Chapter 15. Emotions, Aggression, and Stress

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By Jelena Kecmanovic Across the spectrum, mental health problems seem to be on the rise. One-quarter of Americans reported moderate to severe depression this summer and another quarter said they suffered from mild depression, a recent study reported. These findings are similar to surveys done by the Census Bureau and the Centers for Disease Control and Prevention. A third of Americans now show signs of clinical anxiety or depression, Census Bureau finds. Former first lady Michelle Obama highlighted the problem for many when she said in August that she has been dealing with “low-grade depression.” As a psychologist, I hear almost daily how the combination of coronavirus, racial unrest, economic uncertainty and political crisis are leading many people to feel a lot worse than usual. “It is not at all surprising that we are seeing the significant increase in distress. It’s a normal reaction to an abnormal situation,” said Judy Beck, president of the Beck Institute for Cognitive Behavior Therapy in Philadelphia and author of the widely used mental health textbook “Cognitive Behavior Therapy: Basics and Beyond.” But an important difference exists between having depressive symptoms — such as sadness, fatigue and loss of motivation — and a full-blown major depressive episode that can affect your ability to function at work and home for weeks or months. The amount and duration of the symptoms, as well as the degree to which they impair one’s life all play a role in diagnosing clinical depression. Extensive research suggests that certain ways of thinking and behaving can hasten the plunge into clinical depression, while others can prevent it. As we head into winter, which can stress the coping skills of many people, here are some strategies that can help you resist the depressive downward spiral. 1. Reduce overthinking. When we feel down, we tend to think about the bad things repeatedly, often trying to figure out why they’ve happened. Research shows that some people are especially prone to this kind of “depressive rumination.” They overanalyze everything, hoping to think their way out of feeling bad, and fret about consequences of their sadness.

Keyword: Depression; Emotions
Link ID: 27599 - Posted: 11.30.2020

Janet M. Gibson Amusement and pleasant surprises – and the laughter they can trigger – add texture to the fabric of daily life. Those giggles and guffaws can seem like just silly throwaways. But laughter, in response to funny events, actually takes a lot of work, because it activates many areas of the brain: areas that control motor, emotional, cognitive and social processing. As I found when writing “An Introduction to the Psychology of Humor,” researchers now appreciate laughter’s power to enhance physical and mental well-being. People begin laughing in infancy, when it helps develop muscles and upper body strength. Laughter is not just breathing. It relies on complex combinations of facial muscles, often involving movement of the eyes, head and shoulders. Laughter – doing it or observing it – activates multiple regions of the brain: the motor cortex, which controls muscles; the frontal lobe, which helps you understand context; and the limbic system, which modulates positive emotions. Turning all these circuits on strengthens neural connections and helps a healthy brain coordinate its activity. By activating the neural pathways of emotions like joy and mirth, laughter can improve your mood and make your physical and emotional response to stress less intense. For example, laughing may help control brain levels of the neurotransmitter serotonin, similar to what antidepressants do. By minimizing your brain’s responses to threats, it limits the release of neurotransmitters and hormones like cortisol that can wear down your cardiovascular, metabolic and immune systems over time. Laughter’s kind of like an antidote to stress, which weakens these systems and increases vulnerability to diseases. © 2010–2020, The Conversation US, Inc.

Keyword: Emotions; Neuroimmunology
Link ID: 27597 - Posted: 11.30.2020

By Bethany Brookshire A hungry brain craves food. A lonely brain craves people. After spending a day completely isolated from anyone else, people’s brains perked up at the sight of social gatherings, like a hungry person’s brain seeing food, scientists report November 23 in Nature Neuroscience. Cognitive neuroscientist Livia Tomova, then at MIT, and her colleagues had 40 participants fast for 10 hours. At the end of the day, certain nerve cells in the midbrain fired up in response to pictures of pizza and chocolate cake. Those neurons — in the substantia nigra pars compacta and ventral tegmental area — produce dopamine, a chemical messenger associated with reward (SN: 8/27/15). On a different day, the same people underwent 10 hours of isolation (no friends, no Facebook and no Instagram). That evening, neurons in the same spot activated in response to pictures of people chatting or playing team sports. The more hunger or isolation the subject reported, the stronger the effect (SN: 10/4/17). In people who reported that they were generally more lonely, the social responses were blunted. “We don’t really know what causes that,” Tomova says. “Maybe being isolated doesn’t really affect them as much, because it’s something that is not that different, perhaps, from their everyday life.” The midbrain, which plays an important role in people’s motivation to seek food, friends, gambling or drugs, responds to food and social signals even when people aren’t hungry or lonely. After all, a person always could eat or hang out. But hunger and loneliness increased the reaction and made people’s responses specific to the thing they were missing. The findings “speak to our current state,” says Tomova, now at the University of Cambridge. COVID-19 has left many more socially isolated, putting mental as well as physical health at stake (SN: 3/29/20) and leaving people with cravings for more than food. “It’s important to look at the social dimension of this kind of crisis.” L. Tomova et al. Acute social isolation evokes midbrain craving responses similar to hunger. Nature Neuroscience. Published online November 23, 2020. doi: 10.1038/s41593-020-00742-z. = © Society for Science & the Public 2000–2020

Keyword: Stress; Obesity
Link ID: 27594 - Posted: 11.27.2020

By Lisa Feldman Barrett Five hundred million years ago, a tiny sea creature changed the course of history: It became the first predator. It somehow sensed the presence of another creature nearby, propelled or wiggled its way over, and deliberately ate it. This new activity of hunting started an evolutionary arms race. Over millions of years, both predators and prey evolved more complex bodies that could sense and move more effectively to catch or elude other creatures. Eventually, some creatures evolved a command center to run those complex bodies. We call it a brain. This story of how brains evolved, while admittedly just a sketch, draws attention to a key insight about human beings that is too often overlooked. Your brain’s most important job isn’t thinking; it’s running the systems of your body to keep you alive and well. According to recent findings in neuroscience, even when your brain does produce conscious thoughts and feelings, they are more in service to the needs of managing your body than you realize. And in stressful times like right now, this curious perspective on your mental life may actually help to lessen your anxieties. Much of your brain’s activity happens outside your awareness. In every moment, your brain must figure out your body’s needs for the next moment and execute a plan to fill those needs in advance. For example, each morning as you wake, your brain anticipates the energy you’ll need to drag your sorry body out of bed and start your day. It proactively floods your bloodstream with the hormone cortisol, which helps make glucose available for quick energy. Your brain runs your body using something like a budget. A financial budget tracks money as it’s earned and spent. The budget for your body tracks resources like water, salt and glucose as you gain and lose them. Each action that spends resources, such as standing up, running, and learning, is like a withdrawal from your account. Actions that replenish your resources, such as eating and sleeping, are like deposits. The scientific name for body budgeting is allostasis. It means automatically predicting and preparing to meet the body’s needs before they arise. © 2020 The New York Times Company

Keyword: Stress
Link ID: 27593 - Posted: 11.27.2020

By Lindsay Gray When Herbert Weinstein stood trial for the murder of his wife in 1992, his attorneys were struck by the measured calm with which he recounted her death and the events leading up to it. He made no attempt to deny that he was culpable, and yet his stoicism in the face of his wildly uncharacteristic actions led his defense to suspect that he might not be. Weinstein underwent neuroimaging tests, which confirmed what his attorneys had suspected: a cyst had impinged upon large parts of Weinstein’s frontal lobe, the seat of impulse control in the brain. On these grounds, they reasoned he should be found not guilty by reason of insanity, despite Weinstein’s free admission of guilt. Guilt is difficult to define, but it pervades every aspect of our lives, whether we’re chastising ourselves for skipping a workout, or serving on the jury of a criminal trial. Humans seem to be hardwired for justice, but we’re also saddled with a curious compulsion to diagram our own emotional wiring. This drive to assign a neurochemical method to our madness has led to the generation of vast catalogs of neuroimaging studies that detail the neural underpinnings of everything from anxiety to nostalgia. In a recent study, researchers now claim to have moved us one step closer to knowing what a guilty brain looks like. Since guilt carries different weight depending on context or culture, the authors of the study chose to define it operationally as the awareness of having harmed someone else. A series of functional magnetic resonance imaging (fMRI) experiments across two separate cohorts, one Swiss and one Chinese, revealed what they refer to as a “guilt-related brain signature” that persists across groups. Since pervasive guilt is a common feature in severe depression and PTSD, the authors suggest that a neural biomarker for guilt could offer more precise insight into these conditions and, potentially, their treatment. But brain-based biomarkers for complex human behaviors also lend themselves to the more ethically fraught discipline of neuroprediction, an emergent branch of behavioral science that combines neuroimaging data and machine learning to forecast how an individual is likely to act based on how their brain scans compare to those of other groups. © 2020 Scientific American,

Keyword: Stress; Brain imaging
Link ID: 27591 - Posted: 11.21.2020

By Lisa Sanders, M.D. It started to drizzle just moments after the 24-year-old man crossed the finish line of the 2017 New York City Marathon. It was his first marathon, and he felt both elated and exhausted as the medal given for completing the brutal race was draped around his neck. A goody bag containing an energy drink was put in his left hand. It felt strangely heavy. His whole body ached and trembled with fatigue, but somehow that left arm felt even more tired. Unconcerned, he switched the bag to his right hand and went in search of his partner. Recovery took longer than he expected. It was a day and a half before his legs were strong enough for him to walk down stairs facing forward, rather than the sideways shuffle that his tired muscles insisted on. But by the end of the week he felt mostly normal. Only that left shoulder remained tired, sore and stiff. He went to a nearby walk-in clinic just south of City Hall. The nurse practitioner who examined him thought he had a rotator-cuff injury. She recommended a nonsteroidal anti-inflammatory like ibuprofen, physical therapy and time. The ibuprofen didn’t help much; neither did the physical therapy. That weekend he headed to the gym — his first workout since the race. He did his usual set of reps on his right biceps and triceps. But when he transferred the 25-pound dumbbell to his left hand, it seemed heavier. He struggled through two curls, but on the third the muscles in his arm turned wobbly. He grabbed the weight with his right hand and lowered it to the ground. By the time he got home, straightening his aching arm was excruciating, as if the muscles were too short to allow a full extension. That scared him. And it only got worse. The next day his whole arm was achy and tight. He couldn’t even work on his computer. Thinking back, the young runner questioned the assumption — shared by both him and the nurse practitioner — that the injury had occurred during the race. Now he suspected it started weeks earlier. © 2020 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 27587 - Posted: 11.21.2020

Diana Kwon It all began with a cough. Three years ago Tracey McNiven, a Scottish woman in her mid-30s, caught a bad chest infection that left her with a persistent cough that refused to subside, even after medication. A few months later strange symptoms started to appear. McNiven noticed numbness spreading through her legs and began to feel that their movement was out of her control. When she walked, she felt like a marionette, with someone else pulling the strings. Over the course of two weeks the odd loss of sensation progressively worsened. Then, one evening at home, McNiven's legs collapsed beneath her. “I was lying there, and I felt like I couldn't breathe,” she recalls. “I couldn't feel below my waist.” McNiven's mother rushed her to the hospital where she remained for more than half a year. During her first few weeks in the hospital, McNiven endured a barrage of tests as doctors tried to uncover the cause of her symptoms. It could be a progressive neurodegenerative condition such as motor neuron disease, they thought. Or maybe it was multiple sclerosis, a disease in which the body's own immune cells attack the nervous system. Bafflingly, however, the brain scans, blood tests, spinal taps and everything else came back normal. McNiven's predicament is not uncommon. According to one of the most comprehensive assessments of neurology clinics to date, roughly a third of patients have neurological symptoms that are deemed to be either partially or entirely unexplained. These may include tremor, seizures, blindness, deafness, pain, paralysis and coma and can parallel those of almost any neurological disease. In some patients, such complications can persist for years or even decades; some people require wheelchairs or cannot get out of bed. Although women are more often diagnosed than men, such seemingly inexplicable illness can be found in anyone and across the life span. © 2020 Scientific American

Keyword: Attention; Emotions
Link ID: 27586 - Posted: 11.18.2020

By Jessica Wapner We are living through an inarguably challenging time. The U.S. has been facing its highest daily COVID-19 case counts yet. Uncertainty and division continue to dog the aftermath of the presidential election. And we are heading into a long, cold winter, when socializing outdoors will be less of an option. We are a nation and a world under stress. But Andrew Huberman, a neuroscientist at Stanford University who studies the visual system, sees matters a bit differently. Stress, he says, is not just about the content of what we are reading or the images we are seeing. It is about how our eyes and breathing change in response to the world and the cascades of events that follow. And both of these bodily processes also offer us easy and accessible releases from stress. Huberman’s assertions are based on both established and emerging science. He has spent the past 20 years unraveling the inner workings of the visual system. In 2018, for example, his lab reported its discovery of brain pathways connected with fear and paralysis that respond specifically to visual threats. And a small but growing body of research makes the case that altering our breathing can alter our brain. In 2017 Mark Krasnow of Stanford University, Jack Feldman of the University of California, Los Angeles, and their colleagues identified a tight link between neurons responsible for controlling breathing and the region of the brain responsible for arousal and panic. This growing understanding of how vision and breathing directly affect the brain—rather than the more nebulous categories of the mind and feelings—can come in handy as we continue to face mounting challenges around the globe, across the U.S. and in our own lives. Scientific American spoke with Huberman about how it all works. © 2020 Scientific American

Keyword: Stress; Vision
Link ID: 27584 - Posted: 11.18.2020

By Catherine Zuckerman It’s 3 a.m. and you’ve been struggling for hours to fall asleep. Morning draws nearer and your anxiety about being exhausted the next day intensifies — yet again. If this sounds familiar, you’re not alone. Among the many disruptions of 2020, insomnia may rank high on the list. Data on how the pandemic has affected sleep is limited because biomedical research can take years to shake out and most studies to date have been small. But evidence from China and Europe suggests that prolonged confinement is altering sleep in adults as well as children. Doctors in the United States are seeing it too. “I think Covid and the election have affected sleep and could be considered a kind of trauma,” said Nancy Foldvary-Schaefer, director of the Cleveland Clinic Sleep Disorders Center. “A lot of people that I talk to — patients and non-patients and colleagues and family — have more anxiety generally now probably because of these two stressors, and high anxiety is clearly associated with insomnia.” Whether you’re suddenly tossing and turning at bedtime or waking up in the middle of the night, the first step toward better sleep is to figure out what’s triggering your insomnia. Once you do that, you can take action to prevent it from becoming chronic — a clinical sleep disorder that should be treated by a sleep-medicine specialist. Stressful and upsetting experiences like the death of a loved one or the loss of a job — two widespread realities of Covid-19 — are known psychological triggers for insomnia. If your insomnia is tied to such an event, the quickest way to get help is to call your doctor. One thing many doctors suggest is cognitive behavioral therapy, or C.B.T. C.B.T., or C.B.T.-I. for insomnia, is a standard treatment for both acute and chronic insomnia and includes a variety of techniques. Meditation, mindfulness and muscle relaxation can help people whose sleep problems are tied to a stressful event. C.B.T. for insomnia typically lasts from six to eight weeks and “works in about two-thirds to three-quarters of patients,” said Jennifer Martin, a psychologist and professor of medicine at the University of California, Los Angeles, David Geffen School of Medicine. © 2020 The New York Times Company

Keyword: Sleep; Stress
Link ID: 27581 - Posted: 11.16.2020

Alison Abbott Two years ago, immunologist and medical-publishing entrepreneur Leslie Norins offered to award US$1 million of his own money to any scientist who could prove that Alzheimer’s disease was caused by a germ. The theory that an infection might cause this form of dementia has been rumbling for decades on the fringes of neuroscience research. The majority of Alzheimer’s researchers, backed by a huge volume of evidence, think instead that the key culprits are sticky molecules in the brain called amyloids, which clump into plaques and cause inflammation, killing neurons. Norins wanted to reward work that would make the infection idea more persuasive. The amyloid hypothesis has become “the one acceptable and supportable belief of the Established Church of Conventional Wisdom”, says Norins. “The few pioneers who did look at microbes and published papers were ridiculed or ignored.” In large part, this was because some early proponents of the infection theory saw it as a replacement for the amyloid hypothesis. But some recent research has provided intriguing hints that the two ideas could fit together — that infection could seed some cases of Alzheimer’s disease by triggering the production of amyloid clumps. The data hint at a radical role for amyloid in neurons. Instead of just being a toxic waste product, amyloid might have an important job of its own: helping to protect the brain from infection. But age or genetics can interrupt the checks and balances in the system, turning amyloid from defender into villain. And that idea suggests new avenues to explore for potential therapies. To test the theory further, scientists are now developing animal models that mimic Alzheimer’s disease more closely. “We are taking the ideas seriously,” says neuroscientist Bart de Strooper, director of the UK Dementia Research Institute at University College London. © 2020 Springer Nature Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 27571 - Posted: 11.07.2020

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.”

Keyword: Neuroimmunology
Link ID: 27569 - Posted: 11.07.2020

Elena Renken More than a century ago, the zoologist Richard Semon coined the term “engram” to designate the physical trace a memory must leave in the brain, like a footprint. Since then, neuroscientists have made progress in their hunt for exactly how our brains form memories. They have learned that specific brain cells activate as we form a memory and reactivate as we remember it, strengthening the connections among the neurons involved. That change ingrains the memory and lets us keep memories we recall more often, while others fade. But the precise physical alterations within our neurons that bring about these changes have been hard to pin down — until now. In a study published last month, researchers at the Massachusetts Institute of Technology tracked an important part of the memory-making process at the molecular scale in engram cells’ chromosomes. Neuroscientists already knew that memory formation is not instantaneous, and that the act of remembering is crucial to locking a memory into the brain. These researchers have now discovered some of the physical embodiment of that mechanism. The MIT group worked with mice that had a fluorescent marker spliced into their genome to make their cells glow whenever they expressed the gene Arc, which is associated with memory formation. The scientists placed these mice in a novel location and trained them to fear a specific noise, then returned them to this location several days later to reactivate the memory. In the brain area called the hippocampus, the engram cells that formed and recalled this memory lit up with color, which made it easy to sort them out from other brain cells under the microscope during a postmortem examination. All Rights Reserved © 2020

Keyword: Learning & Memory; Stress
Link ID: 27567 - Posted: 11.04.2020

By James Gorman It’s good to have friends, for humans and chimpanzees. But the nature and number of those friends change over time. In young adulthood, humans tend to have a lot of friendships. But as they age, social circles narrow, and people tend to keep a few good friends around and enjoy them more. This trend holds across many cultures, and one explanation has to do with awareness of one’s own mortality. Zarin P. Machanda, an anthropologist at Tufts University, and her own good friend, Alexandra G. Rosati, a psychologist and anthropologist at the University of Michigan, wondered whether chimpanzees, which they both study, would show a similar pattern even though they don’t seem to have anything like a human sense of their own inevitable death. The idea, in humans, Dr. Machanda said, is that as we get older we think, “I don’t have time for these negative people in my life, or I don’t want to waste my time with all of this negativity.” So we concentrate on a few good friends and invest in them. This explanation is called socioemotional selectivity theory. Dr. Rosati and Dr. Machanda, who is the director of long-term research at the Kibale Chimpanzee Project in Uganda, drew on many years of observations of chimps at Kibale. Along with several colleagues, they reported Thursday in the journal Science that male chimps, at least, display the very same inclinations as humans. The team looked only at interactions of male chimpanzees because males are quite gregarious and form a lot of friendships, whereas females are more tied to family groups. So male relationships were easier to analyze. The finding doesn’t prove or disprove anything about whether knowledge of death is what drives the human behavior. But it does show that our closest primate relative displays the same bonding habits for some other reason, perhaps something about aging that the two species have in common. At the very least, the finding raises questions about humans. © 2020 The New York Times Company

Keyword: Aggression; Stress
Link ID: 27542 - Posted: 10.24.2020

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.

Keyword: Neuroimmunology
Link ID: 27540 - Posted: 10.21.2020

By Rachel Nuwer With their bright saucer eyes, button noses and plump, fuzzy bodies, slow lorises — a group of small, nocturnal Asian primates — resemble adorable, living stuffed animals. But their innocuous looks belie a startling aggression: They pack vicious bites loaded with flesh-rotting venom. Even more surprising, new research reveals that the most frequent recipients of their toxic bites are other slow lorises. “This very rare, weird behavior is happening in one of our closest primate relatives,” said Anna Nekaris, a primate conservationist at Oxford Brookes University and lead author of the findings, published Monday in Current Biology. “If the killer bunnies on Monty Python were a real animal, they would be slow lorises — but they would be attacking each other.” Even before this new discovery, slow lorises already stood out as an evolutionary oddity. Scientists know of just five other types of venomous mammals: vampire bats, two species of shrew, platypuses and solenodons (an insectivorous mammal found in Cuba, the Dominican Republic and Haiti). Researchers are just beginning to untangle the many mysteries of slow loris venom. One key component resembles the protein found in cat dander that triggers allergies in humans. But other unidentified compounds seem to lend additional toxicity and cause extreme pain. Strangely, to produce the venom, the melon-sized primates raise their arms above their head and quickly lick venomous oil-secreting glands located on their upper arms. The venom then pools in their grooved canines, which are sharp enough to slice into bone. “The result of their bite is really, really horrendous,” Dr. Nekaris says. “It causes necrosis, so animals may lose an eye, a scalp or half their face.” © 2020 The New York Times Company

Keyword: Aggression; Neurotoxins
Link ID: 27539 - Posted: 10.21.2020

Catherine Offord Overactivation of the brain’s immune cells, called microglia, may play a role in cognitive impairments associated with Down syndrome, according to research published today (October 6) in Neuron. Researchers in Italy identified elevated numbers of the cells in an inflammation-promoting state in the brains of mice with a murine version of the syndrome as well as in postmortem brain tissue from people with the condition. The team additionally showed that drugs that reduce the number of activated microglia in juvenile mice could boost the animals’ performance on cognitive tests. “This is a fabulous study that gives a lot of proof of principle to pursuing some clinical trials in people,” says Elizabeth Head, a neuroscientist at the University of California, Irvine, who was not involved in the work. “The focus on microglial activation, I thought, was very novel and exciting,” she adds, noting that more research will be needed to see how the effects of drugs used in the study might translate from mice to humans. Down syndrome is caused by an extra copy of part or all of human chromosome 21, and is the most commonly occurring chromosomal condition in the US. Children with Down syndrome often experience cognitive delays compared to typically developing children, although there’s substantial variation and the effects are usually mild or moderate. People with the syndrome also have a higher risk of certain medical conditions, including Alzheimer’s disease. © 1986–2020 The Scientist.

Keyword: Development of the Brain; Glia
Link ID: 27537 - Posted: 10.21.2020

By Benedict Carey Scott Lilienfeld, an expert in personality disorders who repeatedly disturbed the order in his own field, questioning the science behind many of psychology’s conceits, popular therapies and prized tools, died on Sept. 30 at his home in Atlanta. He was 59. The cause was pancreatic cancer, his wife, Candice Basterfield, said. Dr. Lilienfeld’s career, most of it spent at Emory University in Atlanta, proceeded on two tracks: one that sought to deepen the understanding of so-called psychopathic behavior, the other to expose the many faces of pseudoscience in psychology. Psychopathy is characterized by superficial charm, grandiosity, pathological lying and a lack of empathy. Descriptions of the syndrome were rooted in research in the criminal justice system, where psychopaths often end up. In the early 1990s, Dr. Lilienfeld worked to deepen and clarify the definition. In a series of papers, he anchored a team of psychologists who identified three underlying personality features that psychopaths share, whether they commit illegal acts or not: fearless dominance, meanness and impulsivity. The psychopath does what he or she wants, without anxiety, regret or regard for the suffering of others. “When you have these three systems interacting, it’s a bad brew, and it creates the substrate for what can become psychopathy,” said Mark F. Lenzenweger, a professor of psychology at the State University of New York at Binghamton. “This was Scott’s great contribution: He helped change the thinking about psychopathy, in a profound way, by focusing on aspects of personality, rather than on a list of bad behaviors.” Dr. Lilienfeld’s parallel career encompassed clinical psychology and aimed to shake it free of empty theorizing, softheadedness and bad practice. In the late 1990s and early 2000s, he led a loose group of researchers who began to question the validity of some of the field’s favored constructs, like repressed memories of abuse and multiple personality disorder. The Rorschach inkblot test took a direct hit as largely unreliable. The group also attacked treatments including psychological debriefing and eye movement desensitization and reprocessing, or E.M.D.R., both of which are used for trauma victims. © 2020 The New York Times Company

Keyword: Aggression; Learning & Memory
Link ID: 27529 - Posted: 10.19.2020

By Pam Belluck After contracting the coronavirus in March, Michael Reagan lost all memory of his 12-day vacation in Paris, even though the trip was just a few weeks earlier. Several weeks after Erica Taylor recovered from her Covid-19 symptoms of nausea and cough, she became confused and forgetful, failing to even recognize her own car, the only Toyota Prius in her apartment complex’s parking lot. Lisa Mizelle, a veteran nurse practitioner at an urgent care clinic who fell ill with the virus in July, finds herself forgetting routine treatments and lab tests, and has to ask colleagues about terminology she used to know automatically. “I leave the room and I can’t remember what the patient just said,” she said, adding that if she hadn’t exhausted her medical leave she’d take more time off. “It scares me to think I’m working,” Ms. Mizelle, 53, said. “I feel like I have dementia.” It’s becoming known as Covid brain fog: troubling cognitive symptoms that can include memory loss, confusion, difficulty focusing, dizziness and grasping for everyday words. Increasingly, Covid survivors say brain fog is impairing their ability to work and function normally. “There are thousands of people who have that,” said Dr. Igor Koralnik, chief of neuro-infectious disease at Northwestern Medicine in Chicago, who has already seen hundreds of survivors at a post-Covid clinic he leads. “The impact on the work force that’s affected is going to be significant. Scientists aren’t sure what causes brain fog, which varies widely and affects even people who became only mildly physically ill from Covid-19 and had no previous medical conditions. Leading theories are that it arises when the body’s immune response to the virus doesn’t shut down or from inflammation in blood vessels leading to the brain. © 2020 The New York Times Company

Keyword: Alzheimers; Learning & Memory
Link ID: 27522 - Posted: 10.12.2020

By Eddie Jacobs How would you feel about a new therapy for your chronic pain, which—although far more effective than any available alternative—might also change your religious beliefs? Or a treatment for lymphoma that brings one in three patients into remission, but also made them more likely to vote for your least preferred political party? These seem like idle hypothetical questions about impossible side effects. After all, this is not how medicine works. But a new mental health treatment, set to be licensed next year, poses just this sort of problem. Psychotherapy assisted by psilocybin, the psychedelic compound in “magic mushrooms,” seems to be remarkably effective in treating a wide range of psychopathologies, but also causes a raft of unusual nonclinical changes not seen elsewhere in medicine. Although its precise therapeutic mechanisms remain unclear, clinically relevant doses of psilocybin can induce powerful mystical experiences more commonly associated with extended periods of fasting, prayer or meditation. Arguably, then, it is unsurprising that it can generate long-lasting changes in patients: studies report increased prosociality and aesthetic appreciation, plus robust shifts in personality, values and attitudes to life, even leading some atheists to find God. What’s more, these experiences appear to be a feature, rather than a bug, of psilocybin-assisted psychotherapy, with the intensity of the mystical experience correlating with the extent of clinical benefit. © 2020 Scientific American,

Keyword: Drug Abuse; Emotions
Link ID: 27521 - Posted: 10.12.2020

By Benedict Carey The swarm of insects — sometimes gnats, sometimes wasps or flying ants — arrived early in this year of nightmares. With summer came equally unsettling dreams: of being caught in a crowd, naked and mask-less; of meeting men in white lab coats who declared, “We dispose of the elders.” Autumn has brought still other haunted-house dramas, particularly for women caring for a vulnerable relative or trying to manage virtual home-schooling. “I am home-schooling my 10-year-old,” one mother told researchers in a recent study of pandemic dreams. “I dreamed that the school contacted me to say it had been decided that his whole class would come to my home and I was supposed to teach all of them for however long the school remained closed.” Deirdre Barrett, a psychologist at Harvard Medical School and the author of “Pandemic Dreams,” has administered dream surveys to thousands of people in the last year, including the one with the home-schooling mother. “At least qualitatively, you see some shifts in content of dreams from the beginning of the pandemic into the later months,” Dr. Barrett said. “It’s an indication of what is worrying people most at various points during the year.” Dr. Barrett is the editor in chief of the journal Dreaming, which in its September issue posted four new reports on how the sleeping brain has incorporated the threat of Covid-19. The findings reinforce current thinking about the way that waking anxiety plays out during REM sleep: in images or metaphors representing the most urgent worries, whether these involve catching the coronavirus (those clouds of insects) or violating mask-wearing protocols. Taken together, the papers also hint at an answer to a larger question: What is the purpose of dreaming, if any? The answers that science has on offer can seem mutually exclusive, or near so. Freud understood dreams as wish fulfillment; the Finnish psychologist Antti Revonsuo saw them as simulations of pending threats. In recent years, brain scientists have argued that REM sleep — the period of sleep during which most dreaming occurs — bolsters creative thinking, learning and emotional health, providing a kind of unconscious psychotherapy. Then again, there is some evidence that dreaming serves little or no psychological purpose — that it is no more than a “tuning of the mind in preparation for awareness,” as Dr. J. Allan Hobson, a Harvard psychiatrist, has said. © 2020 The New York Times Company

Keyword: Sleep; Stress
Link ID: 27514 - Posted: 10.07.2020