Chapter 11. Emotions, Aggression, and Stress

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 3192

Researchers at the National Institutes of Health found evidence that specific immune cells may play a key role in the devastating effects of cerebral malaria, a severe form of malaria that mainly affects young children. The results, published in the Journal of Clinical Investigation, suggest that drugs targeting T cells may be effective in treating the disease. The study was supported by the NIH Intramural Research Program. “This is the first study showing that T cells target blood vessels in brains of children with cerebral malaria,” said Dorian McGavern, Ph.D., chief of the Viral Immunology and Intravital Imaging Section at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) who co-directed the study with Susan Pierce, Ph.D., chief of the Laboratory of Immunogenetics at the National Institute of Allergy and Infectious Diseases (NIAID). “These findings build a bridge between mouse and human cerebral malaria studies by implicating T cells in the development of disease pathology in children. It is well established that T cells cause the brain vasculature injury associated with cerebral malaria in mice, but this was not known in humans.” More than 200 million people worldwide are infected annually with mosquito-borne parasites that cause malaria. In a subset of those patients, mainly young children, the parasites accumulate in brain blood vessels causing cerebral malaria, which leads to increased brain pressure from swelling. Even with available treatment, cerebral malaria still kills up to 25% of those affected resulting in nearly 400,000 deaths annually. Children who survive the infection will often have long-lasting neurological problems such as cognitive impairment.

Keyword: Neuroimmunology
Link ID: 27049 - Posted: 02.19.2020

Nicola Davis Parents should not worry about their teenagers’ delinquent behaviour provided they were well behaved in their earlier childhood, according to researchers behind a study that suggests those who offend throughout their life showed antisocial behaviour from a young age and have a markedly different brain structure as adults. According to figures from the Ministry of Justice, 24% of males in England and Wales aged 10–52 in 2006 had a conviction, compared with 6% of females. Previous work has shown that crime rises in adolescence and young adulthood but that most perpetrators go on to become law-abiding adults, with only a minority – under 10% of the general population – continuing to offend throughout their life. Such trends underpin many modern criminal justice strategies, including in the UK where police can use their discretion as to whether to a young offender should enter the formal justice system. Now researchers say they have found that adults with a long history of offences show striking differences in brain structure compared with those who have stuck to the straight and narrow or who transgressed only as adolescents. “These findings underscore prior research that really highlights that there are different types of young offenders – they are not all the same. They should not all be treated the same,” said Prof Essi Viding, a co-author of the study from University College London. Prof Terrie Moffitt, another co-author of the research from Duke University in North Carolina, said the study helped to shed light on what may be behind persistent antisocial behaviour. © 2020 Guardian News & Media Limited

Keyword: Aggression; Brain imaging
Link ID: 27048 - Posted: 02.18.2020

By Laura Sanders SEATTLE — Live bits of brain look like any other piece of meat — pinkish, solid chunks of neural tissue. But unlike other kinds of tissue or organs donated for research, they hold the memories, thoughts and feelings of a person. “It is identified with who we are,” Karen Rommelfanger, a neuroethicist at Emory University in Atlanta, said February 13 in a news conference at the annual meeting of the American Association for the Advancement of Science. That uniqueness raises a whole new set of ethical quandaries when it comes to experimenting with living brain tissue, she explained. Such donations are crucial to emerging research aimed at teasing out answers to what makes us human. For instance, researchers at the Seattle-based Allen Institute for Brain Science conduct experiments on live brain tissue to get clues about how the cells in the human brain operate (SN: 8/7/19). These precious samples, normally discarded as medical waste, are donated by patients undergoing brain surgery and raced to the lab while the nerve cells are still viable. Other experiments rely on systems that are less sophisticated than a human brain, such as brain tissue from other animals and organoids. These clumps of neural tissue, grown from human stem cells, are still a long way from mimicking the complexities of the human brain (SN: 10/24/19). But with major advances, these systems might one day be capable of much more advanced behavior, which might ultimately lead to awareness, a conundrum that raises ethical issues. © Society for Science & the Public 2000–2020

Keyword: Consciousness; Emotions
Link ID: 27047 - Posted: 02.18.2020

By Jade Wu 3 Anxiety-Related Disorders You Might Not Know About Person suffering from trichotillomania, an obsessive compulsive condition where sufferers can't resist pulling their hair out. Credit: Ryan Jackson Getty Images Most people know what it’s like to feel anxious. That tension in your muscles, those butterflies in your stomach, and the drumming of your heart tells you that you’re not calm. And this is totally normal. Where would we be if genuinely dangerous situations like dark alleys at night didn’t give us the heebie-jeebies? And would we take important tasks very seriously if we didn’t get nervous in the spotlight, like when giving a wedding toast? Sometimes, anxiety goes too far and gets in the way of our everyday functioning. It can mess up our health, relationships, work, and fun. It’s not hard to imagine the pain of being plagued by non-stop worries or feeling so shy as to have trouble with dating. But sometimes, anxiety and anxiety-related processes can show up in more unusual ways, even ways that don’t seem at first to have anything to do with emotions. The Diagnostic and Statistics Manual - 5th Edition is the official American Psychiatric Association’s list of psychological disorders. It’s a huge bible detailing everything that’s considered a disorder and how it’s categorized. It takes experts years to update it in response to ongoing scientific findings. Advertisement The Anxiety Disorders section got a big makeover in the last update, which came out in 2013. It’s now split into a few different sections, including Trauma and Stress-Related Disorders and Obsessive-Compulsive Disorders. Some of the less common disorders got shuffled around, some got new names, but experts still agree that the line between categories is blurry at best. Overlapping and related to some of the most common anxiety disorders, such as generalized anxiety disorder and social anxiety disorder, are some that are less well-known.

Keyword: Stress; Emotions
Link ID: 27041 - Posted: 02.14.2020

By Randi Hutter Epstein It was a staple of medical thinking dating to the 1910s that stress was the body’s alarm system, switching on only when terrible things happened, often leaving a person with an either-or choice: fight or flight. The neuroscientist Bruce S. McEwen trailblazed a new way of thinking about stress. Beginning in the 1960s, he redefined it as the body’s way of constantly monitoring daily challenges and adapting to them. Dr. McEwen, who died on Jan. 2 at 81, described three forms of stress: good stress — a response to an immediate challenge with a burst of energy that focuses the mind; transient stress — a response to daily frustrations that resolve quickly; and chronic stress — a response to a toxic, unrelenting barrage of challenges that eventually breaks down the body. It was Dr. McEwen’s research into chronic stress that proved groundbreaking. He and his research team at Rockefeller University in Manhattan discovered in 1968 that stress hormones had a profound effect on the brain. In studies using animals (five rats in the initial one), Dr. McEwen and his colleagues demonstrated that toxic stress atrophied neurons near the hippocampus, the brain’s memory and learning center, while expanding neurons near the amygdala, an area known for vigilance toward threats. Describing the burden of continuing stress, he coined the term “allostatic load” (derived from allostasis, the process by which the body seeks to regain stability, or homeostasis, in response to stressors). Their discoveries, first published in the journal Nature in 1968, ignited a new field of research, one that would reveal how stress hormones and other mediators change the brain, alter behavior and impact health, in some cases accelerating disease. At the time, only a few scientists were asserting that the brain remains malleable throughout life, challenging the dogma that the brain stops changing after adolescence. Dr. McEwen’s studies documenting how hormones alter neurons lent credence to this emerging idea. © 2020 The New York Times Company

Keyword: Stress; Hormones & Behavior
Link ID: 27031 - Posted: 02.11.2020

By Everyday Einstein Sabrina Stierwalt People from all cultures laugh, although we may laugh at different things. (I once interviewed for a job in the Netherlands and none of my jokes landed. I didn’t get that job.) Apes also laugh. We know this because there are scientists whose job it is to tickle animals. I’m not even kidding. What a life! Advertisement Humans start laughing as early as 3 months into life, even before we can speak. This is true even for babies who are deaf or blind. Peekaboo, it turns out, is particularly a global crowd-pleaser. And we know this because studying baby laughter is an actual job, too. So, the ubiquitous nature of laughter suggests that it must serve a purpose, but what? Why do we laugh? Here are a few scientific reasons Laughter clearly serves a social function. It is a way for us to signal to another person that we wish to connect with them. In fact, in a study of thousands of examples of laughter, the speakers in a conversation were found to be 46 percent more likely to laugh than the listeners. We’re also 30 times more likely to laugh in a group. Young children between the ages of 2.5 and 4 were found to be eight times more likely to laugh at a cartoon when they watched it with another child even though they were just as likely to report that the cartoon was funny whether alone or not. Evolutionarily speaking, this signal of connection likely played an important role in survival. Upon meeting a stranger, we want to know: What are your intentions with me? And who else are you aligned with? © 2020 Scientific American

Keyword: Emotions
Link ID: 27029 - Posted: 02.10.2020

By Laura Sanders Immune cells in the brain chew up memories, a new study in mice shows. The finding, published in the Feb. 7 Science, points to a completely new way that the brain forgets, says neuroscientist Paul Frankland of the Hospital for Sick Children Research Institute in Toronto, who wasn’t involved in the study. That may sound like a bad thing, but forgetting is just as important as remembering. “The world constantly changes,” Frankland says, and getting rid of unimportant memories — such as a breakfast menu from two months ago — allows the brain to collect newer, more useful information. Exactly how the brain stores memories is still debated, but many scientists suspect that connections between large groups of nerve cells are important (SN: 1/24/18). Forgetting likely involves destroying or changing these large webs of precise connections, called synapses, other lines of research have suggested. The new result shows that microglia, immune cells that can clear debris from the brain, “do exactly that,” Frankland says. Microglia are master brain gardeners that trim extra synapses away early in life, says Yan Gu, a neuroscientist at Zhejiang University School of Medicine in Hangzhou, China. Because synapses have a big role in memory storage, “we started to wonder whether microglia may induce forgetting by eliminating synapses,” Gu says. Gu’s team first gave mice an unpleasant memory: mild foot shocks, delivered in a particular cage. Five days after the shocks, the mice would still freeze in fear when they were placed in the cage. But 35 days later, they had begun to forget and froze less often in the room. © Society for Science & the Public 2000–2020

Keyword: Learning & Memory; Neuroimmunology
Link ID: 27026 - Posted: 02.07.2020

By Sue Halpern During the 2016 Presidential primary, SPARK Neuro, a company that uses brain waves and other physiological signals to delve into the subliminal mind, decided to assess people’s reactions to the Democratic candidates. The company had not yet launched, but its C.E.O., Spencer Gerrol, was eager to refine its technology. In a test designed to uncover how people are actually feeling, as opposed to how they say they are feeling, SPARK Neuro observed, among other things, that the cadence of Bernie Sanders’s voice grabbed people’s attention, while Hillary Clinton’s measured tones were a bore. A few months later, Katz Media Group, a radio-and-television-ad representative firm, hired Gerrol’s group to study a cohort of undecided voters in Florida and Pennsylvania. The company’s chief marketing officer, Stacey Schulman, picked SPARK Neuro because its algorithm took into account an array of neurological and physiological signals. “Subconscious emotion underlies conscious decision-making, which is interesting for the marketing world but critically important in the political realm,” Schulman told me. “This measures how the body is responding, and it happens before you articulate it.” Neuromarketing—gauging consumers’ feelings and beliefs by observing and measuring spontaneous, unmediated physiological responses to an ad or a sales pitch—is not new. “For a while, using neuroscience to do marketing was something of a fad, but it has been applied to commerce for a good ten years now,” Schulman said. Nielsen, the storied media-insight company, has a neuromarketing division. Google has been promoting what it calls “emotion analytics” to advertisers. A company called Realeyes claims to have trained artificial intelligence to “read emotions” through Webcams; another called Affectiva says that it “provides deep insight into unfiltered and unbiased consumer emotional response to brand content” through what it calls “facial coding.” Similarly, ZimGo Polling, a South Korean company that operates in the United States, has paired facial-recognition technology with “automated emotion understanding” and natural language processing to give “insights into how people feel about real-time issues,” and “thereby enables a virtual 24/7 town hall meeting with citizens.” This is crucial, according to the C.E.O. of ZimGo’s parent company, because “people vote on emotion.” © 2020 Condé Nast

Keyword: Attention; Emotions
Link ID: 27017 - Posted: 02.04.2020

By Theodor Schaarschmidt A 51-year-old man I will call “Mr. Pinocchio” had a strange problem. When he tried to tell a lie, he often passed out and had convulsions. In essence, he became a kind of Pinocchio, the fictional puppet whose nose grew with every fib. For the patient, the consequences were all too real: he was a high-ranking official in the European Economic Community (since replaced by the European Union), and his negotiating partners could tell immediately when he was bending the truth. His condition, a symptom of a rare form of epilepsy, was not only dangerous, it was bad for his career. Doctors at the University Hospitals of Strasbourg in France discovered that the root of the problem was a tumor about the size of a walnut. The tumor was probably increasing the excitability of a brain region involved in emotions; when Mr. Pinocchio lied, this excitability caused a structure called the amygdala to trigger seizures. Once the tumor was removed, the fits stopped, and he was able to resume his duties. The doctors, who described the case in 1993, dubbed the condition the “Pinocchio syndrome.” Mr. Pinocchio’s plight demonstrates the far-reaching consequences of even minor changes in the structure of the brain. But perhaps just as important, it shows that lying is a major component of the human behavioral repertoire; without it, we would have a hard time coping. When people speak unvarnished truth all the time—as can happen when Parkinson’s disease or certain injuries to the brain’s frontal lobe disrupt people’s ability to lie—they tend to be judged tactless and hurtful. In everyday life, we tell little white lies all the time, if only out of politeness: Your homemade pie is awesome (it’s awful). No, Grandma, you’re not interrupting anything (she is). A little bit of pretense seems to smooth out human relationships without doing lasting harm. © 2020 Scientific American

Keyword: Emotions
Link ID: 27006 - Posted: 01.29.2020

Elena Renken The sting of a paper cut or the throb of a dog bite is perceived through the skin, where cells react to mechanical forces and send an electrical message to the brain. These signals were believed to originate in the naked endings of neurons that extend into the skin. But a few months ago, scientists came to the surprising realization that some of the cells essential for sensing this type of pain aren’t neurons at all. It’s a previously overlooked type of specialized glial cell that intertwines with nerve endings to form a mesh in the outer layers of the skin. The information the glial cells send to neurons is what initiates the “ouch”: When researchers stimulated only the glial cells, mice pulled back their paws or guarded them while licking or shaking — responses specific to pain. This discovery is only one of many recent findings showing that glia, the motley collection of cells in the nervous system that aren’t neurons, are far more important than researchers expected. Glia were long presumed to be housekeepers that only nourished, protected and swept up after the neurons, whose more obvious role of channeling electric signals through the brain and body kept them in the spotlight for centuries. But over the last couple of decades, research into glia has increased dramatically. “In the human brain, glial cells are as abundant as neurons are. Yet we know orders of magnitude less about what they do than we know about the neurons,” said Shai Shaham, a professor of cell biology at the Rockefeller University who focuses on glia. As more scientists turn their attention to glia, findings have been piling up to reveal a family of diverse cells that are unexpectedly crucial to vital processes. All Rights Reserved © 2020

Keyword: Glia; Pain & Touch
Link ID: 27002 - Posted: 01.28.2020

By Jane E. Brody My husband and I were psychological opposites. I’ve always seen the glass as half-full; to him it was half-empty. That difference, research findings suggest, is likely why I pursue good health habits with a vengeance while he was far less inclined to follow the health-promoting lifestyle I advocated. I’m no cockeyed optimist, but I’ve long believed that how I eat and exercise, as well as how I view the world, can benefit my mental and physical well-being. An increasing number of recent long-term studies have linked greater optimism to a lower risk of developing cardiovascular disease and other chronic ailments and to fostering “exceptional longevity,” a category one team of researchers used for people who live to 85 and beyond. Admittedly, the relationship between optimism and better health and a longer life is still only a correlation that doesn’t prove cause and effect. But there is also now biological evidence to suggest that optimism can have a direct impact on health, which should encourage both the medical profession and individuals to do more to foster optimism as a potential health benefit. According to Dr. Alan Rozanski, one of the field’s primary researchers, “It’s never too early and it’s never too late to foster optimism. From teenagers to people in their 90s, all have better outcomes if they’re optimistic.” Dr. Rozanski is a cardiologist at Mount Sinai St. Luke’s Hospital in New York who became interested in optimism while working in a cardiac rehabilitation program early in his career. In an interview, he explained, “Many heart-attack patients who had long been sedentary would come into the gym and say ‘I can’t do that!’ But I would put them on the treadmill, start off slowly and gradually build them up. Their attitude improved, they became more confident. One woman in her 70s said her heart attack may have been the best thing that had happened to her because it transformed what she thought she could do.” © 2020 The New York Times Company

Keyword: Emotions; Neuroimmunology
Link ID: 26995 - Posted: 01.27.2020

Katarina Zimmer Around 30 years ago, researchers in the UK discovered DNA strands of herpes simplex virus 1 in postmortem brain samples of Alzheimer’s patients at much higher levels than in healthy brains, hinting that viral infection could be somehow involved in the disease. Since then, a string of studies has bolstered the association between Alzheimer’s disease and HSV1, as well as other pathogens, particularly the herpesviruses HHV6A and HHV6B, yet proving causality has remained elusive. Now, in an extensive screen of hundreds of diseased brains from three separate cohorts, a collaboration of US-based researchers reports no evidence for increased RNA or DNA levels of HHV6A or HHV6B in tissue from people with Alzheimer’s disease relative to that from healthy individuals, contradicting the results of some previous results. The scientists also failed to find an association between transcripts of other viruses that have been linked to Alzheimer’s, such as Epstein-Barr virus and cytomegalovirus, and Alzheimer’s, they report today (January 23) in Neuron. “I’m very surprised,” Ruth Itzhaki, an Alzheimer’s disease researcher currently at the University of Oxford who was among those who first associated HSV1, and later HHV6, with the disease, writes to The Scientist in an email. “If their findings are correct, absence of HHV6 would make any involvement in Alzheimer’s disease unlikely,” although not impossible, she notes. Several groups have reported the presence of HHV6 viruses in the brains of Alzheimer’s patients, most notably in a 2018 Neuron study. In that investigation, researchers had found higher levels of HHV6A in patients than in healthy controls, largely based on RNA and DNA sequencing data. © 1986–2020 The Scientist

Keyword: Alzheimers; Neuroimmunology
Link ID: 26989 - Posted: 01.24.2020

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