Chapter 15. Emotions, Aggression, and Stress

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By Knvul Sheikh There is some truth to the longstanding anecdote that your locks can lose color when you’re stressed. A team of researchers has found that in mice, stressful events trigger damage the stem cells that are responsible for producing pigment in hair. These stem cells, found near the base of each hair follicle, differentiate to form more specialized cells called melanocytes, which generate the brown, black, red and yellow hues in hair and skin. Stress makes the stem cells differentiate faster, exhausting their number and resulting in strands that are more likely to be transparent — gray. The study, published Wednesday in Nature, also found that the sympathetic nervous system, which prepares the body to respond to threats, plays an important role in the graying process. “Normally, the sympathetic nervous system is an emergency system for fight or flight, and it is supposed to be very beneficial or, at the very least, its effects are supposed to be transient and reversible,” said Ya-Chieh Hsu, a stem cell biologist at Harvard University who led the study. The sympathetic nervous system helps mobilize many biological responses, including increasing the flow of blood to muscles and sharpening mental focus. But the researchers found that in some cases the same system of nerves permanently depleted the stem cell population in hair follicles. The findings provide the first scientific link between stress and hair graying, Dr. Hsu said. Stress affects the whole body, so the researchers had to do some sleuthing to figure out which physiological system was conveying its effects to hair follicles. At first, the team hypothesized that stress might cause an immune attack on melanocyte stem cells. They exposed mice to acute stress by injecting the animals with an analogue of capsaicin, the chemical in chili peppers that causes irritation. But even mice that lacked immune cells ended up with gray hair. Next, the scientists looked at the effects of the stress hormone cortisol. Mice that had their adrenal glands removed so they couldn’t produce cortisol still had hair that turned gray under stress. © 2020 The New York Times Company

Keyword: Stress
Link ID: 26987 - Posted: 01.23.2020

Sydney Lupkin Sometimes, the approval of a new generic drug offers more hype than hope for patients' wallets, as people with multiple sclerosis know all too well. New research shows just how little the introduction of a generic version of Copaxone — one of the most popular MS drugs — did to lower their medicine costs. MS is an autoimmune disease that gradually damages the central nervous system, disrupting communication between the brain and the rest of the body. Its symptoms are different from patient to patient across a lifetime but can include weakness, numbness, vision problems, tremors and even paralysis. There's no cure for MS, though some patients experience long remissions of symptoms. Several prescription drugs can stave off multiple sclerosis attacks and slow down the disease, says Deborah Ewing-Wilson, a neurologist with University Hospitals Cleveland Medical Center. But the cost of some of the most effective medicines — which have undergone frequent price hikes over the years — can put added stress on her patients. "They are extremely expensive," says Ewing-Wilson. On average, the medicines cost $70,000 per year, according to a 2017 study. Some prices have increased fivefold from when the drugs were first approved by the Food and Drug Administration. Even with insurance, says Ewing-Wilson, patients can be left on the hook for anywhere from $3,000 to more than $50,000 a year. Some patients tell her they need to skip their medications altogether because they're unaffordable. So when a generic version of the injectable MS drug Copaxone — also known as glatiramer acetate — was launched in 2015, Dan Hartung, a drug policy researcher at Oregon Health & Science University, and his colleagues thought that might spur some price relief. After all, if a cheap multiple sclerosis drug were available, wouldn't patients flock to it, forcing other manufacturers to lower their prices to compete? © 2020 npr

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26980 - Posted: 01.22.2020

By Tina Hesman Saey Some hairy cells in the nose may trigger sneezing and allergies to dust mites, mold and other substances, new work with mice suggests. When exposed to allergens, these “brush cells” make chemicals that lead to inflammation, researchers report January 17 in Science Immunology. Only immune cells previously were thought to make such inflammatory chemicals — fatty compounds known as lipids. The findings may provide new clues about how people develop allergies. Brush cells are shaped like teardrops topped by tufts of hairlike projections. In people, mice and other animals, these cells are also found in the linings of the trachea and the intestines, where they are known as tuft cells (SN: 4/13/18). However, brush cells are far more common in the nose than in other tissues, and may help the body identify when pathogens or noxious chemicals have been inhaled, says Lora Bankova, an allergist and immunologist at Brigham and Women’s Hospital in Boston. Bankova and her colleagues discovered that, when exposed to certain molds or dust mite proteins, brush cells in mice’s noses churn out inflammation-producing lipids, called cysteinyl leukotrienes. The cells also made the lipids when encountering ATP, a chemical used by cells for energy that also signals when nearby cells are damaged, as in an infection. Mice exposed to allergens or ATP developed swelling of their nasal tissues. But mice that lacked brush cells suffered much less inflammation. Such inflammation may lead to allergies in some cases. The researchers haven’t yet confirmed that brush cells in human noses respond to allergens in the same way as these cells do in mice. © Society for Science & the Public 2000–2020

Keyword: Chemical Senses (Smell & Taste); Neuroimmunology
Link ID: 26974 - Posted: 01.21.2020

Ashley Yeager About four years ago, pathologist Matthew Anderson was examining slices of postmortem brain tissue from an individual with autism under a microscope when he noticed something extremely odd: T cells swarming around a narrow space between blood vessels and neural tissue. The cells were somehow getting through the blood-brain barrier, a wall of cells that separates circulating blood from extracellular fluid, neurons, and other cell types in the central nervous system, explains Anderson, who works at Beth Israel Deaconess Medical Center in Boston. “I just have seen so many brains that I know that this is not normal.” He soon identified more T-cell swarms, called lymphocytic cuffs, in a few other postmortem brains of people who had been diagnosed with autism. Not long after that, he started to detect another oddity in the brain tissue—tiny bubbles, or blebs. “I’d never seen them in any other brain tissue that I’ve looked at for many, many different diseases,” he says. Anderson began to wonder whether the neurological features he was observing were specific to autism. To test the idea, he and his colleagues examined postmortem brain tissue samples from 25 people with autism spectrum disorder (ASD) and 30 developmentally normal controls. While the lymphocytic cuffs only sporadically turned up in the brains of neurotypical individuals, the cuffs were abundant in a majority of the brains from individuals who had had ASD. Those same samples also had blebs that appeared in the same spots as the cuffs. Staining the brain tissue revealed that the cuffs were filled with an array of different types of T cells, while the blebs contained fragments of astrocytes, non-neuronal cells that support the physical structure of the brain and help to maintain the blood-brain barrier. © 1986–2020 The Scientist

Keyword: Autism; Neuroimmunology
Link ID: 26966 - Posted: 01.17.2020

By Laura Sanders A parasite common in cats can eliminate infected mice’s fear of felines — a brain hijack that leads to a potentially fatal attraction. But this cat-related boldness (SN: 9/18/13) isn’t the whole story. Once in the brain, the single-celled parasite Toxoplasma gondii makes mice reckless in all sorts of dangerous scenarios, researchers write January 14 in Cell Reports. Infected mice spent more time in areas that were out in the open, exposed places that uninfected mice usually avoid. Infected mice also prodded an experimenter’s hand inside a cage — an intrusion that drove uninfected mice to the other side of the cage. T. gondii–infected mice were even unfazed by an anesthetized rat, a mouse predator, the researchers from the University of Geneva and colleagues found. And infected mice spent more time than uninfected mice exploring the scents of foxes and relatively harmless guinea pigs. The extent of mice’s infections, measured by the load of parasite cysts in the brain, seemed to track with the behavior changes, the researchers report. Toxoplasma gondiiToxoplasma gondii, tweaked to glow green, was isolated from the brain of an infected mouse.Pierre-Mehdi Hammoudi, Damien Jacot The parasite needs to get into the guts of cats to sexually reproduce. Other animals can become infected by ingesting T. gondii through direct or indirect contact with cat feces. The parasite can then spread throughout the body and ultimately form cysts in the brain. People can become infected with T. gondii, though usually not as severely as mice. Some studies have hinted, however, at links between the parasite and human behaviors such as inattention and suicide, as well as mental disorders such as schizophrenia. © Society for Science & the Public 2000–2020

Keyword: Emotions
Link ID: 26963 - Posted: 01.15.2020

By Eryn Brown On March 30, 1981, 25-year-old John W. Hinckley Jr. shot President Ronald Reagan and three other people. The following year, he went on trial for his crimes. Defense attorneys argued that Hinckley was insane, and they pointed to a trove of evidence to back their claim. Their client had a history of behavioral problems. He was obsessed with the actress Jodie Foster, and devised a plan to assassinate a president to impress her. He hounded Jimmy Carter. Then he targeted Reagan. In a controversial courtroom twist, Hinckley’s defense team also introduced scientific evidence: a computerized axial tomography (CAT) scan that suggested their client had a “shrunken,” or atrophied, brain. Initially, the judge didn’t want to allow it. The scan didn’t prove that Hinckley had schizophrenia, experts said — but this sort of brain atrophy was more common among schizophrenics than among the general population. It helped convince the jury to find Hinckley not responsible by reason of insanity. Nearly 40 years later, the neuroscience that influenced Hinckley’s trial has advanced by leaps and bounds — particularly because of improvements in magnetic resonance imaging (MRI) and the invention of functional magnetic resonance imaging (fMRI), which lets scientists look at blood flows and oxygenation in the brain without hurting it. Today neuroscientists can see what happens in the brain when a subject recognizes a loved one, experiences failure, or feels pain. Despite this explosion in neuroscience knowledge, and notwithstanding Hinckley’s successful defense, “neurolaw” hasn’t had a tremendous impact on the courts — yet. But it is coming. Attorneys working civil cases introduce brain imaging ever more routinely to argue that a client has or has not been injured. Criminal attorneys, too, sometimes argue that a brain condition mitigates a client’s responsibility. Lawyers and judges are participating in continuing education programs to learn about brain anatomy and what MRIs and EEGs and all those other brain tests actually show.

Keyword: Brain imaging; Aggression
Link ID: 26960 - Posted: 01.15.2020

Katarina Zimmer As early as the 1990s, researchers proposed that a very common type of herpes virus—then known as human herpesvirus 6 (HHV6)—could be somehow involved in the development of multiple sclerosis, a neurodegenerative disease characterized by autoimmune reactions against the protective myelin coating of the central nervous system. However, the association between HHV6 and the disease soon became fraught with controversy as further studies produced discordant results. Complicating matters further, HHV6 turned out to be two related, but distinct variants—HHV6A and HHV6B. Because the two viruses are similar, for a while no method existed to tell whether a patient had been infected with one or the other, or both—making it difficult to draw a definitive association between either of the viruses and the disease. Now, a collaboration of European researchers has developed a technique capable of distinguishing antibodies against one variant from the other. Using that method in a Swedish cohort of more than 8,700 multiple sclerosis patients and more than 7,200 controls, they found that patients were much more likely to carry higher levels of anti-HHV6A antibodies than healthy people, while they were likelier to carry fewer antibodies against HHV6B. The findings, published last November in Frontiers in Immunology, hint that previous contradictory results may at least be partially explained by the fact that researchers couldn’t distinguish between the two viruses. “This article now makes a pretty convincing case that it is HHV6A that correlates with multiple sclerosis, and not HHV6B,” remarks Margot Mayer-Pröschel, a neuroscientist at the University of Rochester Medical Center who wasn’t involved in the study. “Researchers can now focus on one of these viruses rather than looking at [both] of them together.” © 1986–2020 The Scientist.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26956 - Posted: 01.14.2020

Nell Greenfieldboyce Parrots can perform impressive feats of intelligence, and a new study suggests that some of these "feathered apes" may also practice acts of kindness. African grey parrots voluntarily helped a partner get a food reward by giving the other bird a valuable metal token that could be exchanged for a walnut, according to a newly published report in the journal Current Biology. "This was really surprising that they did this so spontaneously and so readily," says Désirée Brucks, a biologist at ETH Zürich in Switzerland who is interested in the evolution of altruism. Children as young as 1 seem highly motivated to help others, and scientists used to think this kind of prosocial behavior was uniquely human. More recent research has explored "helping" behavior in other species, everything from nonhuman primates to rats and bats. To see whether intelligent birds might help out a feathered pal, Brucks and Auguste von Bayern of the Max Planck Institute for Ornithology in Germany tested African grey parrots. They used parrots that had previously been trained to understand that specific tokens, in the form of small metal rings, could be traded for a food treat through an exchange window. In their experiment, this exchange window was covered up and closed on one bird's cage, making it impossible for that bird to trade. The bird had a pile of tokens in its cage but no way to use them. Meanwhile, its neighbor in an adjacent cage had an open exchange window — but no tokens for food. © 2020 npr

Keyword: Emotions; Evolution
Link ID: 26948 - Posted: 01.10.2020

Emily Makowski Bruce McEwen, a neuroendocrinologist at Rockefeller University, died January 2 after a brief illness. He was 81 years old. McEwen is best known for his research on how stress hormones can reconfigure neural connections in the brain, according to a university statement. In 1968, McEwen and his colleagues discovered that the rat hippocampus is affected by the hormone cortisol, sparking further research into how hormones can enter the brain and affect mental functioning and mood. At the time, most scientists believed that the brain was not malleable after becoming fully developed, a line of thinking that McEwen’s research findings contradicted. In 1993, he coined the term allostatic load, which describes the physiological effects of chronic stress. With his wife, Karen Bulloch, a Rockefeller professor, he studied how immune cells in the brain increase during a person’s lifespan and can contribute to neurodegenerative disease. He also researched how sex hormones affect the central nervous system. Over the course of his career, which spanned six decades, McEwen received many accolades including the Pasarow Foundation award in neuropsychiatry, the Fondation Ipsen Neuronal Plasticity and Endocrine Regulation prizes, the Scolnick Prize in Neuroscience, and the William James Lifetime Achievement Award for Basic Research. He was a member of the National Academy of Sciences, the National Academy of Medicine, and the American Society of Arts and Sciences. “Bruce was a giant in the field of neuroendocrinology,” McEwen’s colleague Leslie Vosshall, a neuroscientist at Rockefeller, says in the statement. “He was a world leader in studying the impact of stress hormones on the brain, and led by example to show that great scientists can also be humble, gentle, and generous human beings.” © 1986–2020 The Scientist

Keyword: Stress; Hormones & Behavior
Link ID: 26942 - Posted: 01.09.2020

By James Gallagher Health and science correspondent An early life full of neglect, deprivation and adversity leads to people growing up with smaller brains, a study suggests. The researchers at King's College London were following adopted children who spent time in "hellhole" Romanian orphanages. They grew up with brains 8.6% smaller than other adoptees. The researchers said it was the "most compelling" evidence of the impact on the adult brain. The appalling care at the orphanages came to light after the fall of Romania's communist dictator Nicolae Ceausescu in 1989. "I remember TV pictures of those institutions, they were shocking," Prof Edmund Sonuga-Barke, who now leads the study following those children, told the BBC. He described the institutions as "hellholes" where children were "chained into their cots, rocking, filthy and emaciated". The children were physically and psychologically deprived with little social contact, no toys and often ravaged by disease. The children studied had spent between two weeks and nearly four years in such institutions. Previous studies on children who were later adopted by loving families in the UK showed they were still experiencing mental health problems in adulthood. Higher levels of traits including autism, attention deficit hyperactivity disorder (ADHD) and a lack of fear of strangers (disinhibited social engagement disorder) have all been documented. The latest study, published in Proceedings of the National Academy of Sciences, is the first to scan the brains for answers. There were 67 Romanian adoptees in the study and their brains were compared to 21 adoptees who did not suffer early life deprivation. "What we found is really quite striking," Prof Sonuga-Barke told the BBC. First the total brain volume - the size of the brain - was 8.6% smaller in the Romanian adoptees on average. And the longer they spent in the Romanian orphanages, the greater the reduction in brain size. © 2020 BBC.

Keyword: Development of the Brain; Stress
Link ID: 26935 - Posted: 01.07.2020

By Nicholas Bakalar Living with a pet dog in childhood may be linked to a reduced risk of schizophrenia in adulthood. Researchers studied adult patients at Sheppard Pratt Health System in Baltimore, 396 with schizophrenia and 381 with bipolar disorder. They compared them with 594 healthy controls. The participants reported whether they had had a dog or a cat in the household when they were children and, if so, the first and most recent time they had contact with the animal. The findings appeared this month in PLOS One. More than half of the subjects had dogs, and about a third had cats before their 13th birthdays. After adjusting for other characteristics, the scientists found that exposure to a dog at any time in childhood was associated with a 24 percent reduced risk for schizophrenia. Those exposed to dogs at birth were 55 percent less likely to have schizophrenia than people who had not been exposed at all. There was no significant effect of exposure to cats, and no effect of either animal on the risk for bipolar disorder. “We don’t know the mechanism,” said the lead author, Dr. Robert H. Yolken, a professor of pediatrics at Johns Hopkins University in Baltimore, though he noted that the microbiome, or collection of gut bacteria, of people with schizophrenia is different from that of controls. “One possibility is that having a dog in the house causes a different microbiome and changes the likelihood of developing a psychiatric disorder,” he said. © 2019 The New York Times Company

Keyword: Schizophrenia; Stress
Link ID: 26911 - Posted: 12.26.2019

By Catherine Matacic Falling in love is never easy. But do it in a foreign language, and complications pile up quickly, from your first fumbling attempts at deep expression to the inevitable quarrel to the family visit punctuated by remarks that mean so much more than you realize. Now, a study of two dozen terms related to emotion in nearly 2500 languages suggests those misunderstandings aren’t all in your head. Instead, emotional concepts like love, shame, and anger vary in meaning from culture to culture, even when we translate them into the same words. “I wish I had thought of this,” says Lisa Feldman Barrett, a neuroscientist and psychologist at Northeastern University in Boston. “It’s a very, very well-reasoned, clever approach.” People have argued about emotions since the ancient Greeks. Aristotle suggested they were essential to virtue. The stoics called them antithetical to reason. And in his “forgotten” masterpiece, The Expression of the Emotions in Man and Animals, Charles Darwin wrote that they likely had a single origin. He thought every culture the world over shared six basic emotions: happiness, sadness, fear, anger, surprise, and disgust. Since then, psychologists have looked for traces of these emotions in scores of languages. And although one common experiment, which asks participants to identify emotions from photographs of facial expressions, has led to many claims of universality, critics say an overreliance on concepts from Western, industrialized societies dooms such attempts from the start. © 2019 American Association for the Advancement of Science.

Keyword: Emotions; Language
Link ID: 26907 - Posted: 12.21.2019

Joshua Schrock You know what it’s like to be sick. You feel fatigued, maybe a little depressed, less hungry than usual, more easily nauseated and perhaps more sensitive to pain and cold. The fact that illness comes with a distinct set of psychological and behavioral features is not a new discovery. In medical terminology, the symptom of malaise encompasses some of the feelings that come with being ill. Animal behaviorists and neuroimmunologists use the term sickness behavior to describe the observable behavior changes that occur during illness. Health care providers often treat these symptoms as little more than annoying side effects of having an infectious disease. But as it turns out, these changes may actually be part of how you fight off infection. I’m an anthropologist interested in how illness and infection have shaped human evolution. My colleagues and I propose that all these aspects of being sick are features of an emotion that we call “lassitude.” And it’s an important part of how human beings work to recover from illness. The human immune system is a complex set of mechanisms that help you suppress and eliminate organisms – such as bacteria, viruses and parasitic worms – that cause infection. Activating the immune system, however, costs your body a lot of energy. This presents a series of problems that your brain and body must solve to fight against infection most effectively. Where will this extra energy come from? What should you do to avoid additional infections or injuries that would increase the immune system’s energy requirements even more? © 2010–2019, The Conversation US, Inc.

Keyword: Neuroimmunology; Emotions
Link ID: 26899 - Posted: 12.18.2019

By Jade Wu What do the sounds of whispering, crinkling paper, and tapping fingernails have in common? What about the sight of soft paint brushes on skin, soap being gently cut to pieces, and hand movements like turning the pages of a book? Well, if you are someone who experiences the autonomous sensory meridian response—or ASMR, for short—you may recognize these seemingly ordinary sounds and sights as “triggers” for the ASMR experience. No idea what I’m talking about? Don’t worry, you’re actually in the majority. Most people, myself included, aren’t affected by these triggers. But what happens to those who are? What is the ASMR experience? It’s described as a pleasantly warm and tingling sensation that starts on the scalp and moves down the neck and spine. ASMR burst onto the Internet scene in 2007, according to Wikipedia, when a woman with the username “okaywhatever” described her experience of ASMR sensations in an online health discussion forum. At the time, there was no name for this weird phenomenon. But by 2010, someone called Jennifer Allen had named the experience, and from there, ASMR became an Internet sensation. Today, there are hundreds of ASMR YouTubers who collectively post over 200 videos of ASMR triggers per day, as reported by a New York Times article in April, 2019. Some ASMR YouTubers have become bona fide celebrities with ballooning bank accounts, millions of fans, and enough fame to be stopped on the street for selfies. There’s been some controversy. Some people doubt whether this ASMR experience is “real,” or just the result of recreational drugs or imagined sensations. Some have chalked the phenomenon up to a symptom of loneliness among Generation Z, who get their dose of intimacy from watching strangers pretend to do their makeup without having to interact with real people. Some people are even actively put off by ASMR triggers. One of my listeners, Katie, said that most ASMR videos just make her feel agitated. But another listener, Candace, shared that she has been unknowingly chasing ASMR since she was a child watching BBC. © 2019 Scientific American

Keyword: Hearing; Emotions
Link ID: 26873 - Posted: 12.05.2019

By David Brooks This has been a golden age for brain research. We now have amazing brain scans that show which networks in the brain ramp up during different activities. But this emphasis on the brain has subtly fed the illusion that thinking happens only from the neck up. It’s fed the illusion that the advanced parts of our thinking are the “rational” parts up top that try to control the more “primitive” parts down below. So it’s interesting how many scientists are now focusing on the thinking that happens not in your brain but in your gut. You have neurons spread through your innards, and there’s increasing attention on the vagus nerve, which emerges from the brain stem and wanders across the heart, lungs, kidney and gut. The vagus nerve is one of the pathways through which the body and brain talk to each other in an unconscious conversation. Much of this conversation is about how we are relating to others. Human thinking is not primarily about individual calculation, but about social engagement and cooperation. One of the leaders in this field is Stephen W. Porges of Indiana University. When you enter a new situation, Porges argues, your body reacts. Your heart rate may go up. Your blood pressure may change. Signals go up to the brain, which records the “autonomic state” you are in. Maybe you walk into a social situation that feels welcoming. Green light. Your brain and body get prepared for a friendly conversation. But maybe the person in front of you feels threatening. Yellow light. You go into fight-or-flight mode. Your body instantly changes. Your ear, for example, adjusts to hear high and low frequencies — a scream or a growl — rather than midrange frequencies, human speech. Or maybe the threat feels like a matter of life and death. Red light. Your brain and body begin to shut down. According to Porges’s “Polyvagal Theory,” the concept of safety is fundamental to our mental state. People who have experienced trauma have bodies that are highly reactive to perceived threat. They don’t like public places with loud noises. They live in fight-or-flight mode, stressed and anxious. Or, if they feel trapped and constrained, they go numb. Their voice and tone go flat. Physical reactions shape our way of seeing and being. © 2019 The New York Times Company

Keyword: Emotions
Link ID: 26869 - Posted: 12.04.2019

By Austin Frakt Some days I’m grumpy; other times, my head hurts or my feet or my arms do. Yet when I play the trumpet, my mood improves and the pain disappears. Why? Alternative medicine — including music therapy — is full of pain-relief claims. Although some are simply too good to be true, the oddities of pain can explain why others hold up, as well as why my trumpet playing helps. One thing we tend to believe about pain, but is wrong, is that it always stems from a single, fixable source. Another is that pain is communicated from that source to our brains by “pain nerves.” That’s so wrong it’s called “the naïve view” by neuroscientists. In truth, pain is in our brain. Or as the author and University of California, San Diego, neuroscientist V. S. Ramachandran put it, “Pain is an opinion.” We feel it because of how our brain interprets input transmitted to it from all our senses, not necessarily because of the inherent properties of the input itself. There are no nerves dedicated to sensing and transmitting pain. Anyone who has willed themselves to not feel a tickle as ticklish can appreciate the difference between stimulation and our perception of it. Pain can be experienced and relieved in phantom limbs. Discomfort and swelling increase when people believe a painful hand or knee is larger. They decrease when it seems smaller, for example in a distorted image or based on virtual reality technology. Injections are less painful when we don’t watch them. Using our brains, we can exert some control over it. © 2019 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 26865 - Posted: 12.02.2019

By Sofie Bates In multiple sclerosis, barriers that guard the brain become leaky, allowing some disease-causing immune cells to invade. Now scientists have identified a key molecule in the process that helps B cells breach the barriers. ALCAM, a protein produced by B cells, helps the immune cells sneak into the central nervous system, researchers report November 13 in Science Translational Medicine. Tests in mice and in artificial human brain barriers show that B cells without ALCAM, or activated leukocyte cell adhesion molecule, had trouble getting through the brain’s barriers. And in mice with a disease with some characteristics similar to MS, blocking ALCAM seemed to alleviate the disease’s severity. These early results indicate that the protein may be a good target for new treatments for multiple sclerosis in people, the researchers say. “This is a very important puzzle piece in how we understand multiple sclerosis,” says David Leppert, a neurologist at the University Hospital Basel in Switzerland who was not involved in the work. “How it translates into clinical applications is yet another question.” Worldwide, over 2.3 million people have multiple sclerosis, including nearly 1 million adults in the United States. Scientists think that rogue immune cells invade the brain and strip away the protective coating on nerve cells — leading to neurological issues and physical disability as the disease progresses. There’s no cure, and treatments don’t work for advanced stages of multiple sclerosis. Scientists have developed over a dozen medications to treat MS symptoms (SN: 11/29/17), one of which uses antibodies to destroy the body’s B cells. But that approach weakens patients’ immune systems, opening the door for future infections or cancer. In the new study, the researchers are instead focusing on preventing disease-causing B cells from entering the brain. © Society for Science & the Public 2000–2019

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26859 - Posted: 11.29.2019

Correspondent Lesley Stahl Who among us hasn't wished we could read someone else's mind, know exactly what they're thinking? Well that's impossible, of course, since our thoughts are, more than anything else, our own. Private, personal, unreachable. Or at least that's what we've always, well, thought. Advances in neuroscience have shown that, on a physical level, our thoughts are actually a vast network of neurons firing all across our brains. So if that brain activity could be identified and analyzed, could our thoughts be decoded? Could our minds be read? Well, a team of scientists at Carnegie Mellon University in Pittsburgh has spent more than a decade trying to do just that. We started our reporting on their work 10 years ago, and what they've discovered since, has drawn us back. In Carnegie Mellon's scanner room, two floors underground, a steady stream of research subjects come to have their brains and thoughts "read" in this MRI machine. It's a type of scanning called functional MRI, FMRI. That looks at what's happening inside the brain as a person thinks. Marcel Just: It's like being an astronomer when the first telescope is discovered, or being a biologist when the first microscope is-- is developed. Neuroscientist Marcel Just says this technology has made it possible for the first time to see the physical makeup of our thoughts. When we first visited Dr. Just's lab ten years ago, he and his team had conducted a study. They put people in the scanner and asked them to think about ten objects, five of them tools like screwdriver and hammer and five of them dwellings like igloo and castle, while measuring activity levels throughout their brains. The idea was to crunch the data and try to identify distinctive patterns of activity for each object. Lesley Stahl: You had them think about a screwdriver. Marcel Just: Uh-huh. Lesley Stahl: And the computer found the place in the brain where that person was thinking "screwdriver?" Marcel Just: Screwdriver isn't one place in the brain. It's many places in the brain. When you think of a screwdriver, you think about how you hold it, how you twist it, what it looks like… Lesley Stahl: And each of those functions are in different places? Marcel Just: Correct. He showed us that by dividing the brain into thousands of tiny cubes and analyzing the amount of activity in each one, his team was able to identify unique patterns for each object. © 2019 CBS Interactive Inc.

Keyword: Emotions; Brain imaging
Link ID: 26853 - Posted: 11.26.2019

Ashley P. Taylor Autoimmune diseases tend to ease up during pregnancy, and for women with multiple sclerosis, physicians have documented fewer relapses of the condition while women are pregnant compared to before and after having a baby. Anecdotally, many MS patients also feel better when they’re expecting. Researchers believe that this happens because during pregnancy, the body reins in its immune response so as to not reject the fetus—and in doing so counteracts autoimmune diseases. But as to how exactly this all works, scientists are uncertain. “Obviously, everybody would love to understand why it happens because if you could bottle that property of pregnancy, perhaps you could use it therapeutically,” Adrian Erlebacher, a reproductive immunologist at the University of California, San Francisco, tells The Scientist. To investigate why this happens in pregnant women with multiple sclerosis (MS), Stefan Gold, a neuroscientist at the Institute of Neuroimmunology and Multiple Sclerosis at the Universitätsklinikum Hamburg-Eppendorf, in Hamburg, Germany, and colleagues examined T cell populations in 11 MS patients before, during, and after pregnancy and in 12 women without MS during and after pregnancy. They categorized the T cells into different groups based on a genetic analysis of the cells’ receptors. In the first trimester, they found, MS patients’ T cells were dominated by just a few types, called clones, each with a different T cell receptor. Between the first and third trimesters, those dominant clones declined in abundance, and T cells became more evenly distributed across the different populations, Gold says. In women without MS, the pregnancy-associated changes in the T cell repertoire were not significant. Gold and his colleagues reported their results in Cell Reports on October 22. © 1986–2019 The Scientist.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 26830 - Posted: 11.19.2019

By Jane E. Brody There‌ are‌ ‌some‌ ‌crimes‌ ‌that‌ ‌are‌ almost‌ ‌impossible‌ ‌to‌ ‌forget. ‌ ‌ For‌ me, ‌they‌ ‌include‌ ‌the‌ ‌death‌ ‌in‌ ‌1999‌ ‌of‌ ‌Kendra‌ ‌Webdale, ‌an‌ ‌aspiring‌ ‌young‌ ‌journalist‌ ‌who‌ ‌was‌ ‌pushed‌ ‌in‌ ‌front‌ ‌of‌ ‌a‌ ‌New‌ ‌York‌ ‌subway‌ ‌train‌ ‌by‌ ‌a‌ ‌29-year-old‌ ‌man‌ ‌with‌ ‌schizophrenia‌ ‌who‌ ‌had‌ ‌stopped‌ ‌taking‌ ‌his‌ ‌medication. ‌That‌ ‌same‌ ‌year, ‌two‌ ‌mentally‌ ‌ill‌ ‌teenage‌‌‌ ‌boys‌ ‌massacred‌ ‌12‌ ‌students‌ ‌and‌ ‌one‌ ‌teacher‌ ‌at‌ ‌Columbine‌ ‌High‌ ‌School‌ ‌in‌ ‌Colorado. ‌ ‌ Thirteen‌ ‌years‌ ‌later, ‌a‌ ‌seriously‌ ‌emotionally‌ ‌disturbed‌ ‌20-year-old‌ ‌man‌ ‌murdered‌ ‌20‌ ‌young‌ ‌children‌ ‌and‌ ‌six‌ ‌adults‌ ‌at‌ ‌Sandy‌ ‌Hook‌ ‌Elementary‌ ‌School‌ ‌in‌ ‌Connecticut. ‌This‌ ‌year, ‌a‌ ‌homeless‌ ‌24-year-old‌ ‌man‌ ‌bludgeoned‌ ‌four‌ ‌men‌ ‌to‌ ‌death‌ ‌while‌ ‌they‌ ‌slept‌ ‌on‌ ‌the‌ ‌streets‌ ‌of‌ ‌my‌ ‌city. ‌ ‌ Although‌ ‌New York is now far‌ ‌safer‌ ‌than‌ ‌when‌ ‌I‌ ‌was‌ ‌a‌ ‌child‌ ‌in‌ ‌the‌ ‌1940s‌ ‌and‌ ‌’50s‌ ‌who‌ ‌walked‌ ‌to‌ ‌and‌ ‌from‌ ‌school‌ ‌unescorted, ‌like‌ ‌most‌ ‌big‌ ‌cities, ‌it still‌ ‌harbors‌ ‌untold‌ ‌numbers‌ ‌of‌ ‌men‌ ‌and‌ ‌women‌ ‌with‌ ‌known‌ ‌or‌ ‌undiagnosed‌ ‌severe‌ ‌mental‌ ‌illness‌ ‌that‌ ‌can‌ ‌and‌ ‌should‌ ‌be‌ ‌treated‌ ‌before‌ ‌yet‌ ‌another‌ ‌personal‌ ‌or‌ ‌societal‌ ‌tragedy‌ ‌occurs. ‌ ‌ What, ‌I‌ ‌wondered, ‌is‌ ‌or‌ ‌can‌ ‌be‌ ‌done‌ ‌to‌ ‌help‌ ‌them‌ ‌and‌ ‌avert‌ ‌further‌ ‌disasters? ‌ ‌ Contrary‌ ‌to‌ ‌politically‌ ‌motivated‌ ‌claims, ‌I‌ ‌learned‌ ‌that‌ ‌people‌ ‌with‌ ‌serious‌ ‌mental‌ ‌ills‌ ‌are‌ ‌not‌ ‌necessarily‌ ‌prone‌ ‌to‌ ‌commit‌ ‌violent‌ acts‌ ‌ — ‌they‌ ‌are‌ ‌far‌ ‌more‌ ‌likely‌ ‌to‌ ‌become‌ ‌‌victims‌‌ ‌of‌ ‌crime. ‌Rather, ‌the‌ ‌issue‌ ‌is‌ ‌that‌ ‌treatments‌ ‌known‌ ‌to‌ ‌be‌ ‌effective‌ ‌are‌ ‌underfunded‌ ‌or‌ ‌wrongly‌ ‌dismissed‌ ‌as‌ ‌ineffective‌ ‌or‌ ‌too‌ ‌dangerous; ‌basic‌ ‌research‌ ‌in‌ ‌university‌ ‌and‌ ‌government‌ ‌laboratories‌ ‌into‌ ‌new‌ ‌and‌ ‌better‌ ‌drugs‌ ‌is‌ ‌limited‌ ‌and‌ ‌also‌ ‌underfunded; ‌and‌ ‌pharmaceutical‌ ‌companies‌ ‌have‌ ‌shown‌ ‌little‌ ‌interest‌ ‌in‌ ‌developing‌ ‌and‌ ‌testing‌ ‌treatments‌ ‌for‌ ‌severe‌ ‌mental‌ ‌illness. ‌ ‌ Also‌ ‌at‌ ‌issue‌ ‌is‌ ‌that, ‌as‌ ‌was‌ true‌ for‌ ‌cancer‌ ‌until‌ ‌recently, ‌acknowledgment‌ ‌of‌ ‌mental‌ ‌illness‌ ‌carries‌ ‌a‌ ‌stigma‌ ‌that‌ ‌impedes‌ ‌its‌ ‌early‌ ‌recognition, ‌when‌ ‌it‌ ‌can‌ ‌be‌ ‌most‌ ‌effectively‌ ‌treated‌ ‌or‌ ‌reversed. ‌ ‌ © 2019 The New York Times Company

Keyword: Schizophrenia; Aggression
Link ID: 26829 - Posted: 11.18.2019