Links for Keyword: Neuroimmunology

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Ashley Yeager Tiroyaone Brombacher sat in her lab at the University of Cape Town watching a video of an albino mouse swimming around a meter-wide tub filled with water. The animal, which lacked an immune protein called interleukin 13 (IL-13), was searching for a place to rest but couldn’t find the clear plexiglass stand that sat at one end of the pool, just beneath the water’s surface. Instead, it swam and swam, crisscrossing the tub several times before finally finding the platform on which to stand. Over and over, in repeated trials, the mouse failed to learn where the platform was located. Meanwhile, wildtype mice learned fairly quickly and repeatedly swam right to the platform. “When you took out IL-13, [the mice] just could not learn,” says Brombacher, who studies the intersection of psychology, neuroscience, and immunology. Curious as to what was going on, Brombacher decided to dissect the mice’s brains and the spongy membranes, called the meninges, that separate neural tissue from the skull. She wanted to know if the nervous system and the immune system were communicating using proteins such as IL-13. While the knockout mice had no IL-13, she reported in 2017 that the meninges of wildtype mice were chock full of the cytokine. Sitting just outside the brain, the immune protein did, in fact, seem to be playing a critical role in learning and memory, Brombacher and her colleagues concluded. As far back as 2004, studies in rodents suggested that neurons and their support cells release signals that allow the immune system to passively monitor the brain for pathogens, toxins, and debris that might form during learning and memory-making, and that, in response, molecules of the immune system could communicate with neurons to influence learning, memory, and social behavior. Together with research on the brain’s resident immune cells, called microglia, the work overturned a dogma, held since the 1940s, that the brain was “immune privileged,” cut off from the immune system entirely. © 1986–2020 The Scientist.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 27540 - Posted: 10.21.2020

By Christa Lesté-Lasserre The bacteria that live in our bodies, particularly our guts, play key roles in immunity and development. But babies born by cesarean section don’t get the rich blend of microbes that come from a vaginal birth—microbes that may help prevent disorders such as asthma and allergies. Now, a study suggests feeding these infants a small amount of their mothers’ feces could “normalize” their gut microbiome—the ecosystem of bacteria, viruses, and fungi in the digestive system—and possibly give their immune systems a healthier start. Newborns’ guts are blank slates: Babies born vaginally get microbes from their mother’s perineum (the area around the vulva and anus), and those born by C-section get them from mom’s skin. Within just a few hours, the differences are stark. For example, Bacteroides and Bifidobacteria bacteria are abundant in the guts of babies born vaginally, but “almost absent in C-section babies,” says Willem de Vos, a microbiome scientist at the University of Helsinki. Because babies born by C-section have higher rates of immune-related disorders later in life, researchers think this early-life bacteria could “prime” the immune system during a critical development period. To lessen the damage, previous studies have “seeded” C-section babies with their mothers’ vaginal microbiota. But when those efforts didn’t seem to do the trick, de Vos and colleagues theorized that vaginally born babies might get their microbes from accidentally ingesting a smidgen of their mother’s stool during the birthing process. So they recruited 17 mothers preparing to give birth via C-section. Three weeks before the women were to give birth, their fecal samples were scanned for pathogens including group B Streptococcus and herpesvirus. © 2020 American Association for the Advancement of Science.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 27502 - Posted: 10.03.2020

By Apoorva Mandavilli The coronavirus targets the lungs foremost, but also the kidneys, liver and blood vessels. Still, about half of patients report neurological symptoms, including headaches, confusion and delirium, suggesting the virus may also attack the brain. A new study offers the first clear evidence that, in some people, the coronavirus invades brain cells, hijacking them to make copies of itself. The virus also seems to suck up all of the oxygen nearby, starving neighboring cells to death. It’s unclear how the virus gets to the brain or how often it sets off this trail of destruction. Infection of the brain is likely to be rare, but some people may be susceptible because of their genetic backgrounds, a high viral load or other reasons. “If the brain does become infected, it could have a lethal consequence,” said Akiko Iwasaki, an immunologist at Yale University who led the work. The study was posted online on Wednesday and has not yet been vetted by experts for publication. But several researchers said it was careful and elegant, showing in multiple ways that the virus can infect brain cells. Scientists have had to rely on brain imaging and patient symptoms to infer effects on the brain, but “we hadn’t really seen much evidence that the virus can infect the brain, even though we knew it was a potential possibility,” said Dr. Michael Zandi, consultant neurologist at the National Hospital for Neurology and Neurosurgery in Britain. “This data just provides a little bit more evidence that it certainly can.” Dr. Zandi and his colleagues published research in July showing that some patients with Covid-19, the illness caused by the coronavirus, develop serious neurological complications, including nerve damage. © 2020 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 15: Language and Lateralization
Link ID: 27469 - Posted: 09.12.2020

By Lucy Hicks “Social distancing” has become one of the buzz phrases of the year. But it turns out humans aren’t the only animals that put some space between themselves and others to reduce the transmission of disease. Wildlife—from finches to mandrills—use similar tactics, according to a paper published this week in the Proceedings of the Royal Society B. Science chatted with two of the study’s authors—Andrea Townsend, a behavioral ecologist at Hamilton College, and Dana Hawley, a biologist at the Virginia Polytechnic Institute and State University—about how self-isolating works throughout the animal kingdom. This interview has been edited for clarity and length. Get more great content like this delivered right to you! Q: How do animals know when they need to socially distance? Andrea Townsend: COVID-19 has so many symptoms that it’s hard to know when someone is sick. But some animals like house finches use very general behavioral cues, such as lethargy, to assess potential infections and avoid certain individuals. Dana Hawley: In other cases, animals have evolved fairly complex cues to induce social distancing. The Caribbean spiny lobster [a social lobster that normally lives in groups] has evolved to detect a chemical cue in the urine of sick lobsters and avoid areas that these sick lobsters occupy. Another example is in mandrills. Researchers took the feces of animals that did or did not have parasites and basically put a tiny amount on the side of a tree. They found that the primates were much more strongly drawn to the feces of unparasitized animals than those that were parasitized. © 2020 American Association for the Advancement of Science.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 27420 - Posted: 08.15.2020

By Roni Caryn Rabin Neurologists around the world say that a small subset of patients with Covid-19 are developing serious impairments of the brain. Although fever, cough and difficulty breathing are the typical hallmarks of infection with the new coronavirus, some patients exhibit altered mental status, or encephalopathy, a catchall term for brain disease or dysfunction that can have many underlying causes, as well as other serious conditions. These neurological syndromes join other unusual symptoms, such as diminished sense of smell and taste as well as heart ailments. In early March, a 74-year-old man came to the emergency room in Boca Raton, Fla., with a cough and a fever, but an X-ray ruled out pneumonia and he was sent home. The next day, when his fever spiked, family members brought him back. He was short of breath, and could not tell doctors his name or explain what was wrong — he had lost the ability to speak. The patient, who had chronic lung disease and Parkinson’s, was flailing his arms and legs in jerky movements, and appeared to be having a seizure. Doctors suspected he had Covid-19, and were eventually proven right when he was finally tested. On Tuesday, doctors in Detroit reported another disturbing case involving a female airline worker in her late 50s with Covid-19. She was confused, and complained of a headache; she could tell the physicians her name but little else, and became less responsive over time. Brain scans showed abnormal swelling and inflammation in several regions, with smaller areas where some cells had died. Physicians diagnosed a dangerous condition called acute necrotizing encephalopathy, a rare complication of influenza and other viral infections. “The pattern of involvement, and the way that it rapidly progressed over days, is consistent with viral inflammation of the brain,” Dr. Elissa Fory, a neurologist with Henry Ford Health System, said through an email. “This may indicate the virus can invade the brain directly in rare circumstances.” The patient is in critical condition. © 2020 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 15: Language and Lateralization
Link ID: 27164 - Posted: 04.03.2020

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.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 27049 - Posted: 02.19.2020

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.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 26899 - Posted: 12.18.2019

By Matt Richtel Should you pick your nose? Don’t laugh. Scientifically, it’s an interesting question. Should your children pick their noses? Should your children eat dirt? Maybe: Your body needs to know what immune challenges lurk in the immediate environment. Should you use antibacterial soap or hand sanitizers? No. Are we taking too many antibiotics? Yes. “I tell people, when they drop food on the floor, please pick it up and eat it,” said Dr. Meg Lemon, a dermatologist in Denver who treats people with allergies and autoimmune disorders. Advertisement “Get rid of the antibacterial soap. Immunize! If a new vaccine comes out, run and get it. I immunized the living hell out of my children. And it’s O.K. if they eat dirt.” Dr. Lemon’s prescription for a better immune system doesn’t end there. “You should not only pick your nose, you should eat it,” she said. She’s referring, with a facetious touch, to the fact our immune system can become disrupted if it doesn’t have regular interactions with the natural world. “Our immune system needs a job,” Dr. Lemon said. “We evolved over millions of years to have our immune systems under constant assault. Now they don’t have anything to do.” She isn’t alone. Leading physicians and immunologists are reconsidering the antiseptic, at times hysterical, ways in which we interact with our environment. Sign up for Science Times We’ll bring you stories that capture the wonders of the human body, nature and the cosmos. Why? Let us turn to 19th-century London. The British Journal of Homeopathy, volume 29, published in 1872, included a startlingly prescient observation: “Hay fever is said to be an aristocratic disease, and there can be no doubt that, if it is not almost wholly confined to the upper classes of society, it is rarely, if ever, met with but among the educated.” Hay fever is a catchall term for seasonal allergies to pollen and other airborne irritants. With this idea that hay fever was an aristocratic disease, British scientists were on to something. © 2019 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 26027 - Posted: 03.13.2019

Nicola Davis An overactive immune response appears to be a trigger for persistent fatigue, say researchers in a study that could shed light on the causes of chronic fatigue syndrome. Chronic fatigue syndrome (CFS) is a debilitating long-term condition in which individuals experience exhaustion that is not helped by rest, as well as pain, mental fogginess and trouble with memory and sleep. It is also known as myalgic encephalomyelitis (ME). Some studies into the condition have suggested the immune system could be involved, with viral infections one potential trigger for CFS. “The evidence is largely inconclusive – there are studies which have shown elevated levels of the inflammatory markers, but such abnormalities are quite inconsistent across studies,” said Alice Russell, first author of the research from King’s College London. Because it is not possible to predict who will get a virus, it is impossible to look at levels of biological molecules before, during and after a potential CFS “trigger” infection. Experts say they have used a group of people with a different condition as a model to explore how immune response might be linked to persistent fatigue. Writing in the journal Psychoneuroendocrinology, Russell and colleagues describe how they recruited 55 patients with a chronic hepatitis C infection. To treat the condition, all were given a six- to 12-month course of injections of interferon alpha, a protein that is produced naturally by the body and stimulates the white blood cells to provoke an immune response. The treatment has previously been linked to a side effect of ongoing fatigue in some patients. © 2018 Guardian News and Media Limited

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 25792 - Posted: 12.17.2018

Laura Sanders Skulls seem solid, but the thick bones are actually riddled with tiny tunnels. Microscopic channels cut through the skull bones of people and mice, scientists found. In mice, inflammatory immune cells use these previously hidden channels to travel from the bone marrow of the skull to the brain, the team reports August 27 in Nature Neuroscience. It’s not yet known whether immune cells travel these paths through people’s skulls. If so, these tunnels represent a newfound way for immune cells to reach — and possibly inflame — the brain. Along with other blood cells, immune cells are made in bones including those in the arm, leg, pelvis and skull. Researchers injected tracking dyes into bone marrow in the skull and other bones of mice, marking immune cells called neutrophils that originated in each locale. After a stroke, neutrophils flocked to the brain. Instead of coming equally from all sources of bone marrow, as some scientists had thought, most of these responding cells came from skull marrow, study coauthor Matthias Nahrendorf of Massachusetts General Hospital and Harvard Medical School and colleagues found. Curious about cells’ journeys from skull marrow to the brain, the researchers used powerful microscopes to look where skull meets brain. Tiny rivulets through the skull bone connected bone marrow inside the skull to the outer covering of the brain. In mice, neutrophils used these channels, which averaged about 22 micrometers across, as shortcuts to reach the brain. |© Society for Science & the Public 2000 - 2018

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 25411 - Posted: 09.04.2018

Bone marrow, the spongy tissue inside most of our bones, produces red blood cells as well as immune cells that help fight off infections and heal injuries. According to a new study of mice and humans, tiny tunnels run from skull bone marrow to the lining of the brain and may provide a direct route for immune cells responding to injuries caused by stroke and other brain disorders. The study was funded in part by the National Institutes of Health and published in Nature Neuroscience. “We always thought that immune cells from our arms and legs traveled via blood to damaged brain tissue. These findings suggest that immune cells may instead be taking a shortcut to rapidly arrive at areas of inflammation,” said Francesca Bosetti, Ph.D., program director at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS), which provided funding for the study. “Inflammation plays a critical role in many brain disorders and it is possible that the newly described channels may be important in a number of conditions. The discovery of these channels opens up many new avenues of research.” Using state-of-the-art tools and cell-specific dyes in mice, Matthias Nahrendorf, M.D., Ph.D., professor at Harvard Medical School and Massachusetts General Hospital in Boston, and his colleagues were able to distinguish whether immune cells traveling to brain tissue damaged by stroke or meningitis, came from bone marrow in the skull or the tibia, a large legbone. In this study, the researchers focused on neutrophils, a particular type of immune cell, which are among the first to arrive at an injury site.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 25388 - Posted: 08.28.2018

By Esther Landhuis From savoring a piece of cake to hugging a friend, many of life’s pleasures trigger a similar reaction in the brain—a surge of chemicals that tell the body “that was good, do it again.” Research published Friday in Nature Communications suggests this feel-good circuit may do much more. Using lab tools to activate that reward circuit in mice, scientists discovered that its chemical signals reach the immune system, empowering a subset of bone marrow cells to slow the growth of tumors. The findings have yet to be confirmed in humans. But given the reward system is linked with positive emotions, the research offers a physiological mechanism for how a person’s psychological state could help to stall cancer progression. Plenty of research measures the health impact of stress and negative feelings, says Erica Sloan, a biologist at Monash University in Melbourne, Australia. But the potential for immune activity to shift in response to positive influences through the brain’s reward center—“that’s what I think is really exciting,” says Sloan, who studies neural-immune activity in cancer but was not involved in the present study. The notion that the brain talks to the immune system isn’t new. One of the most compelling examples is the placebo effect—the centuries-old observation that sugar pills can work as well as evidence-based medicine in some people. For years scientists have tried to unravel the biology behind this mysterious phenomenon. © 2018 Scientific American

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory and Learning
Link ID: 25205 - Posted: 07.14.2018

Hartmut Wekerle Some immunologists regard the central nervous system (CNS) as a no-man’s-land, avoided by immune cells and therefore uninteresting. But, in fact, the CNS has a vigorous immune potential that remains dormant in normal conditions but is awakened after injury. The switch that controls the brain’s immune microenvironment involves non-neuronal cells called glia — not only microglia, which are sometimes called the immune cells of the CNS, but also multifunctional cells called astrocytes1. In a paper in Nature, Rothhammer et al.2 describe how these two glial cell types communicate on a molecular level to influence inflammation in the CNS, and show that this interaction is controlled remotely by microbes that inhabit the gut. A decade ago, the group that performed the current study, along with another research group, discovered3,4 an unexpected immunoregulatory role for a ligand-activated transcription factor called the aryl hydrocarbon receptor (AHR), which at the time was best known as a receptor for environmental toxins5. The two groups showed that AHR modulates the progression of experimental autoimmune encephalomyelitis (EAE) — an autoimmune disease in mice in which the immune system becomes overactive and attacks the CNS. EAE is often used a model of multiple sclerosis (MS). Initially, the groups focused on how AHR might affect EAE by regulating pathogenic and protective subsets of immune cells outside the CNS. But it later emerged that AHR is also strongly expressed in the CNS, particularly in microglia and astrocytes6, raising the question of whether AHR in the CNS has a role in autoimmune diseases. © 2018 Macmillan Publishers Limited,

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 25010 - Posted: 05.23.2018

Nancy Shute It's just a cold. But even though I know I'm not horribly ill, I feel this overwhelming need to skip work, ignore my family and retreat to the far corner of the sofa. I'm not being a wimp, it turns out. Those feelings are a real thing called sickness behavior, which is sparked by the body's response to infection. The same chemicals that tell the immune system to rush in and fend off invading viruses also tell us to slow down, skip the eating, drinking and sex, shun social interactions and rest. "Those messages are so powerful they can't be ignored," says Philip Chen, a rhinologist at the University of Texas, San Antonio. But that doesn't mean we don't try. Symptoms like a stuffy nose are obvious, Chen notes, but we're less aware that changes in mood and behavior are also part of our bodies' natural response to infection. It might behoove us to pay attention. There's plenty of evidence that having a cold impairs mood, alertness and working memory, and that brain performance falls off with even minor symptoms. But for most people, having a cold does not equal "take the week off." And that means many people work sick, even when it can put others in danger. A 2015 survey of food workers found that half "always" or "frequently' went to work while sick. © 2018 npr

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 24494 - Posted: 01.06.2018

Douglas Fox Six times a day, Katrin pauses whatever she's doing, removes a small magnet from her pocket and touches it to a raised patch of skin just below her collar bone. For 60 seconds, she feels a soft vibration in her throat. Her voice quavers if she talks. Then, the sensation subsides. The magnet switches on an implanted device that emits a series of electrical pulses — each about a milliamp, similar to the current drawn by a typical hearing aid. These pulses stimulate her vagus nerve, a tract of fibres that runs down the neck from the brainstem to several major organs, including the heart and gut. The technique, called vagus-nerve stimulation, has been used since the 1990s to treat epilepsy, and since the early 2000s to treat depression. But Katrin, a 70-year-old fitness instructor in Amsterdam, who asked that her name be changed for this story, uses it to control rheumatoid arthritis, an autoimmune disorder that results in the destruction of cartilage around joints and other tissues. A clinical trial in which she enrolled five years ago is the first of its kind in humans, and it represents the culmination of two decades of research looking into the connection between the nervous and immune systems. For Kevin Tracey, a neurosurgeon at the Feinstein Institute for Medical Research in Manhasset, New York, the vagus nerve is a major component of that connection, and he says that electrical stimulation could represent a better way to treat autoimmune diseases, such as lupus, Crohn's disease and more. Several pharmaceutical companies are investing in 'electroceuticals' — devices that can modulate nerves — to treat cardiovascular and metabolic diseases. But Tracey's goal of controlling inflammation with such a device would represent a major leap forward, if it succeeds. © 2017 Macmillan Publishers Limited

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 5: The Sensorimotor System
Link ID: 23573 - Posted: 05.04.2017

By Matt Blois A ruthless killer may soon help brain cancer patients. The rabies virus, which kills tens of thousands of people a year, has a rare ability to enter nerve cells and use them as a conduit to infect brain tissue. Now, scientists are trying to mimic this strategy to ferry tumor-killing nanoparticles into brain tumors. So far the approach has been shown to work only in mice. If successful in people, these nanoparticles could one day help doctors send treatment directly to tumors without harming healthy cells. The rabies virus, transmitted largely through the bites of infected animals, has evolved over thousands of years to hijack nerve cells, which it uses to climb from infected muscle tissue into the brain. That allows it to bypass a major hurdle: the blood-brain barrier, a selective membrane that keeps out most pathogens that travel through the bloodstream. But the barrier also prevents treatments—like cancer drugs—from reaching infected cells, limiting options for patients. To get around this problem, scientists are looking to the virus for inspiration. Already, researchers have packaged cancer-fighting drugs into nanoparticles coated with part of a rabies surface protein that lets the virus slip into the central nervous system. Now, a team of researchers from Sungkyunkwan University in Suwon, South Korea, has taken things one step further. Nanoparticle expert Yu Seok Youn and his team have engineered gold particles so that they have the same rodlike shape and size as the virus. The nanoparticle’s shape gives it more surface area than spherical particles, improving the surface protein’s ability to bind with receptors on nerve cells that serve as a gateway to the nervous system. The particles don’t carry any drugs, but the tiny gold rods readily absorb laser light, which heats them up and kills surrounding tissue. © 2017 American Association for the Advancement of Science.

Related chapters from BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 11: Emotions, Aggression, and Stress
Link ID: 23216 - Posted: 02.11.2017

By JAMES HAMBLIN In 1997, a few hundred people who responded to a job posting in a Pittsburgh newspaper agreed to let researchers spray their nostrils with a rhinovirus known to cause the common cold. The people would then be quarantined in hotel rooms for five days and monitored for symptoms. In return they’d get $800. “Hey, it’s a job,” some presumably said. Compensation may also have come from the knowledge that, as they sat alone piling up tissues, they were contributing to scientific understanding of our social-microbial ecosystem. The researchers wanted to investigate a seemingly basic question: Why do some people get more colds than others? To Gene Brody, a professor at the University of Georgia, the answer was “absolutely wild.” (Dr. Brody is a public-health researcher, so “wild” must be taken in that context.) He and colleagues recently analyzed the socio-economic backgrounds and personalities of the people in the Pittsburgh study and found that those who were “more diligent and tended to strive for success” were more likely than the others to get sick. To Dr. Brody, the implication was that something suffers in the immune systems of people who persevere in the face of adversity. Over the past two years, Dr. Brody and colleagues have amassed more evidence supporting this theory. In 2015, they found that white blood cells among strivers were prematurely aged relative to those of their peers. Ominous correlations have also been found in cardiovascular and metabolic health. In December, Dr. Brody and colleagues published a study in the journal Pediatrics that said that among black adolescents from disadvantaged backgrounds, “unrelenting determination to succeed” predicted an elevated risk of developing diabetes. The focus on black adolescents is significant. In much of this research, white Americans appeared somehow to be immune to the negative health effects that accompany relentless striving. As Dr. Brody put it when telling me about the Pittsburgh study, “We found this for black persons from disadvantaged backgrounds, but not white persons.” © 2017 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 23167 - Posted: 01.30.2017

By Mitch Leslie When we have food poisoning, the last thing we want to do is eat. But in mice, a microbe that causes this ailment actually increases appetite, a new study reveals. Researchers say they might be able to use the same trick to increase eating in cancer patients and old folks, who often lose their desire for food. “I think it’s a fantastic paper,” says immunophysiologist Keith Kelley of the University of Illinois in Urbana, who wasn’t connected to the study. The researchers deserve praise for combining approaches from several disciplines such as microbiology, neurobiology, and immunology to draw a surprising conclusion, he says. “It’s the way disease responses should be investigated.” Some of the symptoms you endure when you are ill, such as lethargy and fever, are actually good for you. Lolling on the couch all day, for instance, saves energy for your immune cells. But the picture is more complex for another of these so-called sickness behaviors—reduced appetite. Animal studies have found that eating less seems to improve the odds of surviving some infections, perhaps because it robs the invading microbes of key nutrients, but in other cases the loss of appetite often proves fatal. © 2017 American Association for the Advancement of Science

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 23155 - Posted: 01.27.2017

Laura Sanders Feeling good may help the body fight germs, experiments on mice suggest. When activated, nerve cells that help signal reward also boost the mice’s immune systems, scientists report July 4 in Nature Medicine. The study links positive feelings to a supercharged immune system, results that may partially explain the placebo effect. Scientists artificially dialed up the activity of nerve cells in the ventral tegmental area — a part of the brain thought to help dole out rewarding feelings. This activation had a big effect on the mice’s immune systems, Tamar Ben-Shaanan of Technion-Israel Institute of Technology in Haifa and colleagues found. A day after the nerve cells in the ventral tegmental area were activated, mice were infected with E. coli bacteria. Later tests revealed that mice with artificially activated nerve cells had less E. coli in their bodies than mice without the nerve cell activation. Certain immune cells seemed to be ramped up, too. Monocytes and macrophages were more powerful E. coli killers after the nerve cell activation. If a similar effect is found in people, the results may offer a biological explanation for how positive thinking can influence health. |© Society for Science & the Public 2000 - 2016

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory and Learning
Link ID: 22395 - Posted: 07.05.2016

By Mitch Leslie The worst part of being sick isn’t always the muscle aches and coughing. It’s the foggy head, the crankiness, the apathy, and the fatigue—in short, what researchers call sickness behavior. A new study uncovers a molecular mechanism that explains why we feel so crummy when we’re under the weather. “It’s a nice study that’s covered a lot of ground,” says neuroimmunologist Colm Cunningham of Trinity College in Dublin who wasn’t connected to the research. “What they’ve found is very plausible.” Although sickness behavior is unpleasant, researchers think the symptoms we suffer during a viral or bacterial infection are beneficial, enabling us to divert our energy to fighting the pathogens that have invaded our bodies. For cancer patients and people with autoimmune diseases, however, sickness behavior can be an unwanted side effect of treatment with immune molecules known as interferons, which our cells naturally release when we have an infection. The condition has posed a puzzle for researchers because they assumed the blood-brain barrier, a protective system that excludes most pathogens and immune molecules from the brain, would block signals from the immune system. Although scientists have identified several mechanisms that allow such messages to cross the barrier and influence behavior, the question of how the immune system and brain communicate “has been only partially answered,” says immunophysiologist Keith Kelley of the University of Illinois, Urbana-Champaign, who wasn’t connected to the new study. © 2016 American Association for the Advancement of Science.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 22121 - Posted: 04.20.2016