Links for Keyword: Neuroimmunology

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Nicola Davis Science correspondent From forgetfulness to difficulties concentrating, many people who have long Covid experience “brain fog”. Now researchers say the symptom could be down to the blood-brain barrier becoming leaky. The barrier controls which substances or materials enter and exit the brain. “It’s all about regulating a balance of material in blood compared to brain,” said Prof Matthew Campbell, co-author of the research at Trinity College Dublin. “If that is off balance then it can drive changes in neural function and if this happens in brain regions that allow for memory consolidation/storage then it can wreak havoc.” Writing in the journal Nature Neuroscience, Campbell and colleagues report how they analysed serum and plasma samples from 76 patients who were hospitalised with Covid in March or April 2020, as well 25 people before the pandemic. Among other findings, the team discovered that samples from the 14 Covid patients who self-reported brain fog contained higher levels of a protein called S100β than those from Covid patients without this symptom, or people who had not had Covid. caskets at a funeral home This protein is produced by cells within the brain, and is not normally found in the blood, suggesting these patients had a breakdown of the blood-brain barrier. The researchers then recruited 10 people who had recovered from Covid and 22 people with long Covid – 11 of whom reported having brain fog. None had, at that point, received a Covid vaccine, or been hospitalised for Covid. These participants underwent an MRI scan in which a dye was administered intravenously. The results reveal long Covid patients with brain fog did indeed show signs of a leaky blood-brain barrier, but not those without this symptom, or who had recovered. © 2024 Guardian News & Media Limited

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 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 29158 - Posted: 02.22.2024

By Pam Belluck Jennifer Caldwell was active and energetic, working two jobs and taking care of her daughter and her parents, when she developed a bacterial infection that was followed by intense lightheadedness, fatigue and memory problems. That was nearly a decade ago, and she has since struggled with the condition known as myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS. Ms. Caldwell, 56, of Hillsborough, N.C., said she went from being able to ski, dance and work two jobs as a clinical research coordinator and a caterer to needing to stay in bed most of every day. “I haven’t been right since, and I haven’t worked a day since,” said Ms. Caldwell, whose symptoms include severe dizziness whenever her legs are not elevated. The condition has also “messed me up cognitively,” she said. “I can’t read something and comprehend it very well at all, I can’t remember new things. It’s kind of like being in a limbo state. That’s how I describe it, lost in limbo.” Seven years ago, the National Institutes of Health began a study of patients with ME/CFS, and Ms. Caldwell became one of 17 participants who engaged in a series of tests and evaluations of their blood, bodies and brains. Findings from the study, which was published on Wednesday in the journal Nature Communications, showed notable physiological differences in the immune system, cardio-respiratory function, gut microbiome and brain activity of the ME/CFS patients compared with a group of 21 healthy study participants. Medical experts said that even though the study was a snapshot of a small number of patients, it was valuable, partly because ME/CFS has long been dismissed or misdiagnosed. The findings confirm that “it’s biological, not psychological,” said Dr. Avindra Nath, the chief of infections of the nervous system at the National Institute of Neurological Disorders and Stroke, who led the study. © 2024 The New York Times Company

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: 29157 - Posted: 02.22.2024

By Claudia Lopez Lloreda Of all of COVID-19’s symptoms, one of the most troubling is “brain fog.” Victims report headaches, trouble concentrating, and forgetfulness. Now, researchers have shown that SARS-CoV-2 can cause brain cells to fuse together, disrupting their communication. Although the study was only done in cells in a lab dish, some scientists say it could help explain one of the pandemic’s most confounding symptoms. “This is a first important step,” says Stefan Lichtenthaler, a biochemist at the German Center for Neurodegenerative Diseases who was not involved with the work. Researchers already knew that SARS-CoV-2 could cause certain cells to fuse together. The lungs of patients who die from severe COVID-19 are often riddled with large, multicellular structures called syncytia, which scientists believe may contribute to the respiratory symptoms of the disease. Like other viruses, SARS-CoV-2 may incite cells to fuse to help it spread across an organ without having to infect new cells. To see whether such cell fusion might happen in brain cells, Massimo Hilliard, a neuroscientist at the University of Queensland, and his colleagues first genetically engineered two populations of mouse neurons: One expressed a red fluorescent molecule, and the other a green fluorescent molecule. If the two fused in a lab dish, they would show up as bright yellow under the microscope. That’s just what the researchers saw when they added SARS-CoV-2 to a dish containing both types of cells, they report today in Science Advances. The same fusion happened in human brain organoids, so-called minibrains that are created from stem cells. The key appears to be angiotensin-converting enzyme 2 (ACE2), the protein expressed on the surface of mammalian cells that SARS-CoV-2 is known to target. The virus uses a surface protein called spike to bind to ACE2, triggering the virus to fuse to a cell and release its genetic material inside. Seemingly, the spike protein in infected cells may also make other ACE2 on a cell trigger fusion to a neighboring cell. When the team engineered neurons to express the spike protein, only cells that also expressed ACE2 were able to fuse with each other. The findings parallel previous work in lung cells: The ACE2 receptor seems to be critical in mediating their fusion during SARS-CoV-2 infection.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 14: Attention and Higher Cognition
Link ID: 28818 - Posted: 06.14.2023

Twelve people with persistent neurological symptoms after SARS-CoV-2 infection were intensely studied at the National Institutes of Health (NIH) and were found to have differences in their immune cell profiles and autonomic dysfunction. These data inform future studies to help explain persistent neurological symptoms in Long COVID. The findings, published in Neurology: Neuroimmunology & Neuroinflammation(link is external), may lead to better diagnoses and new treatments. People with post-acute sequelae of COVID-19 (PASC), which includes Long COVID, have a wide range of symptoms, including fatigue, shortness of breath, fever, headaches, sleep disturbances, and “brain fog,” or cognitive impairment. Such symptoms can last for months or longer after an initial SARS-CoV-2 infection. Fatigue and “brain fog” are among the most common and debilitating symptoms, and likely stem from nervous system dysfunction. Researchers used an approach called deep phenotyping to closely examine the clinical and biological features of Long COVID in 12 people who had long-lasting, disabling neurological symptoms after COVID-19. Most participants had mild symptoms during their acute infection. At the NIH Clinical Center, participants underwent comprehensive testing, which included a clinical exam, questionnaires, advanced brain imaging, blood and cerebrospinal fluid tests, and autonomic function tests. The results showed that people with Long COVID had lower levels of CD4+ and CD8+ T cells—immune cells involved in coordinating the immune system’s response to viruses—compared to healthy controls. Researchers also found increases in the numbers of B cells and other types of immune cells, suggesting that immune dysregulation may play a role in mediating Long COVID.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 28771 - Posted: 05.06.2023

ByClaudia Lopez Lloreda Peanuts have a dark side. In some people, they can cause a dangerous and sometimes deadly allergic reaction marked by a sharp drop in body temperature and blood pressure, as well as difficulty breathing. This anaphylactic shock has typically been blamed on the immune system going into overdrive. But a new study in mice pegs an additional culprit: the nervous system. The findings, reported today in Science Immunology, “are line with what people thought but no one was actually able to demonstrate,” says Sebastien Talbot, a neuroimmunologist at Queen’s University who was not involved in the study. The work, he says, could open up new targets to treat severe allergic reactions in people. Anaphylaxis strikes about one in 50 individuals in the United States every year. Besides peanuts, bee stings and some medicines are common triggers. These allergens cause the immune system’s mast cells to release a barrage of histamine and other molecules that spread throughout the body, dilating blood vessels and narrowing airways. Body temperature can also drop, making people feel cold and clammy, though why this happens has been less clear. Mice experience anaphylaxis, too. When exposed to an allergen, they lie on their bellies and stretch out. Such behaviors are controlled by the central nervous system, which made Soman Abraham, an immunologist at Duke University, suspect nerves may also play a role in severe allergic reactions. To find out, he and colleagues gave the mice ovalbumin—the main protein found in egg whites and a known trigger of anaphylaxis—and used electrodes and microscopy to record and measure neuron activity. As in humans, the rodents’ body temperature dropped—about 10°C. But the mice’s brains didn’t register this as a sudden freeze; instead, brain areas that typically respond to heat had higher levels of activity. This false feeling of warmth explains why the animals stretch out as if they’re overheating even as their body temperature drops.

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: 28706 - Posted: 03.18.2023

By Catherine Offord When you come down with the flu, your body lets you know. You lose your appetite, you feel sluggish, and your mood takes a hit. The infection itself doesn’t cause these symptoms—your brain does. Now, scientists may have figured out a key part of how this happens. Studying mice with influenza, they found a cluster of nerve cells in the back of the throat that detects a virus’ presence and sends signals to the brain, triggering symptoms that respond to the infection. The study is among the first to pin this response on a specific population of nerve cells, says Anoj Ilanges, a biologist at the Howard Hughes Medical Institute’s Janelia Research Campus who was not involved in the work. “They’ve done a really great job of looking at this comprehensively.” Scientists know feeling crummy during an illness is partly the result of chemicals produced by infected tissue. Several of these compounds, such as prostaglandins, are known to trigger sickness behaviors. (Drugs such as ibuprofen work by blocking prostaglandin production.) But it’s often unclear exactly how these chemicals communicate with the brain, says Stephen Liberles, a molecular neuroscientist at Harvard Medical School. “Surprisingly little is understood about how the brain becomes aware that there’s an infection in the body.” In the new study, Liberles, postdoc Na-Ryum Bin, and colleagues focused on influenza, which infects the body’s airways. Previous research hinted that a type of prostaglandin made in response to viral infection called PGE2 could travel via the blood to interact with cells in the brain. But when the researchers infected mice that had been genetically engineered to lack receptors for PGE2 in the central nervous system, the animals still acted sick—avoiding eating and drinking, and moving around less than normal.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 28698 - Posted: 03.11.2023

Rachel Treisman A man in southwest Florida died after becoming infected with a rare brain-eating amoeba, which state health officials say was "possibly as a result of sinus rinse practices utilizing tap water." The Florida Department of Health in Charlotte County confirmed Thursday that the unidentified man died of Naegleria fowleri. State and local health and environmental agencies "continue to coordinate on this ongoing investigation, implement protective measures, and take any necessary corrective actions," they added. The single-celled amoeba lives in warm fresh water and, once ingested through the nose, can cause a rare but almost-always fatal brain infection known as primary amebic meningoencephalitis (PAM). The Centers for Disease Control and Prevention has tallied 157 PAM infections in the U.S. between 1962 and 2022, with only four known survivors (a fifth, a Florida teenager, has been fighting for his life since last summer, according to an online fundraiser by his family). Agency data suggests this is the first such infection ever reported in February or March. Infections are most common in Southern states and during warmer months, when more people are swimming — and submerging their heads — in lakes and rivers. But they can also happen when people use contaminated tap water to rinse their sinuses, either as part of a religious ritual or an at-home cold remedy. The CDC says the disease progresses rapidly and usually causes death within about five days of symptom onset. © 2023 npr

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 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 28685 - Posted: 03.04.2023

By Tara C. Smith In The Last of Us, a video game series and recent television show, fungal pathogens are to blame for a zombie-like plague. Once infected, humans lose control over their bodies and become increasingly aggressive, seeking to infect others through violence. It’s a familiar trope: The same fungus, Ophiocordyceps, torments humanity in the movie The Girl With All the Gifts, while viruses do the work in the film 28 Days Later and the novel World War Z. But the concept of a pathogen that can manipulate its host’s behavior — against their will and often to their detriment — is not purely the work of fiction. In these zombie-like cases, the pathogen (whether it’s a virus, bacteria or fungus, or something else) acts specifically to change the behavior of its host. While we know a decent amount about these pathogens — including the very real Ophiocordyceps fungus, which does turn insects into unwitting agents of societal collapse — there’s still much to learn. So the Cordyceps fungus is real? “Cordyceps” has become a common catch-all name for a group of fungi that infect insects. This grouping includes the species Ophiocordyceps unilateralis, better known as the “zombie ant fungus.” It spreads by sprouting fungal structures that erupt through the ant’s head after its death. A regular column in which top researchers explore the process of discovery. This month’s columnist, Tara C. Smith, is a professor of epidemiology and infectious-disease researcher. The challenge for this reproductive strategy is that ants are social insects, and so they act to protect the colony from infections. As part of this behavior, ants typically remove dead ants from the nest. A lone dead ant outside the nest won’t spread the fungus. All Rights Reserved © 2023

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: 28684 - Posted: 02.25.2023

Diana Kwon Hundreds of scientists around the world are looking for ways to treat heart attacks. But few started where Hedva Haykin has: in the brain. Haykin, a doctoral student at the Technion — Israel Institute of Technology in Haifa, wants to know whether stimulating a region of the brain involved in positive emotion and motivation can influence how the heart heals. Late last year, in a small, windowless microscope room, she pulled out slides from a thin black box, one by one. On them were slices of hearts, no bigger than pumpkin seeds, from mice that had experienced heart attacks. Under a microscope, some of the samples were clearly marred by scars left in the aftermath of the infarction. Others showed mere speckles of damage visible among streaks of healthy, red-stained cells. The difference in the hearts’ appearance originated in the brain, Haykin explains. The healthier-looking samples came from mice that had received stimulation of a brain area involved in positive emotion and motivation. Those marked with scars were from unstimulated mice. “In the beginning we were sure that it was too good to be true,” Haykin says. It was only after repeating the experiment several times, she adds, that she was able to accept that the effect she was seeing was real. Haykin, alongside her supervisors at the Technion — Asya Rolls, a neuroimmunologist, and Lior Gepstein, a cardiologist — are trying to work out exactly how this happens. On the basis of their experiments so far, which have not yet been published, activation of this brain reward centre — called the ventral tegmental area (VTA) — seems to trigger immune changes that contribute to the reduction of scar tissue. This study has its roots in decades of research pointing to the contribution of a person’s psychological state to their heart health1. In a well-known condition known as ‘broken-heart syndrome’, an extremely stressful event can generate the symptoms of a heart attack — and can, in rare cases, be fatal. Conversely, studies have suggested that a positive mindset can lead to better outcomes in those with cardiovascular disease. But the mechanisms behind these links remain elusive.

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 28680 - Posted: 02.25.2023

Diana Kwon The brain is the body’s sovereign, and receives protection in keeping with its high status. Its cells are long-lived and shelter inside a fearsome fortification called the blood–brain barrier. For a long time, scientists thought that the brain was completely cut off from the chaos of the rest of the body — especially its eager defence system, a mass of immune cells that battle infections and whose actions could threaten a ruler caught in the crossfire. In the past decade, however, scientists have discovered that the job of protecting the brain isn’t as straightforward as they thought. They’ve learnt that its fortifications have gateways and gaps, and that its borders are bustling with active immune cells. A large body of evidence now shows that the brain and the immune system are tightly intertwined. Scientists already knew that the brain had its own resident immune cells, called microglia; recent discoveries are painting more-detailed pictures of their functions and revealing the characteristics of the other immune warriors housed in the regions around the brain. Some of these cells come from elsewhere in the body; others are produced locally, in the bone marrow of the skull. By studying these immune cells and mapping out how they interact with the brain, researchers are discovering that they play an important part in both healthy and diseased or damaged brains. Interest in the field has exploded: there were fewer than 2,000 papers per year on the subject in 2010, swelling to more than 10,000 per year in 2021, and researchers have made several major findings in the past few years. No longer do scientists consider the brain to be a special, sealed-off zone. “This whole idea of immune privilege is quite outdated now,” says Kiavash Movahedi, a neuroimmunologist at the Free University of Brussels (VUB). Although the brain is still seen as immunologically unique — its barriers prevent immune cells from coming and going at will — it’s clear that the brain and immune system constantly interact, he adds (see ‘The brain’s immune defences’). © 2022 Springer Nature Limited

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 28344 - Posted: 06.01.2022

By Lisa Sanders, M.D. “You have to take your husband to the hospital right now,” the doctor urged over the phone. “His kidneys aren’t working at all, and we need to find out why.” The woman looked at her 82-year-old spouse. He was so thin and pale. She thanked the doctor and called 911. For the past couple of months, every meal was a struggle. Swallowing food was strangely difficult. Liquids were even worse. Whatever he drank seemed to go down the wrong pipe, and he coughed and sputtered after almost every sip. It was terrifying. He saw an ear, nose and throat specialist, who scoped his mouth and esophagus. There wasn’t anything blocking the way. The doctor recommended that he get some therapy to help him strengthen the muscles he used to swallow, and until he did that, he should thicken his liquids to make drinking easier. The patient tried that once, but it was so disgusting he gave up on it. His wife was worried as she watched him eat and drink less and less. She could see that he was getting weaker every day. He had a stroke four months earlier, and since then his right foot dragged a little. But now she had to help him get out of his recliner. And he wasn’t able to drive — she had to make the 45-minute trip with him each day to his office. Finally, he agreed to see Dr. Richard Kaufman, their primary-care doctor. Kaufman was shocked by the man’s appearance, how the skin on his face hung in folds as if air had been let out of his cheeks. He’d lost nearly 40 pounds. He struggled to walk the few steps to the exam table. His right side, which was weakened by his stroke, was now matched by weakness on his left side. His stroke hadn’t done this. There was something else going on. Kaufman ordered some preliminary blood tests to try to see where the problem might lie. Those were the results that sent the couple to the emergency room. © 2022 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 5: The Sensorimotor System
Link ID: 28339 - Posted: 05.28.2022

By Laura Sanders A tussle with COVID-19 can leave people’s brains fuzzy. SARS-CoV-2, the virus behind COVID-19, doesn’t usually make it into the brain directly. But the immune system’s response to even mild cases can affect the brain, new preliminary studies suggest. These reverberating effects may lead to fatigue, trouble thinking, difficulty remembering and even pain, months after the infection is gone. It’s not a new idea. Immune systems gone awry have been implicated in cognitive problems that come with other viral infections such as HIV and influenza, with disorders such as myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS, and even from the damaging effects of chemotherapy. What’s different with COVID-19 is the scope of the problem. Millions of people have been infected, says neurologist Avindra Nath of the National Institutes of Health in Bethesda, Md. “We are now faced with a public health crisis,” he says. Sign up for e-mail updates on the latest coronavirus news and research To figure out ways to treat people for the fuzzy thinking, headaches and fatigue that hang around after a bout with COVID-19, scientists are racing to figure out what’s causing these symptoms (SN: 4/27/21). Cognitive neurologist Joanna Hellmuth at the University of California, San Francisco had a head start. As someone who had studied the effects of HIV on the brain, she quickly noted similarities in the neurological symptoms of HIV and COVID-19. The infections paint “the same exact clinical picture,” she says. HIV-related cognitive symptoms have been linked to immune activation in the body, including the brain. “Maybe the same thing is happening in COVID,” Hellmuth says. © Society for Science & the Public 2000–2022.

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: 28189 - Posted: 02.05.2022

Esther Landhuis Dogs that habitually hear a bell at chow time become classically conditioned to drool at the mere chime, as the physiologist Ivan Pavlov showed in the 1890s: Their brains learn to associate the bell with food and instruct the salivary glands to respond accordingly. More than a century later, in a paper published today in Cell, the neuroimmunologist Asya Rolls has shown that a similar kind of conditioning extends to immune responses. Using state-of-the-art genetic tools in mice, her team at the Technion in Haifa, Israel, identified brain neurons that became active during experimentally induced inflammation in the abdomen. Later, the researchers showed that restimulating those neurons could trigger the same types of inflammation again. “This is an outstanding body of work,” said Kevin Tracey, a neurosurgeon and president of the Feinstein Institutes for Medical Research in Manhasset, New York. It “establishes that the classic concept of immunological memory can be represented in neurons.” Others before Rolls have suggested that the brain could remember and retrieve immune responses, he said, but “she proved it.” Abstractions navigates promising ideas in science and mathematics. Journey with us and join the conversation. Ruslan Medzhitov, an immunologist at the Yale School of Medicine in New Haven, Connecticut, considers the new research “very provocative.” But unlike other groundbreaking studies that push boundaries and challenge conventional concepts, he said that this one also evokes “the ‘Oh, it makes sense’ type of reaction.” All Rights Reserved © 2021

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 28071 - Posted: 11.13.2021

By Raleigh McElvery While the brain and spinal cord have their own squad of specialized immune cells, the peripheral immune system is armed with a larger battalion of proteins, cells and entire organs, such as the spleen, that ward off invaders. Over the past decade, researchers have made great progress in understanding how the peripheral immune system affects neural activity: how immune signals that originate outside the central nervous system can affect cognitive processes, social behavior, neurodegeneration, and more. In fact, they have learned that immune cells from the periphery routinely patrol the central nervous system and support its function. In a new study, researchers showed for the first time that—just as the brain remembers people, places, smells, and so on—it also stores what they call “memory traces” of the body’s past infections. Reactivating the same brain cells that encode this information is enough to swiftly summon the peripheral immune system to defend at-risk tissues. In some ways, this is not an entire surprise. It is clear the peripheral immune system is capable of retaining information about past infections to fight off future ones—otherwise, vaccines would not work. But Asya Rolls, a neuroimmunologist at Technion–Israel Institute of Technology and the paper’s senior author, says the study expands this concept of classical immunologic memory. Initially, she was taken aback that the brain could store traces of immune activity and use them to trigger such a precise response. “I was amazed,” she says. Rolls’s team focused on a brain region called the insular cortex, which senses the body’s internal state through visceral signals such as temperature, pain, hunger and—the researchers reasoned—perhaps immune activity. They studied strains of mice with a type of gut inflammation known as colitis and used fluorescent markers to take snapshots of the groups of brain cells in the insular cortex that became active during the infection. © 2021 Scientific American

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 28069 - Posted: 11.09.2021

Linda Geddes Science correspondent Fibromyalgia – a poorly understood condition that causes widespread pain throughout the body and extreme tiredness – may be caused by be an autoimmune response that increases the activity of pain-sensing nerves throughout the body. The findings, published in the Journal of Clinical Investigation, challenge the widely held view that the condition originates in the brain, and could pave the way for more effective treatments for the millions of people affected. They could also have implications for patients suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and “long Covid”. “These different syndromes are symptomatically very similar, so I think it could be very relevant to both of these conditions,” said Dr David Andersson from the Institute of Psychiatry, Psychology and Neuroscience at King’s College London, who led the new study. Fibromyalgia affects at least 1 in 40 people worldwide, although some estimates suggest nearly 1 in 20 people may be affected to some degree. It is characterised by widespread pain and crippling fatigue – often referred to as “fibro fog” – and usually develops between the ages of 25 and 55, although children can also get it. Similar to many autoimmune conditions, the vast majority of those affected (80% are women). Current treatment tends to focus on gentle aerobic exercise, as well as drug and psychological therapies designed to manage pain. However, these have proven ineffective in most patients and have left behind an enormous unmet clinical need, said Andersson. “The widespread paradigm at the moment is that this is a disease that emanates from the brain, and I think our findings suggest that that’s not the case,” he said. © 2021 Guardian News & 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: 27888 - Posted: 07.03.2021

Elena Renken A hundred years ago, the Japanese scientist Y. Shirai published a mysterious finding: When Shirai transplanted tumor tissue into a mouse’s body, the tissue was destroyed by its immune system. But when tumors were grafted in various places in the mouse’s brain, they grew. Tumors seemed to be able to safely hide in the brain, escaping the immune system’s notice. Similar results soon piled up, and scientific consensus accepted the brain as having “immune privilege” — a kind of separation from the immune system. This notion made some sense. Immune cells, in the course of fighting infections, can damage or destroy healthy tissue. Protecting neurons from this damage is more crucial than protecting cells like those in the liver or skin, because neurons typically can’t regenerate. “If they die, they die,” said Justin Rustenhoven, an immunologist at Washington University in St. Louis. “We have a very poor ability to replace them.” In the last couple of decades, though, the idea of immune privilege has withered in the face of mounting evidence that the brain and the immune system do interact. Researchers have tracked immune cells crossing from the bloodstream into the nervous system in animals with brain disease, for instance, and they’ve observed cognitive deficits in mice that lack certain immune cells. Now, Rustenhoven and collaborators have identified how evolution achieves a balancing act, limiting the dangers of immune responses in the central nervous system while still providing protection from disease. The researchers reported recently in the journal Cell that the immune system operates from a distance to constantly inspect the brain for signs of trouble. Immune cells, rather than making themselves at home throughout the brain itself, patrol the sidelines until they detect a threat. All Rights Reserved © 2021

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 27799 - Posted: 05.01.2021

The membranes surrounding our brains are in a never-ending battle against deadly infections, as germs constantly try to elude watchful immune cells and sneak past a special protective barrier called the meninges. In a study involving mice and human autopsy tissue, researchers at the National Institutes of Health and Cambridge University have shown that some of these immune cells are trained to fight these infections by first spending time in the gut. “This finding opens a new area of neuroimmunology, showing that gut-educated antibody-producing cells inhabit and defend regions that surround the central nervous system,” said Dorian McGavern, Ph.D., senior investigator at NINDS and co-senior author of the study, which was published in Nature. The central nervous system (CNS) is protected from pathogens both by a three-membrane barrier called the meninges and by immune cells within those membranes. The CNS is also walled off from the rest of the body by specialized blood vessels that are tightly sealed by the blood brain barrier. This is not the case, however, in the dura mater, the outermost layer of the meninges. Blood vessels in this compartment are not sealed, and large venous structures, referred to as the sinuses, carry slow moving blood back to the heart. The combination of slow blood flow and proximity to the brain requires strong immune protection to stop potential infections in their tracks. “The immune system has invested heavily in the dura mater,” said Dr. McGavern. “The venous sinuses within the dura act like drainage bins, and, consequently, are a place where pathogens can accumulate and potentially enter the brain. It makes sense that the immune system would set up camp in this vulnerable area.”

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: 27569 - Posted: 11.07.2020

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