drawing with pen on paper. The winning entries were created by independent artists, as well as working scientists, demonstrating that art and neuroscience can inspire both professions. A winner and four honorable mentions were selected from dozens of submitted works. And seven pieces were chosen by Scientific American as Editors’ Picks. (Photography editor Liz Tormes served on the panel of judges for the competition.) © 2020 Scientific American

Keyword: Brain imaging
Link ID: 27381 - Posted: 07.25.2020

by Peter Hess / Infants with particular patterns of electrical activity in the brain go on to have high levels of autism traits as toddlers, a new study shows1. Specifically, babies who have unusually high or low synchrony between certain brain waves — as measured by electroencephalography (EEG) — at 3 months old tend to score high on a standardized scale of autism-linked behaviors when they are 18 months old. These levels of synchrony reflect underlying patterns of connectivity in the brain. The findings suggest that EEG could help clinicians identify autistic babies long before these children show behaviors flagged by standard diagnostic tests. The work “reinforces the concept and the truism that brain development is affected before autism diagnoses are made,” says lead researcher Shafali Spurling Jeste, associate professor of psychiatry and neurology at the University of California, Los Angeles. “We believe that we could work to start rewiring the brain if we intervene effectively and early enough. That message, quite simply, is a very important one.” The study involved ‘baby sibs,’ the younger siblings of autistic children. Baby sibs are 10 to 20 times more likely to have autism than the general population. Previous research showed similar patterns of altered connectivity in functional magnetic resonance imaging (MRI) data from infants who were later diagnosed with autism, but MRI is costly and prone to errors. EEG measurements, on the other hand, are relatively inexpensive and simple to perform, which makes them more practical for clinical use, says Charles Nelson, professor of pediatrics and neuroscience at Harvard University, who was not involved in the study. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27380 - Posted: 07.25.2020

Laura P.W. Ranum An FDA-approved diabetes drug shows early signs of promise against the most common genetic form of amyotrophic lateral sclerosis, a devastating neurological condition that causes paralysis. ALS is a progressive disease that affects neurons in the brain and spinal cord. Motor neurons transmit signals from our brain to our muscles and allow us to move. ALS causes these motor neurons to die, resulting in the loss of a patient’s ability to speak, eat, move and breathe. Notable ALS patients include New York Yankees baseball star Lou Gehrig (the disease is often called Lou Gehrig’s disease), physicist Stephen Hawking and New Orleans Saints football star Steve Gleason. There are currently more than 30,000 cases of ALS in the United States, and life expectancy after diagnosis is typically 2 to 5 years. There is currently no cure for ALS. I am a scientist who studies neurological diseases that run in families, and I have been working hard to find a treatment to stop ALS. Our team has made a discovery, detailed in a scientific study, that paves the way for further research for improving disease in a genetic type of ALS caused by a mutation in a gene with the unwieldy name chromosome 9 open reading frame 72 (C9orf72), based on its location on chromosome 9. In addition to ALS, mutations in this gene can also cause frontotemporal dementia, which can cause apathy, loss of emotional control and cognitive decline. Some patients with the C9orf72 mutation develop ALS, others develop frontotemporal dementia and some develop both. Together, these diseases are referred to here as C9-ALS/FTD. I have been focusing on C9-ALS, which is the most common genetic type of ALS which is caused by a mutation in the C9orf72 gene. The mutation occurs when six letters of DNA that make up part of the gene’s genetic code – GGGGCC – are repeated hundreds of extra times. It is as if a single word is repeated hundreds of times in the same sentence. © 2010–2020, The Conversation US, Inc.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27379 - Posted: 07.21.2020

By Jane E. Brody Michael Richard Clifford, a 66-year-old retired astronaut living in Cary, N.C., learned before his third spaceflight that he had Parkinson’s disease. He was only 44 and in excellent health at the time, and had no family history of this disabling neurological disorder. What he did have was years of exposure to numerous toxic chemicals, several of which have since been shown in animal studies to cause the kind of brain damage and symptoms that afflict people with Parkinson’s. As a youngster, Mr. Clifford said, he worked in a gas station using degreasers to clean car engines. He also worked on a farm where he used pesticides and in fields where DDT was sprayed. Then, as an aviator, he cleaned engines readying them for test flights. But at none of these jobs was he protected from exposure to hazardous chemicals that are readily inhaled or absorbed through the skin. Now Mr. Clifford, a lifelong nonsmoker, believes that his close contact with these various substances explains why he developed Parkinson’s disease at such a young age. Several of the chemicals have strong links to Parkinson’s, and a growing body of evidence suggests that exposure to them may very well account for the dramatic rise in the diagnosis of Parkinson’s in recent decades. To be sure, the medical literature is replete with associations between people’s habits and exposures and their subsequent risk of developing various ailments, from allergies to heart disease and cancer. Such linkages do not — and cannot by themselves — prove cause and effect. Sometimes, though, the links are so strong and the evidence so compelling that there can be little doubt that one causes the other. The link of cigarette smoking to lung cancer is a classic example. Despite tobacco industry claims that there was no definitive proof, the accumulation of evidence, both experimental and epidemiological, eventually made it impossible to deny that years of smoking can cause cancer even long after a person has quit. © 2020 The New York Times Company

Keyword: Parkinsons; Neurotoxins
Link ID: 27378 - Posted: 07.21.2020

A scientific analysis of more than 2,000 brain scans found evidence for highly reproducible sex differences in the volume of certain regions in the human brain. This pattern of sex-based differences in brain volume corresponds with patterns of sex-chromosome gene expression observed in postmortem samples from the brain’s cortex, suggesting that sex chromosomes may play a role in the development or maintenance of sex differences in brain anatomy. The study, led by researchers at the National Institute of Mental Health (NIMH), part of the National Institutes of Health, is published in Proceedings of the National Academy of Sciences. “Developing a clearer understanding of sex differences in human brain organization has great importance for how we think about well-established sex differences in cognition, behavior, and risk for psychiatric illness. We were inspired by new findings on sex differences in animal models and wanted to try to close the gap between these animal data and our models of sex differences in the human brain,” said Armin Raznahan, M.D., Ph.D., study co-author and chief of the NIMH Section on Developmental Neurogenomics. Researchers have long observed consistent sex-based differences in subcortical brain structures in mice. Some studies have suggested these anatomical differences are largely due to the effects of sex hormones, lending weight to a “gonad-centric” explanation for sex-based differences in brain development. However, more recent mouse studies have revealed consistent sex differences in cortical structures, as well, and gene-expression data suggest that sex chromosomes may play a role in shaping these anatomical sex differences. Although the mouse brain shares many similarities with the human brain, it is not clear whether these key findings in mice also apply to humans.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 27377 - Posted: 07.21.2020

Ruairi J MacKenzie Research into developing treatments for psychiatric illness is missing out vital data from female animals, producing drugs that aren’t optimized for women and contributing to the failure of clinical trials, said a panel of neuroscientists today at FENS Virtual Forum of Neuroscience. In a press conference, Professor Christina Dalla from the National and Kapodistrian University of Athens, Dr Debra Bangasser from Temple University and Professor Mohammed Milad at New York University Grossman School of Medicine spoke of the impacts of the inequitable use of female animals on their research areas. Dalla reviewed the targeting of the hypothalamic–pituitary–adrenal (HPA) axis using antidepressants. The HPA axis is a major neuroendocrine system that regulates responses to stress and many other bodily processes. Dysfunctions in the HPA axis have long thought to be a factor in the onset of depression, but drugs targeting this axis have roundly failed in clinical trials. Dalla proposed that this failure may partly be the result of pre-clinical studies using male animals, followed by clinical trials that often recruit more women than men. Bangasser and Milad respectively showed how responses to stress and fear also vary between male and female mice. The Forum, held online for the first time, has extensively addressed the representation of women in the field in its program, opening with a Mini-Conference led by the Cajal Club that celebrated the impact of women in the development of neuroscience.

Keyword: Sexual Behavior
Link ID: 27376 - Posted: 07.21.2020

by Angie Voyles Askham The autism gene SHANK3 is crucial for the development and function of muscles and the motor neurons that control them, according to a new study1. This relationship may explain why some people with mutations in the gene have low muscle tone, says co-lead investigator Maria Demestre, senior researcher at the Institute for Bioengineering of Catalonia in Barcelona. “It opens an avenue for treatment.” Between 1 and 2 percent of people with autism have a mutation in SHANK3. Deletions of the chromosomal region containing SHANK3 lead to Phelan-McDermid syndrome, characterized by intellectual disability, speech delay and, often, autism. One of the earliest signs of the syndrome in infants is hypotonia, or low muscle tone, which can result in difficulty feeding and a delay in reaching developmental milestones such as crawling and walking. SHANK3 encodes a protein that helps neurons communicate throughout the brain. But studies have shown that the gene is also found in other parts of the body and that mutations or deletions of genes in peripheral cells can contribute to autism traits2. SHANK3 is heavily expressed throughout the motor system of both mice and people, the new work shows. Muscle cells derived from people with Phelan-McDermid syndrome fail to mature, and mice deficient in SHANK3 have poor muscle function. The results add to “the growing appreciation of the role of autism-associated genes — in this case, SHANK3 — outside of the brain,” says David Ginty, professor of neurobiology at Harvard Medical School, who was not involved in the study. © 2020 Simons Foundation

Keyword: Autism; Movement Disorders
Link ID: 27375 - Posted: 07.21.2020

By Erik Stokstad Dogs are renowned for their world-class noses, but a new study suggests they may have an additional—albeit hidden—sensory talent: a magnetic compass. The sense appears to allow them to use Earth’s magnetic field to calculate shortcuts in unfamiliar terrain. The finding is a first in dogs, says Catherine Lohmann, a biologist at the University of North Carolina, Chapel Hill, who studies “magnetoreception” and navigation in turtles. She notes that dogs’ navigational abilities have been studied much less compared with migratory animals such as birds. “It’s an insight into how [dogs] build up their picture of space,” adds Richard Holland, a biologist at Bangor University who studies bird navigation. There were already hints that dogs—like many animals, and maybe even humans—can perceive Earth’s magnetic field. In 2013, Hynek Burda, a sensory ecologist at the Czech University of Life Sciences Prague who has worked on magnetic reception for 3 decades, and colleagues showed dogs tend to orient themselves north-south while urinating or defecating. Because this behavior is involved in marking and recognizing territory, Burda reasoned the alignment helps dogs figure out the location relative to other spots. But stationary alignment isn’t the same thing as navigation. In the new study, Burda’s graduate student, Kateřina Benediktová, initially put video cameras and GPS trackers on four dogs and took them on trips into the forest. The dogs would scamper off to chase the scent of an animal for 400 meters on average. The GPS tracks showed two types of behavior during their return trips to their owner (see map, below). In one, dubbed tracking, a dog would retrace its original route, presumably following the same scent. In the other behavior, called scouting, the dog would return along a completely new route, bushwhacking without any backtracking. Benediktová et al., eLife (2020) 10.7554 (CC BY) © 2020 American Association for the Advancement of Science.

Keyword: Animal Migration
Link ID: 27374 - Posted: 07.18.2020

Salvatore Domenic Morgera How the brain works remains a puzzle with only a few pieces in place. Of these, one big piece is actually a conjecture: that there’s a relationship between the physical structure of the brain and its functionality. The brain’s jobs include interpreting touch, visual and sound inputs, as well as speech, reasoning, emotions, learning, fine control of movement and many others. Neuroscientists presume that it’s the brain’s anatomy – with its hundreds of billions of nerve fibers – that make all of these functions possible. The brain’s “living wires” are connected in elaborate neurological networks that give rise to human beings’ amazing abilities. It would seem that if scientists can map the nerve fibers and their connections and record the timing of the impulses that flow through them for a higher function such as vision, they should be able to solve the question of how one sees, for instance. Researchers are getting better at mapping the brain using tractography – a technique that visually represents nerve fiber routes using 3D modeling. And they’re getting better at recording how information moves through the brain by using enhanced functional magnetic resonance imaging to measure blood flow. But in spite of these tools, no one seems much closer to figuring out how we really see. Neuroscience has only a rudimentary understanding of how it all fits together. To address this shortcoming, my team’s bioengineering research focuses on relationships between brain structure and function. The overall goal is to scientifically explain all the connections – both anatomical and wireless – that activate different brain regions during cognitive tasks. We’re working on complex models that better capture what scientists know of brain function. t © 2010–2020, The Conversation US, Inc.

Keyword: Brain imaging
Link ID: 27373 - Posted: 07.18.2020

by Jonathan Moens / Autistic people with deletions in the chromosomal region 22q11.2 have a brain structure that’s distinct from that of autistic people without the deletions, according to a new brain imaging study1. The findings suggest that brain changes related to autism vary depending on the condition’s etiology, says study investigator Carrie Bearden, professor of clinical psychology at the University of California, Los Angeles. “[Autism is] really not one thing.” Deletions in 22q11.2 cause a syndrome characterized by heart defects, learning difficulties and an increased risk of psychiatric conditions such as schizophrenia. About 16 percent of people with the syndrome have autism2. Brain anatomy differs between people with the syndrome who have autism and those who do not, past studies by the same team show3. The new work is the first to compare these two groups with people who have ‘idiopathic’ autism, meaning its etiology is unknown. Disentangling these brain differences may be key to understanding if clinicians should treat autistic people with 22q deletions differently than people with autism without the deletions, Bearden says. “Maybe we’re treating these [conditions] as all the same at one level when we really need to dissect this a bit more.” Some experts say these findings could also be a first step toward dividing autism’s broad spectrum of traits into smaller sets of genetic conditions. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27372 - Posted: 07.18.2020

By Serena Puang When I was in elementary school, I occasionally had trouble falling asleep, and people would tell me to count sheep. I had seen the activity graphically depicted in cartoons, but when I tried it, I never saw anything — just black. I’ve been counting silently into the darkness for years. There were other puzzling comments about visualizing things. My dad would poke fun at my bad sense of direction and reference a “mental map” of the city that he used for navigation. I thought he had superhuman powers. But then, in my freshman year of college, I was struggling through Chinese, while my friend Shayley found it easy. I asked her how she did it, and she told me she was just “visualizing the characters.” That’s when I discovered I had aphantasia, the inability to conjure mental images. Little is known about the condition, but its impact on my education led me to wonder about how it might be impacting others. Aphantasia was first described by Sir Francis Galton in 1880 but remained largely neglected until Dr. Adam Zeman, a cognitive neurologist at the University of Exeter in England, began his work in the early 2000s and coined the name from the Greek word “phantasia,” which means “imagination.” “My interest in it was sparked by a patient who had lost the ability to visualize following a cardiac procedure,” Dr. Zeman said. “He gave a very compelling account. His dreams became avisual; he ceased to enter a visual world when he read a novel.” Dr. Zeman wrote about the case, calling the patient MX, and in 2010, the science journalist Carl Zimmer wrote about it in Discover magazine, and later, in The Times. Hundreds of people started contacting Dr. Zeman, saying they were just like MX, except that they had never had the ability to visualize. © 2020 The New York Times Company

Keyword: Attention
Link ID: 27371 - Posted: 07.16.2020

Kayt Sukel A 44-year-old male patient, with no history of cardiovascular disease, arrived at an emergency room in New York City after experiencing difficulty speaking and moving the right side of his body. The on-call physician quickly determined he had suffered a stroke—a condition that normally affects people who are decades older. In Italy, a 23-year-old man sought care for a complete facial palsy and feelings of “pins and needles” in his legs. Doctors discovered axonal sensory-motor damage suggesting Guillain Barré Syndrome, a rare autoimmune neurological disorder where the immune system, sometimes following an infection, mistakes some of the body’s own peripheral nerve cells as foreign invaders and attacks them. A 58-year-old woman in Detroit was rushed to the hospital with severe cognitive impairment, unable to remember anything beyond her own name. MRI scans showed widespread inflammation across the patient’s brain, leading doctors to diagnose a rare but dangerous neurological condition called acute necrotizing hemorrhagic encephalopathy. At first glance, it may seem that these patients have little in common. Yet all three were also suffering from severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) disease, better known as Covid-19. While most individuals infected with this new virus exhibit fever, cough, and respiratory symptoms, doctors across the globe are also documenting patients presenting with a handful of neurological manifestations—leading clinicians and researchers to wonder if Covid-19 also has the ability to invade the human nervous system. “As more people are being tested and diagnosed with this virus, physicians are starting to see more uncommon symptoms and complications, including neurological ones,” says Diane Griffin, M.D., Ph.D., a researcher at Johns Hopkins University’s Bloomberg School of Public Health. “But as Covid-19 is a new virus, we aren’t yet sure why these things are happening. Is the virus getting into the brain directly? Is it affecting the brain through other means? These are important questions to answer.” © 2020 The Dana Foundation

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27370 - Posted: 07.16.2020

by Chloe Williams A new wireless device activates a mouse’s neurons as it navigates a cage with food, hiding places and other mice, allowing researchers to study social behavior in a realistic environment1. Experiments using this setup suggest that oxytocin has distinct effects in different contexts — which may be particularly important as researchers explore the hormone’s value as a potential treatment for autism. The device makes use of optogenetics, a technique in which researchers use pulses of light to activate or silence neurons. Autism researchers have used the approach to manipulate neural circuits in mice, but traditional optogenetic devices involve a fiber-optic cable, which tethers the animal and interferes with social interactions. Other wireless devices have been able to activate neurons without a tether, but researchers have mostly used them to study social behavior involving just two mice interacting for only about 15 minutes in an otherwise empty cage — a scenario that fails to capture a full range of mouse behaviors2. The new wireless device, powered by two watch batteries, consists of a light-emitting diode attached to an optical fiber that is implanted into the brain. It has an on-off switch that allows researchers to control it remotely using a magnet placed inside the cage. Using this setup, researchers can modulate brain activity in a group of mice as they roam for days through a cage that has hiding places, platforms, a nest, food and water. The device’s designers tested it in mice engineered to express light-sensitive proteins in part of the hypothalamus. This region produces the hormone oxytocin, generally thought to reduce aggression and enhance social bonds. When delivered as a nasal spray, it improves social skills in some people with autism. © 2020 Simons Foundation

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 27369 - Posted: 07.16.2020

By Gretchen Reynolds Exercise may help change exercisers’ brains in surprising ways, according to a new study of physical activity and brain health. The study, which included both mice and people, found that exercise prompts the liver to pump out a little-known protein, and that chemically upping the levels of that protein in out-of-shape, elderly animals rejuvenates their brains and memories. The findings raise provocative questions about whether the brain benefits of exercise might someday be available in a capsule or syringe form — essentially “exercise in a pill.” We already have considerable evidence, of course, that physical activity protects brains and minds from some of the declines that otherwise accompany aging. In past rodent studies, animals that ran on wheels or treadmills produced more new neurons and learned and remembered better than sedentary mice or rats. Similarly, older people who took up walking for the sake of science added tissue volume in portions of their brains associated with memory. Even among younger people, those who were more fit than their peers tended to perform better on cognitive tests. But many questions remain unanswered about how, at a cellular level, exercise remodels the brain and alters its function. Most researchers suspect that the process involves the release of a cascade of substances inside the brain and elsewhere in the body during and after exercise. These substances interact and ignite other biochemical reactions that ultimately change how the brain looks and works. But what the substances are, where they originate and how they meet and mingle has remained unclear. So, for the new study, which was published this month in Science, researchers at the University of California, San Francisco, and other institutions decided to look inside the minds and bloodstreams of mice. In past research from the same lab, the scientists had infused blood from young mice into older ones and seen improvements in the aging animals’ thinking. It was like “transferring a memory of youth through blood,” says Saul Villeda, a professor at U.C.S.F., who conducted the study with his colleagues Alana Horowitz, Xuelai Fan and others. © 2020 The New York Times Company

Keyword: Hormones & Behavior
Link ID: 27368 - Posted: 07.16.2020

By Baland Jalal Imagine waking up in the middle of the night to an unearthly figure with blood dripping down its fangs. You try to scream, but you can’t. You can’t move a single muscle! If this sounds familiar, you’ve probably experienced an episode of sleep paralysis, which involves the inability to move or speak upon falling asleep or awakening and is often coupled with hallucinations. About one in five people have had sleep paralysis at least once. But despite its prevalence, it has largely remained a mystery. For centuries, cultures across the world have attributed these hallucinations to black magic, mythical monsters, even paranormal activity. Scientists have since dismissed such explanations, yet these cultural beliefs persist. In fact, my and my colleagues’ research, conducted over roughly a decade in six different countries, suggests that beliefs about sleep paralysis can dramatically shape the physical and psychological experience, revealing a striking type of mind-body interaction. Sleep paralysis is caused by what appears to be a basic brain glitch at the interface between wakefulness and rapid eye movement (REM) sleep. During REM, you have intensely lifelike dreams. To prevent you from acting out these realistic dreams (and hurting yourself!), your brain has a clever solution: it temporarily paralyzes your entire body. Indeed, your brain has a “switch” (a handful of neurochemicals) that tilts you between sleep and wakefulness. Sometimes the “switch” fails, however—your brain inadvertently wakes up while your body is still under the “spell” of REM paralysis, leaving you stuck in a paradoxical state between parallel realities: wakefulness and REM sleep. During sleep paralysis, the crisp dreams of REM “spill over” into waking consciousness like a dream coming alive before your eyes—fanged figures and all. © 2020 Scientific American

Keyword: Sleep
Link ID: 27367 - Posted: 07.16.2020

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

Keyword: Development of the Brain
Link ID: 27366 - Posted: 07.15.2020