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

By Matthew Sitman As I read George Scialabba’s new book How To Be Depressed, I recalled that I’d been introduced to his writing almost a decade ago by a schizophrenic, manic-depressive homeless man. R. might have protested that term—technically, he lived in a small garage that a fellow parishioner at the church we all attended let him use. It was shocking to visit him there for the first time; nearly every square inch of the place was filled with musty stacks of the New York Review of Books, assorted newspapers, and books, leaving only a narrow path that led to a mattress. Before adding something to one of these piles, he’d open his latest acquisition and run his finger down its pages, searching for matches or “sparks” that might cause a destructive fire—a phobia caused by a traumatic incident in R.’s childhood. My friends and I tried to look after R., taking him to dinner or paying his phone bill or letting him do laundry in our homes. I was drawn to R. partly because I couldn’t help but see some of myself in him, and had a gnawing fear that his plight would one day be my own. He was, in his way, an intellectual, who actually read at least a few of the periodicals he collected and enjoyed arguing about politics. I’d often see him in the local used bookstore I frequented, and that must have been where he pressed Scialabba’s What Are Intellectuals Good For? into my hands. “This is the good shit,” he solemnly professed, and he was right. R. had been an alcoholic, and I’d gleaned that when he finally kicked booze the withdrawal caused a breakdown from which he’d never quite recovered. I knew I sometimes drank too much, too, and for the wrong reasons—enough to watch myself. We shared both hypochondria and a dread of visiting the doctor. I wasn’t a manic depressive, but for much of the time I knew R. I was in the throes of the worst severe depression of my life. © 2020 Commonweal Magazine.

Keyword: Depression
Link ID: 27365 - Posted: 07.15.2020

Amy Fleming Taking a stroll with Shane O’Mara is a risky endeavour. The neuroscientist is so passionate about walking, and our collective right to go for walks, that he is determined not to let the slightest unfortunate aspect of urban design break his stride. So much so, that he has a habit of darting across busy roads as the lights change. “One of life’s great horrors as you’re walking is waiting for permission to cross the street,” he tells me, when we are forced to stop for traffic – a rude interruption when, as he says, “the experience of synchrony when walking together is one of life’s great pleasures”. He knows this not only through personal experience, but from cold, hard data – walking makes us healthier, happier and brainier. We are wandering the streets of Dublin discussing O’Mara’s book, In Praise of Walking, a backstage tour of what happens in our brains while we perambulate. Our jaunt begins at the grand old gates of his workplace, Trinity College, and takes in the Irish famine memorial at St Stephen’s Green, the Georgian mile, the birthplace of Francis Bacon, the site of Facebook’s new European mega-HQ and the salubrious seaside dwellings of Sandymount. O’Mara, 53, is in his element striding through urban landscapes – from epic hikes across London’s sprawl to more sedate ambles in Oxford, where he received his DPhil – and waxing lyrical about science, nature, architecture and literature. He favours what he calls a “motor-centric” view of the brain – that it evolved to support movement and, therefore, if we stop moving about, it won’t work as well. © 2020 Read It Later, Inc.

Keyword: Depression
Link ID: 27364 - Posted: 07.15.2020

by Sarah DeWeerdt The amygdala is a deep brain structure about the size and shape of an almond — from which it gets its name. It is commonly described as a center for detecting threats in the environment and for processing fear and other emotions. Researchers who study the region argue that its function is broader — and that it plays a crucial role in autism. “Emotion is such a big part in social function,” says Wei Gao, associate professor of biomedical sciences at Cedars-Sinai Medical Center in Los Angeles, California. “So I think the amygdala has got to have a big role in the emergence or development of autism-related traits.” The amygdala is the brain’s surveillance hub: involved in recognizing when someone with an angry face and hostile body language gets closer, tamping down alarm when a honeybee buzzes past, and paying attention when your mother teaches you how to cross the street safely and points out which direction traffic will be coming from — in other words, things people should run away from, but also those they should look toward, attend to and remember. In that sense, researchers say, this little knot of brain tissue shows just how tangled up emotion and social behavior are for humans. “Important events tend to be emotional in nature,” as do most aspects of social behavior, says John Herrington, assistant professor of psychiatry at the Children’s Hospital of Philadelphia in Pennsylvania. As a result, the amygdala has long been a focus of autism research, but its exact role in the condition is still unclear. © 2020 Simons Foundation

Keyword: Autism; Emotions
Link ID: 27363 - Posted: 07.15.2020

By Nicholas Bakalar Artificial outdoor light at night may disrupt adolescents’ sleep and raise the risk for psychiatric disorders, a new study suggests. Researchers tracked the intensity of outdoor light in representative urban and rural areas across the country using satellite data from the National Oceanic and Atmospheric Administration. They interviewed more than 10,123 adolescents living in these neighborhoods about their sleep patterns, and assessed mental disorders using well-validated structured scales. They also interviewed the parents of more than 6,000 of the teenagers about their children. The study, in JAMA Psychiatry, found that the more intense the lighting in your neighborhood, the more sleep was disrupted and the greater the risk for depression and anxiety. After adjustment for other factors such as sex, race, parental education and population density, they found that compared with the teenagers in the one-quarter of neighborhoods with the lowest levels of outdoor light, those in the highest went to bed, on average, 29 minutes later and reported 11 fewer minutes of sleep. Adolescents living in the most intensely lit neighborhoods had a 19 percent increased risk for bipolar illness, and a 7 percent increased risk for depression. The study is observational, and does not prove cause and effect. The senior author, Kathleen R. Merikangas, a senior investigator with the National Institute of Mental Health, said that future policy changes could make a difference. In the meantime, she said, “At least as individuals, we ought to try to minimize exposure to light at night.” © 2020 The New York Times Company

Keyword: Sleep; Biological Rhythms
Link ID: 27362 - Posted: 07.15.2020

By Erica Rex In 2012, I had my first psychedelic experiences, as a subject in a clinical trial at Johns Hopkins University School of Medicine’s Behavioral Pharmacology Research Unit. I was given two doses of psilocybin spaced a month apart to treat my cancer-related depression. During one session, deep within the world the drug evoked, I found myself inside a steel industrial space. Women were bent over long tables, working. I became aware of my animosity towards my two living siblings. A woman seated at the end of a table wearing a net cap and white clothes, turned and handed me a tall Dixie cup. “You can put that in here,” she said. The cup filled itself with my bilious, sibling-directed feelings. “We’ll put it over there.” She turned and placed the cup matter-of-factly on a table at the back of the room. Then she went back to her tasks. Whenever I speak with her, Mary Cosimano, the director of guide/facilitator services at Johns Hopkins Center for Psychedelic and Consciousness Research, mentions the women in the chamber and the cup. My experience struck a chord. For me, the women in the chamber have become a transcendent metaphor for emotional healing. “I’ve thought about having a necklace made, with the cup, as a momento,” she said the last time I saw her at a conference. “Have you thought about it?” Prior to their 1971 prohibition, psilocybin and LSD were administered to approximately 40,000 patients, among them people with terminal cancer, alcoholics and those suffering from depression and obsessive-compulsive disorder. The results of the early clinical studies were promising, and more recent research has been as well. The treatment certainly helped me. Eight years after my sessions, researchers continue to prove the same point again and again in an ongoing effort to turn psychedelic drug therapy into FDA-sanctioned medical treatment. This can’t happen soon enough. © 2020 Scientific American,

Keyword: Depression; Drug Abuse
Link ID: 27361 - Posted: 07.14.2020

By Anna Goldfarb It’s understandable that you may be struggling to fall asleep these days. Our world has been turned upside down, so it is especially hard to unplug from the day and get the high-quality sleep your body needs. “Almost every single patient I’m speaking with has insomnia,“ said Dr. Alon Y. Avidan, a professor and vice chair in the department of neurology at the David Geffen School of Medicine at the University of California, Los Angeles, and director of the U.C.L.A. Sleep Disorders Center. “Especially now with Covid-19, we have an epidemic of insomnia. We call it Covid-somnia.” An increase in anxiety in both children and adults is affecting our ability to fall asleep. Additionally, our lifestyles have changed drastically as people observe sheltering in place guidelines. With more people staying indoors, it can mean they are not getting enough light exposure. “Without light exposure in the morning,” Dr. Avidan said, people “lose the circadian cues that are so fundamentally important in setting up appropriate and normal sleep-wake time.” There are nonmedical ways to help you sleep better: Meditation, turning off screens early in the night, warm showers and cool bedrooms can help your body rest better. But if these options don’t work, or if you are ready for the next step, you may have considered trying melatonin supplements. These pills are commonplace enough that you have most likely heard of them and seen them in your local pharmacy. Here’s what you need to know about the pros and cons of using melatonin supplements for sleeping difficulties. What is melatonin? Melatonin is a hormone that helps regulate sleep timing. It is produced in the pea-size pineal gland, which is nestled in the middle of your brain and syncs melatonin production with the rising and setting of the sun. According to the National Sleep Foundation, the gland remains inactive during the day but switches on around 9 p.m. (when it’s generally dark) to flood the brain with melatonin for the next 12 hours. © 2020 The New York Times Company

Keyword: Sleep; Biological Rhythms
Link ID: 27360 - Posted: 07.14.2020

For every cell in the body there comes a time when it must decide what it wants to do for the rest of its life. In an article published in the journal PNAS, National Institutes of Health researchers report for the first time that ancient viral genes that were once considered “junk DNA” may play a role in this process. The article describes a series of preclinical experiments that showed how some human endogenous retrovirus (HERV-K) genes inscribed into chromosomes 12 and 19 may help control the differentiation, or maturation, of human stem cells into the trillions of neurons that are wired into our nervous systems. The experiments were performed by researchers in a lab led by Avindra Nath, M.D., clinical director, at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS). Over the course of evolution, the human genome has absorbed thousands of human endogenous retrovirus genes. As a result, nearly eight percent of the DNA that lines our chromosomes includes remnants of these genes. Although once thought to be inactive, or “junk”, recent studies have shown that these genes may be involved in human embryonic development, the growth of some tumors, and nerve damage during multiple sclerosis. Previously, researchers in Dr. Nath’s lab showed that amyotrophic lateral sclerosis (ALS) may be linked to activation of the HERV-K gene. In this study, led by Tongguang (David) Wang, M.D., Ph.D., staff scientist at NINDS, the team showed that deactivation of the gene may free stem cells to become neurons. The researchers performed most of their experiments on blood cells, drawn from healthy volunteers at the NIH’s Clinical Center, that they genetically transformed into induced pluripotent stem cells, which can then turn into any cell type in the body. Surprisingly, they found that the surfaces of the stem cells were lined with high levels of HERV-K, subtype HML-2, an envelope protein, that viruses often use to latch onto and infect cells. These proteins progressively disappeared as the cells were served two rounds of “cocktails.” One round nudged the cells into an intermediate, neural stem cell state followed by a second round that pushed the cells into finally becoming neurons.

Keyword: ALS-Lou Gehrig's Disease ; Development of the Brain
Link ID: 27359 - Posted: 07.14.2020

By Laura Sanders Exercise’s power to boost the brain might require a little help from the liver. A chemical signal from the liver, triggered by exercise, helps elderly mice keep their brains sharp, suggests a study published in the July 10 Science. Understanding this liver-to-brain signal may help scientists develop a drug that benefits the brain the way exercise does. Lots of studies have shown that exercise helps the brain, buffering the memory declines that come with old age, for instance. Scientists have long sought an “exercise pill” that could be useful for elderly people too frail to work out or for whom exercise is otherwise risky. “Can we somehow get people who can’t exercise to have the same benefits?” asks Saul Villeda, a neuroscientist at the University of California, San Francisco. Villeda and colleagues took an approach similar to experiments that revealed the rejuvenating effects of blood from young mice (SN: 5/5/14). But instead of youthfulness, the researchers focused on fitness. The researchers injected sedentary elderly mice with plasma from elderly mice that had voluntarily run on wheels over the course of six weeks. After eight injections over 24 days, the sedentary elderly mice performed better on memory tasks, such as remembering where a hidden platform was in a pool of water, than elderly mice that received injections from sedentary mice. Comparing the plasma of exercised mice with that of sedentary mice showed an abundance of proteins produced by the liver in mice that ran on wheels. The researchers closely studied one of these liver proteins produced in response to exercise, called GPLD1. GPLD1 is an enzyme, a type of molecular scissors. It snips other proteins off the outsides of cells, releasing those proteins to go do other jobs. Targeting these biological jobs with a molecule that behaves like GPLD1 might be a way to mimic the brain benefits of exercise, the researchers suspect. © Society for Science & the Public 2000–2020.

Keyword: Learning & Memory; Development of the Brain
Link ID: 27358 - Posted: 07.11.2020

By Jocelyn Kaiser It’s well established that exercise can sharpen the mind: People and mice who work out do better on cognitive tests, and elderly people who are physically active reduce their risk of dementia. Now, in a surprising finding, researchers report that blood from a mouse that exercises regularly can perk up the brain of a “couch potato” mouse. This effect, traced to a specific liver protein in the blood, could point the way to a drug that confers the brain benefits of exercise to an old or feeble person who rarely leaves a chair or bed. “Can your brain think that you exercised, from just something in your blood?” asks aging researcher Saul Villeda of the University of California, San Francisco (UCSF), who led the rodent research. The study grew out of research in Villeda’s lab and others suggesting blood from a young mouse can rejuvenate the brain and muscles of an old mouse. Some teams have since claimed to find specific proteins that explain the benefits of this “young blood.” Graduate student Alana Horowitz and postdoc Xuelai Fan in Villeda’s group wondered whether exercise—not just youth—could confer similar benefits via the blood. It was easy to enough to test: Put a wheel in a cage full of mice, and the mostly inactive animals will run for miles at night. The researchers collected blood from elderly or middle-aged mice that had an exercise wheel in their cage for 6 weeks and then transfused this blood into old mice without a wheel in their cage. Couch potato mice receiving this blood eight times over 3 weeks did nearly as well on learning and memory tests, such as navigating through a maze, as the exercising mice. A control group of couch potatoes receiving blood from similarly old, nonexercising mice saw no boost. The rodents getting the blood from the active mice also grew roughly twice as many new neurons in the hippocampus, a brain region involved in learning and memory, Villeda’s team reports today in Science. That change is comparable to what’s seen in rodents that directly exercise. © 2020 American Association for the Advancement of Science.

Keyword: Alzheimers; Development of the Brain
Link ID: 27357 - Posted: 07.11.2020