Chapter 11. Emotions, Aggression, and Stress

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Sara Reardon Psychedelic drugs have been undergoing a major makeover in psychiatry, earning mainstream acceptance that has eluded them for decades. In 2019, a variant of ketamine — an animal tranquillizer well known as a club drug — was approved by the US Food and Drug Administration (FDA) for treating post-traumatic stress disorder (PTSD). In May, Oregon opened its first treatment centre for administering psilocybin — the hallucinogenic compound found in magic mushrooms — following the state’s decision to legalize it (psilocybin remains illegal at the federal level). And, after decades of effort, the Multidisciplinary Association for Psychedelic Studies, a non-profit research organization in San Jose, California, formally asked the FDA for approval to market MDMA — also known as molly or ecstasy — as a treatment for PTSD. Most specialists expect the MDMA approval to go through on the weight of clinical evidence and popular support. Two large trials have shown that the drug can reduce the symptoms of PTSD when administered in controlled therapy sessions1,2. And it seems to do so more quickly than other treatments. But how MDMA and other psychedelics work is still largely a mystery, both because the drugs have long been illegal and because psychiatric conditions are difficult to study in animals. Psychedelic drug MDMA moves closer to US approval following success in PTSD trial With the regulatory landscape shifting, legal psychedelic research is becoming easier — and potentially more profitable. Neuroscientists, psychiatrists, pharmacologists, biochemists and others are entering the field, bringing fresh ideas about what the drugs do at a cellular and molecular level and trying to unravel how these mechanisms might help to relieve symptoms of psychiatric conditions. From a clinical perspective, understanding how the drugs work might not matter. “You don’t need to know the mechanism of the drug to have a very effective therapy,” says David Olson, a biochemist at the University of California, Davis. But, understanding more about psychedelics could lead to the development of proprietary drugs that are safer, less hallucinogenic and ultimately more effective. It could also affect the way psychedelics are administered in the clinic — helping providers to tailor treatments to each person. Several key questions are driving the basic research that progresses in the background as MDMA and others march towards the market. © 2023 Springer Nature Limited

Keyword: Depression; Stress
Link ID: 28986 - Posted: 11.04.2023

By Christa Lesté-Lasserre A gray cat stares quietly at a nearby orange tabby, squinting her eyes, flattening her ears, and licking her lips. The tabby glares back, wrinkles his nose, and pulls back his whiskers. Cat people know what’s about to go down: a fight. If looks and growls don’t resolve the budding tiff, claws will pop out and fur will fly. Those faces aren’t the only ones cats make at each other, of course—not by a long shot. In a study published this month in Behavioural Processes, researchers tallied 276 different feline facial expressions, used to communicate hostile and friendly intent and everything in between. What’s more, the team found, we humans might be to thank: Our feline friends may have evolved this range of sneers, smiles, and grimaces over the course of their 10,000-year history with us. “Many people still consider cats—erroneously—to be a largely nonsocial species,” says Daniel Mills, a veterinary behaviorist at the University of Lincoln who was not involved in the study. The facial expressions described in the new study suggest otherwise, he notes. “There is clearly a lot going on that we are not aware of.” Cats can be solitary creatures, but they often form friendships with fellow kitties in people’s homes or on the street; feral cats can live in colonies of thousands, sometimes taking over entire islands. Lauren Scott, a medical student and self-described cat person at the University of Kansas, long wondered how all these felines communicated with one another. There has to be love and diplomacy, not just fighting, yet most studies of feline expression have focused on aggression. Fortunately in 2021, Scott was studying at the University of California, Los Angeles (UCLA), just minutes from the CatCafé Lounge. There, human visitors can interact—and even do yoga—with dozens of group-housed, adoptable cats. From August to June, Scott video recorded 194 minutes of cats’ facial expressions, specifically those aimed at other cats, after the café had closed for the day. Then she and evolutionary psychologist Brittany Florkiewicz, also at UCLA at the time but now at Lyon College, coded all their facial muscle movements—excluding any related to breathing, chewing, yawning, and the like.

Keyword: Emotions; Evolution
Link ID: 28977 - Posted: 10.28.2023

By Charles Digges Is there any kind of fence that can make humans and elephants good neighbors? It’s a question Dominique Gonçalves has had to ponder as she leads the elephant ecology project at Mozambique’s Gorongosa National Park, which is not surrounded by a physical barrier. A number of pioneering studies throughout Sub-Saharan Africa over the past several years showed a solution that was simple and natural: bees. As it turns out, the tiny, ubiquitous honeybee has the power to terrify a mammal that’s 22 million times its size. In fact, even the sound of the insect’s buzz is enough to send a family of elephants into a panic, showed studies by Lucy King, an Oxford zoologist and preeminent researcher in human-elephant coexistence at the nonprofit Save the Elephants. Upon hearing the telltale hum, elephants will run, kick up dust, shake their heads as if trying to swat the bees out of the air, trumpeting distressed warnings to other elephants as they flee. Of course, a bee’s stinger can’t penetrate the thick hide of an elephant. But when bees swarm—and African bees swarm aggressively—hundreds of bees might sting an elephant in its most sensitive areas, like the trunk, the mouth, and eyes. And it works. Building on King’s insights, Paola Branco of the University of Idaho conducted a massive two-year-long experiment in Gorongosa that culminated in a 2019 paper she co-authored with King, Marc Stalmans, Gorongosa’s director of scientific services, Princeton zoologist Robert Pringle, and others.1 Their research aimed to settle tensions between human farmers and the park’s growing population of marauding pachyderms—with the help of bees. © 2023 NautilusNext Inc.,

Keyword: Emotions; Evolution
Link ID: 28976 - Posted: 10.28.2023

Christie Wilcox Adult horsehair worms look about how you’d expect given their name: They’re long, noodlelike creatures that resemble wiggling horse hairs. They live and reproduce in water, but their young only develop inside the bodies of other animals—usually terrestrial insects such as praying mantises. Once they’ve finished growing inside their unwitting vessel, the worms must convince their hosts to drown themselves to complete their life cycle. How these parasites manage to lethally manipulate their hosts has long puzzled scientists. Researchers behind a new study published today in Current Biology suggest horsehair worms possess hundreds of genes that allow them to hijack a mantis’ movement—and they may have acquired these genes directly from their ill-fated hosts. “The results are amazing,” says Clément Gilbert, an evolutionary biologist at the University of Paris-Saclay who wasn’t involved in the work. If it turns out to be true that so many of the mantises’ genes jumped over to the parasitic worms—a process known as horizontal gene transfer—then “this is by far the highest number of horizontally transferred genes that have been reported between two species of animals,” he adds. The phenomenon of parasites mind-controlling their hosts to an early grave has always intrigued Tappei Mishina, an evolutionary biologist at Kyushu University and the RIKEN Center for Biosystems Dynamics Research. “For more than 100 years, there have been horrifying observations of terrestrial insects jumping into water right before our eyes all over the world,” he says. He teamed up with ecologist Takuya Sato of the Center for Ecological Research at Kyoto University to investigate the genetic basis of their parasitism. They focused on horsehair or gordian worms, a group of parasitic animals related to nematodes. Many have complex life cycles involving multiple hosts, and the ones that live in freshwater must generally find their way into an insect to finish developing into adults. The genus Mishina, Sato, and their colleagues specialize in, known as Chordodes, infect mantises and can grow to nearly 1 meter long inside the palm-size insects’ abdomens.

Keyword: Genes & Behavior; Evolution
Link ID: 28971 - Posted: 10.25.2023

Marlys Fassett Itching can be uncomfortable, but it’s a normal part of your skin’s immune response to external threats. When you’re itching from an encounter with poison ivy or mosquitoes, consider that your urge to scratch may have evolved to get you to swat away disease-carrying pests. However, for many people who suffer from chronic skin diseases like eczema, the sensation of itch can fuel a vicious cycle of scratching that interrupts sleep, reduces productivity and prevents them from enjoying daily life. This cycle is caused by sensory neurons and skin immune cells working together to promote itching and skin inflammation. But, paradoxically, some of the mechanisms behind this feedback loop also stop inflammation from getting worse. In our newly published research, my team of immunologists and neuroscientists and I discovered that a specific type of itch-sensing neuron can push back on the itch-scratch-inflammation cycle in the presence of a small protein. This protein, called interleukin-31, or IL-31, is typically involved in triggering itching. This negative feedback loop – like the vicious cycle – is only possible because the itch-sensing nerve endings in your skin are closely intertwined with the millions of cells that make up your skin’s immune system. The protein IL-31 is key to the connection between the nervous and immune systems. This molecule is produced by some immune cells, and like other members of this molecule family, it specializes in helping immune cells communicate with each other. © 2010–2023, The Conversation US, Inc.

Keyword: Pain & Touch; Neuroimmunology
Link ID: 28961 - Posted: 10.14.2023

Perspective by Dan O'Brien I was 12 years old when I developed obsessive-compulsive disorder. My older brother had recently tried to kill himself by jumping from our attic window. I was the one who saw him first, as he limped around the side of the house, his back and hair matted with snow. Inside I found his suicide note and showed it to our mother. She collapsed in my arms, crying, and whispered, “This is a secret we must take to our graves.” Live well every day with tips and guidance on food, fitness and mental health, delivered to your inbox every Thursday. Before long, I found myself obsessing about any number of vague yet existential threats, and compulsively taking defensive action against them. I cycled through most of the classic OCD manifestations: avoiding cracks in the sidewalk, flipping light switches three, six, nine times (depending on my mood), checking and rechecking — and rechecking again — that our front and back doors were indeed locked. I had no idea what was happening to me. I simply knew with certainty that if I did not execute these actions correctly, my loved ones and I would suffer. And hypochondria, too: A book titled “Symptoms” lived in the tall bookcase behind the potted plant in the living room; one searched for one’s symptoms in an index up front, then proceeded to the indicated page where one would be provided with the most dire diagnosis imaginable. “Symptoms,” with its heft, its red-linen hardcover and tissue-thin paper, became my Bible. I touched things and people with trepidation and regret. I probed my body for swollen glands. My frequent handwashing desiccated my skin like a riverbed in drought, blood breaking through the cracks. I was forever certain that I was coming down with something catastrophic, like tuberculosis, AIDS, cancer. I was morally scrupulous, in the clinical sense, and prayed three times a day. (I wasn’t particularly religious; I was trying to cover all my bases.) Morning and evening prayer was easy, at home, but lunchtime at school could be tricky; I’d have to abscond to the boy’s room, or a shadowy, chain-link corner of the playground. I grew adept at praying without moving my lips in rote run-on sentences in which I begged God’s forgiveness for everything and anything I had done wrong in the past and would do wrong in the future.

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 28926 - Posted: 09.27.2023

Sara Reardon The psychedelic drug MDMA, also known as ecstasy or molly, has passed another key hurdle on its way to regulatory approval as a treatment for mental illness. A second large clinical trial has found that the drug — in combination with psychotherapy — is effective at treating post-traumatic stress disorder (PTSD). The results allow the trial’s sponsor to now seek approval from the US Food and Drug Administration (FDA) for MDMA’s use as a PTSD treatment for the general public, which might come as soon as next year. “It’s an important study,” says Matthias Liechti, a psychopharmacologist who studies MDMA at the University of Basel in Switzerland, but who was not involved with the trial or its sponsor. “It confirms MDMA works.” In June, Australia became the first country to allow physicians to prescribe MDMA for treating psychiatric conditions. MDMA is illegal in the United States and other countries because of the potential for its misuse. But the Multidisciplinary Association for Psychedelic Studies (MAPS), a non-profit organization in San Jose, California, has long been developing a proprietary protocol for using MDMA as a treatment for PTSD and other disorders. MAPS has been campaigning for its legalization — a move that could encourage other countries to follow suit. In 2021, researchers sponsored by MAPS reported the results of a study1 in which 90 people received a form of psychotherapy developed by the organization alongside either MDMA or a placebo. After three treatment sessions, 67% of those who received MDMA with therapy no longer qualified for a PTSD diagnosis, compared with 32% of those who received therapy and a placebo. The results were widely hailed as promising, but the FDA typically requires two placebo-controlled trials before a drug can be approved. The results of a second trial, involving 104 further individuals with PTSD and published on 14 September in Nature Medicine2, were similar to those of the original: 71% of people who received MDMA alongside therapy lost their PTSD diagnosis, compared with 48% of those who received a placebo and therapy. © 2023 Springer Nature Limited

Keyword: Drug Abuse; Stress
Link ID: 28911 - Posted: 09.16.2023

By Jonathan Moens When the war in Ukraine broke out, many countries and agencies around the world lent their support in the form of financial aid, weapons, and food. But Olga Chernoloz, a Ukrainian neuroscientist based in Canada, wanted to provide a different kind of assistance: a combination of therapy and the psychedelic drug MDMA. Such therapy, she said, could help countless people on the ground who are suffering from psychological trauma. “I thought that the most efficacious way I could be of help,” she told Undark, “would be to bring psychedelic-assisted therapy to Ukraine.” Chernoloz’s confidence stems in part from the results of clinical trials on MDMA to treat post-traumatic stress disorder in vulnerable populations, which suggest that such treatments may improve symptoms, or do away with them altogether. But the approach is experimental and has not yet cleared major regulatory hurdles in Canada, Europe, or the United States. Still, Chernoloz, who is a professor at the University of Ottawa, plans on carrying out clinical trials with Ukrainian refugees in a psychedelic center in the Netherlands in early 2024. This month, Chernoloz and her colleagues organized an education session for 20 Ukrainian therapists to learn about MDMA-assisted therapy for PTSD from the Multidisciplinary Association for Psychedelic Studies, or MAPS, one of the most influential organizations dedicated to education and promotion of psychedelic drugs.

Keyword: Stress
Link ID: 28878 - Posted: 08.24.2023

Nicola Davis Science correspondent Researchers have discovered a genetic variant that appears to influence the speed at which multiple sclerosis (MS) progresses, potentially paving the way for new treatments. According to the MS International Federation, about 2.9 million people worldwide have MS, a condition in which the insulating coating of the nerves in the brain and spinal cord is damaged by the immune system. The nerve fibres themselves can also become damaged. While some people have a relapsing remitting form of the disease, others experience gradual progression that in some can cause severe disability. Researchers say they have identified a genetic variant that appears to increase the severity of the disease. They found that people who inherit the variant from both parents need a walking aid almost four years sooner than those without. “This is a very substantial effect for a single genetic variant,” said Sergio Baranzini, a professor of neurology at the University of California, San Francisco and co-senior author of the study. “Furthermore, this variant affects genes that are active in the central nervous system, a clear contrast to variants that confer risk [of MS], which overwhelmingly affect the immune system.” The study, published in the journal Nature, was an international endeavour, involving 70 institutions around the world. To make their discovery, the team analysed genetic data from more than 12,000 people with MS, screening more than 7m genetic variants for associations with the speed of disease progression. The team found that one variant, nestled between two genes called DYSF and ZNF638, was associated with a more rapid increase in disability. © 2023 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28840 - Posted: 07.01.2023

By Claudia Lopez Lloreda A baby born through the vaginal canal picks up critical microbes along the way that help it stay healthy later in life. But babies delivered via cesarean section miss out on those useful, gut-colonizing bacteria, which may put them at greater risk of developing certain health conditions and developmental disorders. Now, researchers at Southern Medical University say that by exposing C-section babies to the microbes they’ve missed—an intervention called vaginal seeding—doctors can partially restore these missing gut bacteria. The procedure may even aid in their early development. Newborns delivered via C-section who received their mother’s vaginal microbes had more advanced motor and communication skills than other C-section babies months later, the team reports today in Cell Host & Microbe. But some clinicians argue these benefits for infants have not yet been proved, nor has the procedure’s safety. “This study establishes a link showing that there is a possible benefit in a select group of infants and mothers,” says Mehreen Zaigham, an obstetrician at Lund University who was not involved in the study. “But it has to be proven with larger longitudinal studies.” The microbiomes of C-section babies look a lot different from those of babies born vaginally. In particular, they have lower numbers of Lactobacillus, Escherichia, and Bacteroides bacteria in their guts. These microbes are believed to be critical for growth and are thought to help protect against asthma, allergies, obesity, and autoimmune disorders—all conditions that are more common among C-section babies. A few highly controversial studies have suggested some babies delivered by C-section may be at a greater risk of developing neurodevelopmental conditions such as autism spectrum disorder, which some researchers attribute to their disrupted microbiome. Other researchers have roundly criticized that suggestion, however. To restore the microbiomes of infants delivered by C-section, researchers have come up with a simple solution: Swab them with bacteria from their mother’s vagina shortly after they are born. This method, called vaginal seeding, was first clinically tested 7 years ago by Jose Clemente, a geneticist at the Icahn School of Medicine at Mount Sinai, and Maria Gloria Dominguez Bello, a microbial ecologist at Rutgers University, who found the procedure indeed restored microbes that C-section babies lacked. However, these results were based on a small group of just 11 babies.

Keyword: Development of the Brain; Neuroimmunology
Link ID: 28824 - Posted: 06.17.2023

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