Ian Sample Science editor The sight of their dead comrades is enough to drive fruit flies to an early grave, according to researchers, who suspect the creatures keel over after developing the fly equivalent of depression. For a species that spends much of its life feasting on decayed matter, the insects appear to be particularly sensitive to their own dead. Witnessing an abundance of fruit fly carcasses speeds up the insects’ ageing process, scientists found, cutting their lives short by nearly 30%. While the researchers are cautious about extrapolating from 3mm-long flies to rather larger humans that can live 400 times longer, they speculate that the insights might prove useful for people who are routinely surrounded by death, such as combat troops and healthcare workers. “Could motivational therapy or pharmacologic intervention in reward systems, much like what is done for addiction, slow ageing?” the authors ask in Plos Biology. The possibility could be tested in humans today, they added, using drugs that are already approved. Researchers led by Christi Gendron and Scott Pletcher at the University of Michigan raised fruit flies in small containers filled with food. While some of the containers held only living flies and tasty nutrients, others were dotted with freshly dead fruit flies as well, to see what impact they had on the feeding insects. When fruit flies were raised among dead ones, they tended to die several weeks earlier than those raised without being surrounded by carcasses. Those exposed to death appeared to age faster, losing stored fat and becoming less resilient to starvation. © 2023 Guardian News & Media Limited

Keyword: Stress
Link ID: 28819 - Posted: 06.14.2023

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.

Keyword: Neuroimmunology; Attention
Link ID: 28818 - Posted: 06.14.2023

By Kate Laskowski In the age-old debate about nature versus nurture — whether our characteristics are forged by our genes or our upbringing — I have an answer for you. It is both. And it is neither. I’m a behavioral ecologist who seeks to answer this question by studying a particular kind of fish. The Amazon molly (Poecilia formosa) is an experimental goldmine for these types of questions. She naturally clones herself by giving birth to offspring with identical genomes to her own and to each other’s. A second quirk of this little fish is that her offspring are born live and are completely independent from birth. This means I can control their experiences from the earliest possible age. Essentially, this fish gives me and my colleagues the opportunity to perform “twin studies” to understand how and why individuality develops. And what we’ve found may surprise you. As humans, we know the critical importance of our personalities. These persistent differences among us shape how we navigate our worlds and respond to major life events; whether we are bold or shy; whether we ask someone on a second date or not. Given the obvious importance of personality, it’s perhaps a bit surprising that scientists generally overlooked these kinds of differences in other species for a long time. Up until about 30 years ago, these differences (what I prefer to call “individuality,” as it avoids the human connotation of “personality”) were typically viewed as cute anecdotes with little evolutionary importance. Instead, researchers focused on the typical behavior of a given population. With guppies, for example — a classic workhorse of behavioral ecology research — researchers found that fish will, on average, swim more tightly together if they live among lots of predatory fish, whereas fish from areas with fewer predators spend less time schooling and more time fighting one another, as they don’t have to worry so much about being eaten. © 2023 Annual Reviews

Keyword: Development of the Brain; Genes & Behavior
Link ID: 28815 - Posted: 06.07.2023

Sara Reardon Vaccination against shingles might also prevent dementia, such as that caused by Alzheimer’s disease, according to a study of health records from around 300,000 people in Wales. The analysis found that getting the vaccine lowers the risk of dementia by 20%. But some puzzling aspects of the analysis have stirred debate about the work’s robustness. The study was published on the medRxiv preprint server on 25 May and has not yet been peer reviewed. “If it is true, it’s huge,” says Alberto Ascherio, an epidemiologist at Harvard University in Cambridge, Massachusetts, who was not involved in the study. “Even a modest reduction in risk is a tremendous impact.” Dementia–infection link The idea that viral infection can play a part in at least some dementia cases dates back to the 1990s, when biophysicist Ruth Itzhaki at the University of Manchester, UK, and her colleagues found herpesviruses in the brains of deceased people with dementia2. The theory has been controversial among Alzheimer’s researchers. But recent work has suggested that people infected with viruses that affect the brain have higher rates of neurodegenerative diseases3. Research has also suggested that those vaccinated against certain viral diseases are less likely to develop dementia4. But all these epidemiological studies have shared a key problem: people who get any type of vaccination tend to have healthier lifestyles than those who don’t5, meaning that other factors could account for their lowered risk of diseases such as Alzheimer’s. With that in mind, epidemiologist Pascal Geldsetzer at Stanford University in California and his colleagues turned to a natural experiment: a shingles vaccination programme in Wales, which began on 1 September 2013. Shingles is caused by the reawakening of inactive varicella zoster virus (VZV), the herpesvirus that causes chickenpox and which is present in most people. Shingles is most common in older adults and can cause severe pain and rashes. © 2023 Springer Nature Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 28814 - Posted: 06.07.2023

By Ula Chrobak A couple of weeks after I adopted my dog, Halle, I realized she had a problem. When left alone, she would pace, bark incessantly, and ignore any treats I left her in favor of chewing my belongings. When I returned, I’d find my border collie mix panting heavily with wide, fearful eyes. As frustrated as I was, though, I restrained the urge to scold her, realizing her destruction was born out of panic. Halle’s behavior was a textbook illustration of separation anxiety. Distressed over being left alone, an otherwise perfectly mannered pup might chomp the couch, scratch doors, or relieve themselves on the floor. Problem behaviors like these tend to be interpreted as acts of willful defiance, but they often stem from intense emotions. Dogs, like humans, can act out of character when they are distressed. And, as with people, some dogs may be neurologically more prone to anxiety. So concluded a recent brain imaging study, published in PLOS One, in which researchers performed resting-state functional magnetic resonance imaging on 25 canines that were deemed behaviorally “normal,” and 13 that had been diagnosed with anxiety, based on a behavioral evaluation. The scans revealed that anxious dogs had stronger connections between several of five brain regions that the researchers called the anxiety circuit: the amygdala, frontal lobe, hippocampus, mesencephalon, and thalamus. The team also saw weaker connections between the hippocampus and midbrain in anxious dogs, which can signal difficulties in learning and might explain why the owners reported decreased trainability in these dogs. That the neurological architecture of anxious dogs seems to parallel the signatures of human anxiety comes as little surprise to many animal behavior experts.

Keyword: Emotions; Evolution
Link ID: 28782 - Posted: 05.13.2023

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.

Keyword: Neuroimmunology
Link ID: 28771 - Posted: 05.06.2023

Asher Mullard The US Food and Drug Administration (FDA) is set to rule soon on the approval of a new drug for a rare form of amyotrophic lateral sclerosis (ALS). The hotly anticipated decision is expected to signpost the agency’s vision for neurological drugs — and its willingness to be flexible in the regulation of these therapeutics. People with the disease desperately need new treatments, because they face a degenerative condition that causes neuronal death and typically leads to fatal respiratory failure within three years of symptoms appearing1. Tofersen, developed by the biotechnology firms Biogen in Cambridge, Massachusetts, and Ionis Pharmaceuticals in Carlsbad, California, did not slow patients’ decline in a phase III trial2. However, some say the trial was too short, and point out that there were signs of possible benefit, such as a reduction in a biomarker of neuronal damage and death called neurofilament light chain (NFL). Because of this, Biogen has asked the FDA to approve the drug on an ‘accelerated’ basis, to fast-track it to patients with a guarantee that future trial data will determine whether it works. If approved, tofersen will become the latest example of the agency’s evolving approach to neurological drug development, which could boost industry investment in brain diseases. A vote of confidence for the drug would also supercharge interest in using NFL as a tool to measure brain health and to test drugs in future. “This could be the start of a new era,” says Valentina Bonetto, a neuroscientist at the Mario Negri Institute for Pharmacological Research in Milan, Italy. In March, the FDA convened a panel to discuss the tofersen data set. Its nine independent advisers rallied behind accelerated approval for the drug, voting unanimously that the available evidence supports a “reasonably likely” chance that tofersen will help people with SOD1 ALS. This rare disease is caused by genetic mutations that affect the protein SOD1, leading it to form toxic clumps in motor neurons in the brain, brainstem and spinal cord. The agency usually follows the recommendations of its advisory committee. © 2023 Springer Nature Limited

Keyword: ALS-Lou Gehrig's Disease ; Neuroimmunology
Link ID: 28744 - Posted: 04.18.2023

Functional neurologic disorder (FND) refers to a group of motor, sensory, or cognitive symptoms caused by an abnormality in how the brain functions. FND is distinct from other neurologic conditions such as epilepsy, stroke, and multiple sclerosis in that there is no overt structural damage in the brain. It's a dysfunction of the connections within the brain (the “software”) rather than the structure of the brain itself (the “hardware”). People with FND can experience involuntary movements, nonepileptic seizures, dizziness, blindness, numbness, fatigue, and pain. Memory and concentration also may be affected. An estimated four to 12 people per 100,000 will develop FND, according to the National Institutes of Health. Risk factors include adverse life experiences, having fibromyalgia or other disorders with no identifiable causes, and physical injury. Some people with FND have experienced abuse or neglect in their lives. FND is more common in women and occurs most frequently in people between the ages of 20 and 50, although adolescents and older people also can develop it. Symptoms can include leg and arm weakness or paralysis; nonepileptic convulsions; tremor; sudden, brief involuntary twitching or jerking of a muscle or group of muscles; tics; involuntary muscle contractions that cause slow, repetitive movements or abnormal postures; problems with walking, posture, or balance; speech or voice difficulties; persistent dizziness; and clouded thinking. To diagnose FND and distinguish it from other neurologic conditions, doctors (generally neurologists or neuropsychiatrists) conduct physical and neurologic examinations and ask questions about the person's health and medical and family histories. To evaluate for potential co-occurring conditions and to assist in developing a treatment plan, doctors also may order imaging scans and perform focused mental health and social history screenings. Other tests, which screen for other neurologic disorders, could include electromyography (to record electrical activity in muscles) and electroencephalography (to monitor the brain's electrical activity).

Keyword: Epilepsy; Muscles
Link ID: 28734 - Posted: 04.12.2023

Visual: Andrew Bret Wallis/The Image Bank via Getty Images By Lina Tran At 25, Dasha Kiper moved in with a 98-year-old man. She’d just left a graduate program in clinical psychology; Mr. Kessler was a Holocaust survivor in the early stages of Alzheimer’s disease, whose son had hired Kiper as a live-in caregiver. One day, Mr. Kessler clambers onto a chair to replace the battery in a smoke detector. When he ignores her instructions to come down, Kiper loses her cool. She shouts that he’s incapable of changing the battery and doing much of anything for himself. Later, Kiper is filled with remorse. She should have known better than to yell at a nonagenarian with dementia. This is the focus of Kiper’s “Travelers to Unimaginable Lands: Stories of Dementia, the Caregiver, and the Human Brain” — not the mind of the patient, but the caregiver. Often, the spouses, children, and loved ones of people living with dementia succumb to arguing or pleading with their patients, despite reason. “We want to reestablish a shared reality,” Kiper writes. “It’s not cruelty but desperation that drives us to confront them with the truth.” Caregivers aren’t mere observers to cognitive decline but the “invisible victims” of dementia disorders, Kiper writes. They traverse warped realities that operate under different rules of time and memory. One caregiver says, referring to a famous case study by neurologist and author Oliver Sacks, it’s “like being an anthropologist on Mars.” But a caregiver’s slip-up isn’t necessarily the result of character flaws or a lapse in compassion. Rather, Kiper shows the healthy brain is riddled with cognitive biases that impede the work of caring for a person with an impaired mind. This takes a heavy toll. “People always ask about the patient,” one exasperated woman tells Kiper, after recounting how her husband, who doesn’t recognize her, takes to locking her out of their apartment each night. She starts carrying a spare key to let herself in after he falls asleep. “Let me tell you something, the patient is fine; it’s the caregiver who’s going crazy.”

Keyword: Alzheimers; Stress
Link ID: 28728 - Posted: 04.09.2023

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.

Keyword: Neuroimmunology
Link ID: 28706 - Posted: 03.18.2023

By Bethany Brookshire When you’re stressed and anxious, you might feel your heart race. Is your heart racing because you’re afraid? Or does your speeding heart itself contribute to your anxiety? Both could be true, a new study in mice suggests. By artificially increasing the heart rates of mice, scientists were able to increase anxiety-like behaviors — ones that the team then calmed by turning off a particular part of the brain. The study, published in the March 9 Nature, shows that in high-risk contexts, a racing heart could go to your head and increase anxiety. The findings could offer a new angle for studying and, potentially, treating anxiety disorders. The idea that body sensations might contribute to emotions in the brain goes back at least to one of the founders of psychology, William James, says Karl Deisseroth, a neuroscientist at Stanford University. In James’ 1890 book The Principles of Psychology, he put forward the idea that emotion follows what the body experiences. “We feel sorry because we cry, angry because we strike, afraid because we tremble,” James wrote. The brain certainly can sense internal body signals, a phenomenon called interoception. But whether those sensations — like a racing heart — can contribute to emotion is difficult to prove, says Anna Beyeler, a neuroscientist at the French National Institute of Health and Medical Research in Bordeaux. She studies brain circuitry related to emotion and wrote a commentary on the new study but was not involved in the research. “I’m sure a lot of people have thought of doing these experiments, but no one really had the tools,” she says. Deisseroth has spent his career developing those tools. He is one of the scientists who developed optogenetics — a technique that uses viruses to modify the genes of specific cells to respond to bursts of light (SN: 6/18/21; SN: 1/15/10). Scientists can use the flip of a light switch to activate or suppress the activity of those cells. © Society for Science & the Public 2000–2023.

Keyword: Emotions
Link ID: 28705 - Posted: 03.15.2023

By Elizabeth Preston Several years ago, Christian Rutz started to wonder whether he was giving his crows enough credit. Rutz, a biologist at the University of St. Andrews in Scotland, and his team were capturing wild New Caledonian crows and challenging them with puzzles made from natural materials before releasing them again. In one test, birds faced a log drilled with holes that contained hidden food, and could get the food out by bending a plant stem into a hook. If a bird didn’t try within 90 minutes, the researchers removed it from the dataset. But, Rutz says, he soon began to realize he was not, in fact, studying the skills of New Caledonian crows. He was studying the skills of only a subset of New Caledonian crows that quickly approached a weird log they’d never seen before — maybe because they were especially brave, or reckless. The team changed their protocol. They began giving the more hesitant birds an extra day or two to get used to their surroundings, then trying the puzzle again. “It turns out that many of these retested birds suddenly start engaging,” Rutz says. “They just needed a little bit of extra time.” Scientists are increasingly realizing that animals, like people, are individuals. They have distinct tendencies, habits and life experiences that may affect how they perform in an experiment. That means, some researchers argue, that much published research on animal behavior may be biased. Studies claiming to show something about a species as a whole — that green sea turtles migrate a certain distance, say, or how chaffinches respond to the song of a rival — may say more about individual animals that were captured or housed in a certain way, or that share certain genetic features. That’s a problem for researchers who seek to understand how animals sense their environments, gain new knowledge and live their lives. “The samples we draw are quite often severely biased,” Rutz says. “This is something that has been in the air in the community for quite a long time.” In 2020, Rutz and his colleague Michael Webster, also at the University of St. Andrews, proposed a way to address this problem. They called it STRANGE. © 2023 Annual Reviews

Keyword: Emotions; Evolution
Link ID: 28700 - Posted: 03.11.2023

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.

Keyword: Neuroimmunology
Link ID: 28698 - Posted: 03.11.2023

By Marta Zaraska The Neumayer III polar station sits near the edge of Antarctica’s unforgiving Ekström Ice Shelf. During the winter, when temperatures can plunge below minus 50 degrees Celsius and the winds can climb to more than 100 kilometers per hour, no one can come or go from the station. Its isolation is essential to the meteorological, atmospheric and geophysical science experiments conducted there by the mere handful of scientists who staff the station during the winter months and endure its frigid loneliness. But a few years ago, the station also became the site for a study of loneliness itself. A team of scientists in Germany wanted to see whether the social isolation and environmental monotony marked the brains of people making long Antarctic stays. Eight expeditioners working at the Neumayer III station for 14 months agreed to have their brains scanned before and after their mission and to have their brain chemistry and cognitive performance monitored during their stay. (A ninth crew member also participated but could not have their brain scanned for medical reasons.) As the researchers described in 2019, in comparison to a control group, the socially isolated team lost volume in their prefrontal cortex — the region at the front of the brain, just behind the forehead, that is chiefly responsible for decision-making and problem-solving. They also had lower levels of brain-derived neurotrophic factor, a protein that nurtures the development and survival of nerve cells in the brain. The reduction persisted for at least a month and a half after the team’s return from Antarctica. It’s uncertain how much of this was due purely to the social isolation of the experience. But the results are consistent with evidence from more recent studies that chronic loneliness significantly alters the brain in ways that only worsen the problem. Neuroscience suggests that loneliness doesn’t necessarily result from a lack of opportunity to meet others or a fear of social interactions. Instead, circuits in our brain and changes in our behavior can trap us in a catch-22 situation: While we desire connection with others, we view them as unreliable, judgmental and unfriendly. Consequently, we keep our distance, consciously or unconsciously spurning potential opportunities for connections. Simons Foundation All Rights Reserved © 2023

Keyword: Stress; Attention
Link ID: 28689 - Posted: 03.04.2023

Sara Reardon Emotions such as fear and anxiety can make the heart beat faster. Now a study in mice has found that the reverse is also true — artificially increasing the heart rate can raise anxiety levels1. Links between emotions and physical sensations are familiar to everyone: hairs rising on the backs of your arms when you hear an eerie sound, or the sinking feeling in your gut when you receive bad news. But the question of whether emotions drive bodily functions or vice versa has long vexed researchers, because it is hard to control either factor independently. “It was a chicken-and-egg question that has been the subject of debate for a century,” says Karl Deisseroth, a neuroscientist at Stanford University in California. He learned about this conundrum — first proposed by the psychologist William James in the 1880s — while at medical school and says the question has haunted him ever since. To test the phenomenon directly, Deisseroth and his colleagues turned to optogenetics, a method that involves using light to control cell activity. The team bioengineered mice to make muscle cells in the rodents’ hearts sensitive to light. The authors also designed tiny vests for the animals that emitted red light, which could pass through the rodents’ bodies all the way to their hearts. When a mouse’s vest emitted a pulse of light, the animal’s engineered heart muscles fired, causing the heart to beat. The team trained the animals to expect a shock if they pressed a lever for a water reward. Using the optogenetic system, the team raised the animals’ heart rates from their normal 660 beats per minute to 900. When their hearts started racing, mice became less willing to press the lever or to explore open areas, suggesting that they were more anxious. But for animals in other contexts, the externally increased heart rate had no effect, suggesting that the brain and the heart worked together to produce anxiety. © 2023 Springer Nature Limited

Keyword: Stress; Emotions
Link ID: 28687 - Posted: 03.04.2023

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

Keyword: Neuroimmunology
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

Keyword: Neuroimmunology; Aggression
Link ID: 28684 - Posted: 02.25.2023

By Sujata Gupta Trish Tran narrates her life in staccato notes. “I remember carrying my little sister on my back because she’s too tired and walking through the huge sunflower fields … and me feeling so tired I didn’t think I could walk another step.” “I remember being in a taxi with my mother, coming back to the man who had been violently abusive to all of us…. Her words to me were, ‘Just trust me, Trish. Just trust me.’ ” “I’m waiting at a train station … to meet my mother who I haven’t seen in many years…. Hours pass and eventually I try to call her … and she says to me, ‘I’m sorry, Trish. My neighbor was upset, and I needed to stay back with them.’ And her voice was slurring quite a lot, so I knew she had been drinking.” Tran, who lives in Perth, Australia, is dispassionate as she describes a difficult childhood. Her account lacks what are generally considered classic signs of trauma: She makes no mention of flashbacks, appears to have a generally positive outlook and speaks with relative ease about distressing events. Yet she narrates her life growing up and living in the Australian Outback as a series of disconnected events; her life story lacks connective glue. That disjointed style is not how people, at least people in the West, tend to talk about themselves, says psychologist Christin Camia. Autobiographical accounts, like any good narrative, typically contain a curation of key past experiences, transitions linking those experiences and larger arcs about where life is headed. People use these stories to make sense of their lives, says Camia, of Zayed University’s Abu Dhabi campus in the United Arab Emirates. But a growing body of evidence from fields as wide-ranging as psychology, neuroscience, linguistics, philosophy and literary studies suggests that, as with Tran, trauma can shatter the narrative coherence of one’s life. People lose the plot. © Society for Science & the Public 2000–2023.

Keyword: Stress; Attention
Link ID: 28683 - 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.

Keyword: Neuroimmunology
Link ID: 28680 - Posted: 02.25.2023

Max Kozlov A group of brain cells in mice becomes active both when the animals fight and when they watch other mice fight, a study1 shows. The work hints that such ‘mirror neurons’, which fire when an animal either observes or takes part in a particular activity, could shape complex social behaviours, such as aggression. The mirror neurons described in the study are the first to be found in the hypothalamus, an evolutionarily ancient brain region — suggesting that mirror neurons’ original purpose might have been to enhance defence and, ultimately, reproductive success, the authors speculate. The study was published in Cell on 15 February. “We’ve now shown that mirror neurons functionally participate in the behaviours they’re mirroring,” says Nirao Shah, a neuroscientist at Stanford University in California who co-authored the study. “That changes what we think about mirror neurons.” First identified in monkeys in the 1990s, mirror neurons generally fire when an animal takes a certain action, but they also fire when it sees another animal perform the same action. Previous work has linked mirror neurons’ activity to simple behaviours, such as reaching for an object, but not to complex social behaviours, such as fighting. But exactly how mirror-neuron activity contributes to cognitive functions has been controversial, says Pier Francesco Ferrari, a neuroethologist at the Institute of Cognitive Science Marc Jeannerod in Lyon, France. Some researchers have argued that the fact that mirror neurons fire both when an animal observes a behaviour and when it performs that behaviour itself shows that these neurons are involved in a higher-order awareness of others’ actions — and perhaps even contribute to empathy. But others say that there is little evidence to support this theory. © 2023 Springer Nature Limited

Keyword: Aggression; Attention
Link ID: 28674 - Posted: 02.18.2023