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

By Rachel Nuwer In the years leading up to the roaring 2020s, young people were once again dropping acid. Onetime Harvard psychologist Timothy Leary died almost 25 years ago, after which some of his ashes were launched into space. But from 2015 to 2018, the rate of “turning on and tuning in” with LSD, to paraphrase Leary, increased by more than 50 percent in the U.S.—a rise perhaps fueled by a need for chemical escapism. Those results were published in the July issue of Drug and Alcohol Dependence. The authors of the study suspect that many users may be self-medicating with the illegal substance to find relief from depression, anxiety and general stress over the state of the world. “LSD is used primarily to escape. And given that the world’s on fire, people might be using it as a therapeutic mechanism,” says Andrew Yockey, a doctoral candidate in health education at the University of Cincinnati and lead author of the paper. “Now that COVID’s hit, I’d guess that use has probably tripled.” To arrive at their findings, Yockey and his colleagues turned to data collected from more than 168,000 American adults by the National Survey on Drug Use and Health, an annual, nationally representative questionnaire. They analyzed trends since 2015, partly because of the timing of the 2016 presidential election. The researchers found that past-year LSD use increased by 56 percent over three years. The rise was especially pronounced in certain user groups, including people with college degrees (who saw a 70 percent increase) and people aged 26 to 34 (59 percent), 35 to 49 (223 percent) and 50 or older (45 percent). Younger people aged 18 to 25, on the other hand, decreased their use by 24 percent. © 2020 Scientific American

Keyword: Drug Abuse; Stress
Link ID: 27356 - Posted: 07.11.2020

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

Keyword: Development of the Brain
Link ID: 27355 - Posted: 07.11.2020

Ian Sample Science editor Doctors may be missing signs of serious and potentially fatal brain disorders triggered by coronavirus, as they emerge in mildly affected or recovering patients, scientists have warned. Neurologists are on Wednesday publishing details of more than 40 UK Covid-19 patients whose complications ranged from brain inflammation and delirium to nerve damage and stroke. In some cases, the neurological problem was the patient’s first and main symptom. The cases, published in the journal Brain, revealed a rise in a life-threatening condition called acute disseminated encephalomyelitis (Adem), as the first wave of infections swept through Britain. At UCL’s Institute of Neurology, Adem cases rose from one a month before the pandemic to two or three per week in April and May. One woman, who was 59, died of the complication. A dozen patients had inflammation of the central nervous system, 10 had brain disease with delirium or psychosis, eight had strokes and a further eight had peripheral nerve problems, mostly diagnosed as Guillain-Barré syndrome, an immune reaction that attacks the nerves and causes paralysis. It is fatal in 5% of cases. “We’re seeing things in the way Covid-19 affects the brain that we haven’t seen before with other viruses,” said Michael Zandi, a senior author on the study and a consultant at the institute and University College London Hospitals NHS foundation trust. “What we’ve seen with some of these Adem patients, and in other patients, is you can have severe neurology, you can be quite sick, but actually have trivial lung disease,” he added. “Biologically, Adem has some similarities with multiple sclerosis, but it is more severe and usually happens as a one-off. Some patients are left with long-term disability, others can make a good recovery.” © 2020 Guardian News & Media Limited

Keyword: Stroke; Movement Disorders
Link ID: 27354 - Posted: 07.08.2020

Sherry H-Y. Chou Aarti Sarwal Neha S. Dangayach The patient in the case report (let’s call him Tom) was 54 and in good health. For two days in May, he felt unwell and was too weak to get out of bed. When his family finally brought him to the hospital, doctors found that he had a fever and signs of a severe infection, or sepsis. He tested positive for SARS-CoV-2, the virus that causes COVID-19 infection. In addition to symptoms of COVID-19, he was also too weak to move his legs. When a neurologist examined him, Tom was diagnosed with Guillain-Barre Syndrome, an autoimmune disease that causes abnormal sensation and weakness due to delays in sending signals through the nerves. Usually reversible, in severe cases it can cause prolonged paralysis involving breathing muscles, require ventilator support and sometimes leave permanent neurological deficits. Early recognition by expert neurologists is key to proper treatment. We are neurologists specializing in intensive care and leading studies related to neurological complications from COVID-19. Given the occurrence of Guillain-Barre Syndrome in prior pandemics with other corona viruses like SARS and MERS, we are investigating a possible link between Guillain-Barre Syndrome and COVID-19 and tracking published reports to see if there is any link between Guillain-Barre Syndrome and COVID-19. Some patients may not seek timely medical care for neurological symptoms like prolonged headache, vision loss and new muscle weakness due to fear of getting exposed to virus in the emergency setting. People need to know that medical facilities have taken full precautions to protect patients. Seeking timely medical evaluation for neurological symptoms can help treat many of these diseases. © 2010–2020, The Conversation US, Inc.

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27353 - Posted: 07.08.2020

Edmund Chong When you experience something with your senses, it evokes complex patterns of activity in your brain. One important goal in neuroscience is to decipher how these neural patterns drive the sensory experience. For example, can the smell of chocolate be represented by a single brain cell, groups of cells firing all at the same time or cells firing in some precise symphony? The answers to these questions will lead to a broader understanding of how our brains represent the external world. They also have implications for treating disorders where the brain fails in representing the external world: for example, in the loss of sight of smell. To understand how the brain drives sensory experience, my colleagues and I focus on the sense of smell in mice. We directly control a mouse’s neural activity, generating “synthetic smells” in the olfactory part of its brain in order to learn more about how the sense of smell works. Our latest experiments discovered that scents are represented by very specific patterns of activity in the brain. Like the notes of a melody, the cells fire in a unique sequence with particular timing to represent the sensation of smelling a unique odor. Using mice to study smell is appealing to researchers because the relevant brain circuits have been mapped out, and modern tools allow us to directly manipulate these brain connections. © 2010–2020, The Conversation US, Inc.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27352 - Posted: 07.08.2020

Jon Hamilton The same process that causes dew drops to form on a blade of grass appears to play an important role in Alzheimer's disease and other brain diseases. The process, known as phase transition, is what allows water vapor to condense into liquid water, or even freeze into solid ice. That same sort of process allows brain cells to constantly reorganize their inner machinery. But in degenerative diseases that include amyotrophic lateral sclerosis, frontotemporal dementia and Alzheimer's, the phase transitions inside neurons seem to go awry, says Dr. J. Paul Taylor, a neurogeneticist at St. Jude Children's Research Hospital in Memphis, and an investigator with the Howard Hughes Medical Institute. This malfunctioning prompts the interior of the cell to become too viscous, Taylor says. "It's as if you took a jar of honey [and] left it in the refrigerator overnight." In this sticky environment, structures that previously could nimbly disassemble and move around become "irreversibly glommed together," says Clifford Brangwynne, a professor of chemical and biological engineering at Princeton University and an investigator with the Howard Hughes Medical Institute. "And when they're irreversibly stuck like that, they can no longer leave to perform functions elsewhere in the cell." That glitch seems to allow toxins to begin to build up in and around these dysfunctional cells, Taylor says — including the toxins associated with Alzheimer's and other neurodegenerative diseases. The science behind this view of brain diseases has emerged only in the past decade. In 2009, Brangwynne was part of a team that published a study showing that phase transitions are important inside cells — or at least inside the reproductive cells of worms. © 2020 npr

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 27351 - Posted: 07.08.2020

By Gretchen Reynolds When we start to lift weights, our muscles do not strengthen and change at first, but our nervous systems do, according to a fascinating new study in animals of the cellular effects of resistance training. The study, which involved monkeys performing the equivalent of multiple one-armed pull-ups, suggests that strength training is more physiologically intricate than most of us might have imagined and that our conception of what constitutes strength might be too narrow. Those of us who join a gym — or, because of the current pandemic restrictions and concerns, take up body-weight training at home — may feel some initial disappointment when our muscles do not rapidly bulge with added bulk. In fact, certain people, including some women and most preadolescent children, add little obvious muscle mass, no matter how long they lift. But almost everyone who starts weight training soon becomes able to generate more muscular force, meaning they can push, pull and raise more weight than before, even though their muscles may not look any larger and stronger. Scientists have known for some time that these early increases in strength must involve changes in the connections between the brain and muscles. The process appears to involve particular bundles of neurons and nerve fibers that carry commands from the brain’s motor cortex, which controls muscular contractions, to the spinal cord and, from there, to the muscles. If those commands become swifter and more forceful, the muscles on the receiving end should respond with mightier contractions. Functionally, they would be stronger. But the mechanics of these nervous system changes have been unclear. Understanding the mechanics better could also have clinical applications: If scientists and doctors were to better understand how the nervous system changes during resistance training, they might be better able to help people who lose strength or muscular control after a stroke, for example, or as a result of aging or for other reasons. © 2020 The New York Times Company

Keyword: Muscles
Link ID: 27350 - Posted: 07.08.2020

Jordana Cepelewicz We consider the brain the very center of who we are and what we do: ruler of our senses, master of our movements; generator of thought, keeper of memory. But the brain is also rooted in a body, and the connection between the two goes both ways. If certain internal receptors indicate hunger, for instance, we’re driven to eat; if they indicate cold, we dress more warmly. However, decades of research have also shown that those sensations do much more than alert the brain to the body’s immediate concerns and needs. As the heart, lungs, gut and other organs transmit information to the brain, they affect how we perceive and interact with our environment in surprisingly profound ways. Recent studies of the heart in particular have given scientists new insights into the role that the body’s most basic processes play in defining our experience of the world. In the late 19th century, the psychologist William James and the physician Carl Lange proposed that emotional states are the brain’s perception of certain bodily changes in response to a stimulus — that a pounding heart or shallow breathing gives rise to emotions like fear or anger rather than vice versa. Researchers have since found many examples of physiological arousal leading to emotional arousal, but they wanted to delve deeper into that link. Beginning in the 1930s, scientists found that systole dampens pain and curbs startle reflexes. Further work traced this effect to the fact that during systole, pressure sensors send signals about the heart’s activity to inhibitory regions of the brain. This may be useful because, while the brain must constantly balance and integrate internal and external signals, “you cannot pay attention to everything at once,” said Ofer Perl, a postdoctoral research fellow at the Icahn School of Medicine at Mount Sinai in New York. Experiments even showed that people were more likely to forget words that were presented exactly at systole than words that they saw and encoded during the rest of the cardiac cycle. All Rights Reserved © 2020

Keyword: Emotions
Link ID: 27349 - Posted: 07.08.2020