By Betsy Mason Some fish can recognize their own faces in photos and mirrors, an ability usually attributed to humans and other animals considered particularly brainy, such as chimpanzees, scientists report. Finding the ability in fish suggests that self-awareness may be far more widespread among animals than scientists once thought. “It is believed widely that the animals that have larger brains will be more intelligent than animals of the small brain,” such as fish, says animal sociologist Masanori Kohda of Osaka Metropolitan University in Japan. It may be time to rethink that assumption, Kohda says. Kohda’s previous research showed that bluestreak cleaner wrasses can pass the mirror test, a controversial cognitive assessment that purportedly reveals self-awareness, or the ability to be the object of one’s own thoughts. The test involves exposing an animal to a mirror and then surreptitiously putting a mark on the animal’s face or body to see if they will notice it on their reflection and try to touch it on their body. Previously only a handful of large-brained species, including chimpanzees and other great apes, dolphins, elephants and magpies, have passed the test. In a new study, cleaner fish that passed the mirror test were then able to distinguish their own faces from those of other cleaner fish in still photographs. This suggests that the fish identify themselves the same way humans are thought to — by forming a mental image of one’s face, Kohda and colleagues report February 6 in the Proceedings of the National Academy of Sciences. “I think it’s truly remarkable that they can do this,” says primatologist Frans de Waal of Emory University in Atlanta who was not involved in the research. “I think it’s an incredible study.” © Society for Science & the Public 2000–2023.

Keyword: Attention; Evolution
Link ID: 28659 - Posted: 02.08.2023

By Susan Dominus For the past two or three years, many of my friends, women mostly in their early 50s, have found themselves in an unexpected state of suffering. The cause of their suffering was something they had in common, but that did not make it easier for them to figure out what to do about it, even though they knew it was coming: It was menopause. The symptoms they experienced were varied and intrusive. Some lost hours of sleep every night, disruptions that chipped away at their mood, their energy, the vast resources of good will that it takes to parent and to partner. One friend endured weeklong stretches of menstrual bleeding so heavy that she had to miss work. Another friend was plagued by as many as 10 hot flashes a day; a third was so troubled by her flights of anger, their intensity new to her, that she sat her 12-year-old son down to explain that she was not feeling right — that there was this thing called menopause and that she was going through it. Another felt a pervasive dryness in her skin, her nails, her throat, even her eyes — as if she were slowly calcifying. Then last year, I reached the same state of transition. Technically, it is known as perimenopause, the biologically chaotic phase leading up to a woman’s last period, when her reproductive cycle makes its final, faltering runs. The shift, which lasts, on average, four years, typically starts when women reach their late 40s, the point at which the egg-producing sacs of the ovaries start to plummet in number. In response, some hormones — among them estrogen and progesterone — spike and dip erratically, their usual signaling systems failing. During this time, a woman’s period may be much heavier or lighter than usual. As levels of estrogen, a crucial chemical messenger, trend downward, women are at higher risk for severe depressive symptoms. Bone loss accelerates. In women who have a genetic risk for Alzheimer’s disease, the first plaques are thought to form in the brain during this period. Women often gain weight quickly, or see it shift to their middles, as the body fights to hold onto the estrogen that abdominal fat cells produce. The body is in a temporary state of adjustment, even reinvention, like a machine that once ran on gas trying to adjust to solar power, challenged to find workarounds. © 2023 The New York Times Company

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 28658 - Posted: 02.08.2023

by Peter Hess An autism-linked mutation in the gene CHD8 yields wildly different physical and behavioral traits in mice depending on their genetic backgrounds, according to a study of 33 mouse strains. The findings were published today in Neuron. The results serve as a stark reminder that traits associated with an autism-linked mutation reflect more than just that mutation, says senior investigator Pat Levitt, chair of developmental neurogenetics at Children’s Hospital Los Angeles in California. Differences in genetic background could also explain why some findings from autism model mice have failed to replicate across labs, he adds. People with CHD8 mutations often have autism, intellectual disability, gastrointestinal issues and macrocephaly — larger-than-average head size — but not all of them have all of these traits. This variability may stem from interactions between the mutations and other variants across the genome, says study investigator Manal Tabbaa, a postdoctoral research fellow in Levitt’s lab. The new work does not reveal how the same CHD8 mutation can affect different mice — or people — differently. But researchers could use the genetically diverse rodents to answer this question, and to better understand and model autism’s heterogeneity, Tabbaa and Levitt say. “This is such a comprehensive approach to understand a really clinically relevant question, and it’s almost unbelievable that just three people could do this amount of work, considering how much it looks like was done,” says Joseph Gleeson, professor of neurosciences at the University of California, San Diego, who was not involved in the study. “They are just scratching the surface of what could be really fantastic future efforts.” © 2023 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 28657 - Posted: 02.08.2023

ByKatherine Kornei In the summer of 2021, a 54-year-old man was brought to a hospital in Northern California after an unexplained seizure. When an MRI revealed a mysterious mass in the left side of his brain, he was transferred to the University of California, San Francisco (UCSF), Medical Center. A brain biopsy and other tests revealed not a tumor, but an incredibly rare infection of the central nervous system caused by the amoeba Balamuthia mandrillaris. One of several “brain-eating” amoebae that occasionally spark headlines, the pathogen kills more than 90% of people who contract it. But despite initial setbacks, the patient survived and has largely recovered after experimental treatment with a decades-old drug. As his UCSF medical team recounted in a paper last month, a desperate hunt for a cure led them to a study published several years ago in which researchers showed a drug originally developed in Europe to quell urinary tract infections was effective against Balamuthia in the laboratory. That discovery sent the medical team rushing to obtain the drug, nitroxoline, from abroad so it could be given for the first time to a Balamuthia patient. Researchers not involved with the case call the man’s recovery a breakthrough in treating a brain infection that’s long been presumed to be a death sentence. “It’s the best that I ever remember seeing with Balamuthia,” says Dennis Kyle, a cell biologist at the University of Georgia, Athens, who studies amoebic diseases. The drug, which is not approved for regular use in the United States, has also been effective against other pathogenic amoebae in laboratory tests, according to the UCSF team. Balamuthia mandrillaris was first identified in 1986—not in a hospital but at the San Diego Wild Animal Park, where staff were eagerly anticipating the birth of a mandrill, the largest species of monkey. But one day, Nyani, the mother-to-be, began dragging her right arm on the ground. Within 48 hours she became lethargic, and she eventually stopped moving and died. A postmortem evaluation of Nyani’s brain tissue revealed hemorrhaging and centimeter-scale lesions. The culprits were plainly visible: Amoebae were eating Nyani’s brain.

Keyword: Miscellaneous
Link ID: 28656 - Posted: 02.04.2023

By McKenzie Prillaman A newfound species of frog doesn’t ribbit. In fact, it doesn’t make any sound at all. Many frogs have unusual characteristics, from turning translucent to being clumsy jumpers (SN: 12/22/22; 6/15/22). The recently discovered amphibian lacks a voice. It joins a group of seven other voiceless frog species called spiny-throated reed frogs that reside in East Africa. Instead of croaking, the spines on male frogs’ throats might help their female counterparts recognize potential mates via touch, sort of like braille, says conservation biologist Lucinda Lawson of the University of Cincinnati. Lawson and colleagues spotted the little frog, only about 25 millimeters long, in 2019 while surveying wildlife in Tanzania’s Ukaguru Mountains. The team immediately recognized the animal, now named Hyperolius ukaguruensis, as a spiny-throated reed frog. But something seemed off. “It [was] the wrong color,” Lawson says. Most frogs from this group are green and silver, but this one was gold and brown. Some quick measurements to check if the peculiar frog simply had trivial color variations or if it could be a new species revealed that its eyes were smaller than other spiny-throated reed frogs. The researchers agreed: “Let’s do some genetics,” Lawson says. They ran DNA tests on two frogs that looked like they belonged to the suspected new species, as well as 10 individuals belonging to known spiny-throated species. Comparing the golden frogs’ genetic makeup with that of the others revealed the oddballs were genetically distinct, Lawson and colleagues report February 2 in PLOS ONE. © Society for Science & the Public 2000–2023.

Keyword: Animal Communication; Sexual Behavior
Link ID: 28655 - Posted: 02.04.2023

By Natalia Mesa Most people will learn one or two languages in their lives. But Vaughn Smith, a 47-year-old carpet cleaner from Washington, D.C., speaks 24. Smith is a hyperpolyglot—a rare individual who speaks more than 10 languages. In a new brain imaging study, researchers peered inside the minds of polyglots like Smith to tease out how language-specific regions in their brains respond to hearing different languages. Familiar languages elicited a stronger reaction than unfamiliar ones, they found, with one important exception: native languages, which provoked relatively little brain activity. This, the authors note, suggests there’s something special about the languages we learn early in life. This study “contributes to our understanding of how our brain learns new things,” says Augusto Buchweitz, a cognitive neuroscientist at the University of Connecticut, Storrs, who was not involved in the work. “The earlier you learn something, the more your brain [adapts] and probably uses less resources.” Scientists have largely ignored what’s going on inside the brains of polyglots—people who speak more than five languages—says Ev Fedorenko, a cognitive neuroscientist at the Massachusetts Institute of Technology who led the new study. “There’s oodles of work on individuals whose language systems are not functioning properly,” she says, but almost none on people with advanced language skills. That’s partly because they account for only 1% of people globally, making it difficult to find enough participants for research. But studying this group can help linguists understand the human “language network,” a set of specialized brain areas located in the left frontal and temporal lobes. These areas help humans with the most basic aspect of understanding language: connecting sounds with meaning, Fedorenko says.

Keyword: Language
Link ID: 28654 - Posted: 02.04.2023

Heidi Ledford The humble prairie vole (Microtus ochrogaster) has long been revered for its unusual commitment to family. Pair-bonded couples huddle together, raise pups together and mate exclusively together — at least most of the time. Drop another couple’s pups into a cage with pair-bonded prairie voles and the adults will often foster those young as their own — highly unusual behaviour for a rodent. But a study published on 27 January in Neuron1 challenges decades of research that suggests a protein that detects the ‘love hormone’ oxytocin is responsible for the voles’ domestic bliss. Using CRISPR gene-editing, researchers found that prairie voles lacking the protein were still responsible parents and still formed monogamous relationships. These surprising results highlight the importance of revisiting accepted dogma when new scientific techniques emerge, says neuroscientist Bianca Jones Marlin at the Columbia University Zuckerman Institute in New York City. “Neuroscientists grew up in our field understanding that prairie voles pair bonded because of the distribution of oxytocin receptors and oxytocin,” she says. “That was canon.” For decades, neuroscientists interested in understanding the biological underpinnings of human social behaviours have been fascinated by prairie voles. “There’s a sort of eerie similarity between prairie vole social behaviours and human social behaviours,” says Nirao Shah, a neuroscientist at Stanford University in California. “Prairie voles are one of the few mammalian species that exhibit social attachment.” Social attachment The hormone oxytocin has long been thought to have a pivotal role in social behaviours. A protein that binds to oxytocin, called oxytocin receptor, is expressed differently in prairie vole brains than in the brains of other voles that do not form monogamous relationships. In humans, oxytocin levels rise in response to social interactions, and the hormone is important in stimulating uterine contractions during childbirth and the production of milk afterwards. © 2023 Springer Nature Limited

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 28653 - Posted: 02.01.2023

By John M. Beggs Over the last few decades, an idea called the critical brain hypothesis has been helping neuroscientists understand how the human brain operates as an information-processing powerhouse. It posits that the brain is always teetering between two phases, or modes, of activity: a random phase, where it is mostly inactive, and an ordered phase, where it is overactive and on the verge of a seizure. The hypothesis predicts that between these phases, at a sweet spot known as the critical point, the brain has a perfect balance of variety and structure and can produce the most complex and information-rich activity patterns. This state allows the brain to optimize multiple information processing tasks, from carrying out computations to transmitting and storing information, all at the same time. To illustrate how phases of activity in the brain — or, more precisely, activity in a neural network such as the brain — might affect information transmission through it, we can play a simple guessing game. Imagine that we have a network with 10 layers and 40 neurons in each layer. Neurons in the first layer will only activate neurons in the second layer, and those in the second layer will only activate those in the third layer, and so on. Now, I will activate some number of neurons in the first layer, but you will only be able to observe the number of neurons active in the last layer. Let’s see how well you can guess the number of neurons I activated under three different strengths of network connections. First, let’s consider weak connections. In this case, neurons typically activate independently of each other, and the pattern of network activity is random. No matter how many neurons I activate in the first layer, the number of neurons activated in the last layer will tend toward zero because the weak connections dampen the spread of activity. This makes our guessing game incredibly difficult. The amount of information about the first layer that you can learn from the last layer is practically nothing. All Rights Reserved © 2023

Keyword: Attention; Learning & Memory
Link ID: 28652 - Posted: 02.01.2023

ByEmily Underwood When two male mice meet in a confined space, the rules of engagement are clear: The lower ranking mouse must yield. But when these norms go out the window—say, when researchers rig such an encounter to favor the weakling—it sends the higher ranking male into a depressionlike spiral. That’s the conclusion of a new neuroimaging study that reveals how the mouse brain responds to an unexpected loss of social status, which has been shown to be a major risk factor for depression in humans, particularly men. The new study’s approach is “clever and powerful,” says Neir Eshel, a neuroscientist and psychiatrist at Stanford University who wasn’t involved in the work. But he cautions more work is needed to extend the results to our own species. Groups of mice live in hierarchies, both in the lab and the wild. In the lab, though, the highest ranking males form particularly despotic regimes. One or more dominant “alpha mice” will have privileged access to food and females. They can pee wherever they please, rather than in the designated corner reserved for commoners. Hailan Hu, a neuroscientist at the Zhejiang University School of Medicine, wanted to know what would happen in the brains of these mousy muckety-mucks when their pecking order was upended. She and colleagues set up a battle of wills, designed to avoid any actual fighting or bloodshed. Ten times a day, over 4 days, the researchers put a dominant mouse nose-to-nose with a subordinate in a clear, narrow tube. Then they blocked the lower ranked rodent’s exit, leaving it no choice but to advance on its superior. At first, the dominant mice resisted the upstarts and held their ground. But by the fourth day, they were retreating voluntarily from their opponents after only a few seconds. In doing so, the mouse kings also fell in social status and lost their high-ranking perks, including VIP access to a warm nest in the corner.

Keyword: Aggression; Depression
Link ID: 28651 - Posted: 02.01.2023

By Kelsey Herbers The comments started the day I became engaged in December 2018: “You’re going to be such a beautiful bride.” “I can’t wait to see you in your dress.” “Everything is going to be perfect.” Before my fiancé and I even booked our wedding date, originally April 25, 2020, or saved a color scheme on Pinterest, I felt an intensifying pressure to live up to the high expectations that I thought my friends and family already had for my wedding day. I was determined to meet those expectations. But the innocent, wedding-driven diet that commenced shortly after my engagement ultimately spiraled into a full-fledged eating disorder. I was shocked by how quickly I fell ill and how deep that illness was. There was nothing about my journey, however, that surprised Robyn L. Goldberg, a registered dietitian and author of “The Eating Disorder Trap.” “The research shows one out of three people who diet develop an eating disorder — it’s very, very common,” said Ms. Goldberg, who has worked in private practice for the last 25 years with clients who have eating disorders, including many future brides. Some have ended up in residential treatment, she said. “You get so consumed that to pull yourself out of that dark hole seems impossible.” In the early days of wedding planning, my lifestyle changes were subtle. I bought an elliptical machine, took note of my calorie intake and found healthier meal options. But when the pandemic hit and kept me at home with my gym equipment, measuring cups and extra time on my hands, the opportunities to try new weight loss methods and obsess over my progress grew. It also forced us to postpone our wedding date. In just a few months, I was severely limiting my calorie intake, weighing myself several times a day and adhering to strict, self-proclaimed exercise rules. This included 45 minutes of running on a treadmill and 120 minutes of walking (180 minutes on weekends) daily. Before my engagement, I had never heard of intermittent fasting, but it didn’t take long for me to master it. These behavioral changes happened so gradually that I didn’t even recognize something was wrong until nearly two years later. By then I had lost 50 pounds, though initially I had wanted to shed only 25. © 2023 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 28650 - Posted: 02.01.2023

By Nicola Jones The first hurdle was simply getting hold of some cannabis, given that it was illegal. “I was lucky,” Mechoulam recounts in a personal chronicle of his life’s work, published this month in the Annual Review of Pharmacology and Toxicology. “The administrative head of my Institute knew a police officer. ... I just went to Police headquarters, had a cup of coffee with the policeman in charge of the storage of illicit drugs, and got 5 kg of confiscated hashish, presumably smuggled from Lebanon.” By 1964, Mechoulam and his colleagues had determined, for the first time, the full structure of both delta-9-tetrahydrocannabinol, better known to the world as THC (responsible for marijuana’s psychoactive “high”) and cannabidiol, or CBD. That chemistry coup opened the door for cannabis research. Over the following decades, researchers including Mechoulam would identify more than 140 active compounds, called cannabinoids, in the cannabis plant, and learn how to make many of them in the lab. Mechoulam helped to figure out that the human body produces its own natural versions of similar chemicals, called endocannabinoids, that can shape our mood and even our personality. And scientists have now made hundreds of novel synthetic cannabinoids, some more potent than anything found in nature. Today, researchers are mining the huge number of known cannabinoids — old and new, found in plants or people, natural and synthetic — for possible pharmaceutical uses. But, at the same time, synthetic cannabinoids have become a hot trend in recreational drugs, with potentially devastating impacts. For most of the synthetic cannabinoids made so far, the adverse effects generally outweigh their medical uses says biologist João Pedro Silva of the University of Porto in Portugal, who studies the toxicology of substance abuse, and coauthored a 2023 assessment of the pros and cons of these drugs in the Annual Review of Pharmacology and Toxicology. But, he adds, that doesn’t mean there aren’t better things to come. © 2023 Annual Reviews

Keyword: Drug Abuse
Link ID: 28649 - Posted: 02.01.2023

By Kristen French George Church looks like he needs a nap. I’m talking to him on Zoom, and his eyelids have grown heavy, inclining toward slumber. Or maybe my mind is playing tricks on me. He assures me he is wide awake. But sleeping and waking life are often blurred for Church. One of the world’s most imaginative scientists, Church is a narcoleptic. A rare disorder, narcolepsy causes sudden attacks of sleep, and Church has fallen asleep in some unfortunate circumstances—at The World Economic Forum, just a few feet away from Microsoft founder Bill Gates, for instance. He also had to give up driving due to the risk that a bout of sleepiness will strike while he is behind the wheel. But Church, a Harvard geneticist known for his pathbreaking contributions to numerous fields—from genetics to astrobiology to biomedicine—says the benefits of his condition outweigh the inconveniences. Many of his wildest and most prescient ideas come from his narcoleptic naps. “The fact is, I fall asleep several times a day, and so almost everything comes from there,” Church says. His idea for a quick and simple way to “read” DNA—which resulted in the first commercial genome sequence, of the human pathogen H. pylori—came from a narcoleptic nap. He also conceived of editing genomes with CRISPR and building new genomes with off-the-shelf molecules during narcoleptic naps. More recently, in December, a wild idea for a space probe that could reach distant stars within just 20 years, at one-fifth the speed of light, came to him after a narcoleptic nap. He proposed that these lightning-speed interstellar missions could be launched by microbes and powered by laser sails. The ideas that come to him are often the result of collisions of unexpected images in his head. “I try to turn science fiction into science fact,” Church tells me. © 2023 NautilusNext Inc.,

Keyword: Sleep; Attention
Link ID: 28648 - Posted: 02.01.2023

By Joanna Thompson People often think they know what causes chronic depression. Surveys indicate that more than 80% of the public blames a “chemical imbalance” in the brain. That idea is widespread in pop psychology and cited in research papers and medical textbooks. Listening to Prozac, a book that describes the life-changing value of treating depression with medications that aim to correct this imbalance, spent months on the New York Times bestseller list. The unbalanced brain chemical in question is serotonin, an important neurotransmitter with fabled “feel-good” effects. Serotonin helps regulate systems in the brain that control everything from body temperature and sleep to sex drive and hunger. For decades, it has also been touted as the pharmaceutical MVP for fighting depression. Widely prescribed medications like Prozac (fluoxetine) are designed to treat chronic depression by raising serotonin levels. Yet the causes of depression go far beyond serotonin deficiency. Clinical studies have repeatedly concluded that the role of serotonin in depression has been overstated. Indeed, the entire premise of the chemical-imbalance theory may be wrong, despite the relief that Prozac seems to bring to many patients. If you were still of the opinion that it was simply a chemical imbalance of serotonin, then yeah, it’s pretty damning. A literature review that appeared in Molecular Psychiatry in July was the latest and perhaps loudest death knell for the serotonin hypothesis, at least in its simplest form. An international team of scientists led by Joanna Moncrieff of University College London screened 361 papers from six areas of research and carefully evaluated 17 of them. They found no convincing evidence that lower levels of serotonin caused or were even associated with depression. People with depression didn’t reliably seem to have less serotonin activity than people without the disorder. Experiments in which researchers artificially lowered the serotonin levels of volunteers didn’t consistently cause depression. Genetic studies also seemed to rule out any connection between genes affecting serotonin levels and depression, even when the researchers tried to consider stress as a possible cofactor. All Rights Reserved © 2023

Keyword: Depression; Stress
Link ID: 28647 - Posted: 01.27.2023

By Dana G. Smith Do you: Cut the tags out of your clothes? Relive (and regret) past conversations? Have episodes of burnout and fatigue? Zone out while someone is talking? Become hyper-focused while working on a project? Take on dozens of hobbies? Daydream? Forget things? According to TikTok, you might have attention deficit hyperactivity disorder. Videos about the psychiatric condition are all over the social media app, with the #adhd hashtag receiving more than 17 billion views to date. Many feature young people describing their specific (and sometimes surprising) symptoms, like sensitivity to small sensory annoyances (such as clothing tags) or A.D.H.D. paralysis, a type of extreme procrastination. After viewing these videos, many people who were not diagnosed with A.D.H.D. as children may question whether they would qualify as adults. As with most psychiatric conditions, A.D.H.D. symptoms can range in type and severity. And many of them “are behaviors everyone experiences at some point or another,” said Joel Nigg, a professor of psychiatry at Oregon Health & Science University. The key to diagnosing the condition, however, requires “determining that it’s serious, it’s extreme” and it’s interfering with people’s lives, he said. It’s also critical that the symptoms have been present since childhood. Those nuances can be lost on social media, experts say. In fact, one study published earlier this year found that more than half of the A.D.H.D. videos on TikTok were misleading. If a video (or article) has you thinking you may have undiagnosed A.D.H.D., here’s what to consider. Approximately 4 percent of adults in the United States have enough symptoms to qualify for A.D.H.D., but only an estimated one in 10 of them is diagnosed and treated. For comparison, roughly 9 percent of children in the United States have been diagnosed with the condition, and three-quarters have received medication or behavioral therapy for it. One reason for the lack of diagnoses in adults is that when people think of A.D.H.D., they often imagine a boy who can’t sit still and is disruptive in class, said Dr. Deepti Anbarasan, a clinical associate professor of psychiatry at the NYU Grossman School of Medicine. But those stereotypical hyperactive symptoms are present in just 5 percent of adult cases, she said. © 2023 The New York Times Company

Keyword: ADHD
Link ID: 28646 - Posted: 01.27.2023

Liam Drew The emergence of disease-causing bacteria that are resistant to antibiotics is often attributed to the overuse of antibiotics in people and livestock. But researchers have homed in on another potential driver of resistance: antidepressants. By studying bacteria grown in the laboratory, a team has now tracked how antidepressants can trigger drug resistance1. “Even after a few days exposure, bacteria develop drug resistance, not only against one but multiple antibiotics,” says senior author Jianhua Guo, who works at the Australian Centre for Water and Environmental Biotechnology at the University of Queensland in Brisbane. This is both interesting and scary, he says. Globally, antibiotic resistance is a significant public-health threat. An estimated 1.2 million people died as a direct result of it in 20192, and that number is predicted to climb. Early clues Guo became interested in the possible contributions of non-antibiotic drugs to antibiotic resistance in 2014, after work by his lab found more antibiotic-resistance genes circulating in domestic wastewater samples than in samples of wastewater from hospitals, where antibiotic use is higher. Guo’s group and other teams also observed that antidepressants — which are among the most widely prescribed medicines in the world — killed or stunted the growth of certain bacteria. They provoke “an SOS response”, Guo explains, triggering cellular defence mechanisms that, in turn, make the bacteria better able to survive subsequent antibiotic treatment. © 2023 Springer Nature Limited

Keyword: Depression
Link ID: 28645 - Posted: 01.27.2023

By Annabelle Timsit A new study of more than 29,000 older adults has identified six habits — from eating a variety of foods to regularly reading or playing cards — that are linked with a lower risk of dementia and a slower rate of memory decline. Eating a balanced diet, exercising the mind and body regularly, having regular contact with others, and not drinking or smoking — these six “healthy lifestyle factors” were associated with better cognitive outcomes in older adults, in a large Chinese study conducted over a decade and published in the BMJ on Wednesday. While researchers have long known that there is a link between dementia and factors such as social isolation and obesity, the size and scope of the new study adds substantial evidence to a global body of research that suggests a healthy lifestyle may help brains age better. It also suggests that the effects of a healthy lifestyle are beneficial even for people who are genetically more susceptible to memory decline — a “very hope-giving” finding for the millions of individuals around the world who carry the APOEε4 gene, a major risk factor for Alzheimer’s disease, said Eef Hogervorst, chair of biological psychology at Loughborough University, who was not involved in the study. Memory naturally declines gradually as people age. Some older people may develop dementia, an umbrella term that can include Alzheimer’s, and generally describes a deterioration in cognitive function that goes beyond the normal effects of aging. But for many, “memory loss can merely be senescent forgetfulness,” write the authors of the BMJ study — like forgetting the name of that TV program you used to love, or that pesky fact you wanted to look up. Memory loss is no less damaging for being gradual, and age-related memory decline can in some cases be an early symptom of dementia. But the good news, the researchers say, is that it “can be reversed or become stable rather than progress to a pathological state.” How do you live to be 100? Good genes, getting outside and friends.

Keyword: Alzheimers
Link ID: 28644 - Posted: 01.27.2023

By Jennifer Szalai “‘R’s’ are hard,” John Hendrickson writes in his new memoir, “Life on Delay: Making Peace With a Stutter,” committing to paper a string of words that would have caused him trouble had he tried to say them out loud. In November 2019, Hendrickson, an editor at The Atlantic, published an article about then-presidential candidate Joe Biden, who talked frequently about “beating” his childhood stutter — a bit of hyperbole that the article finally laid to rest. Biden insisted on his redemptive narrative, even though Hendrickson, who has stuttered since he was 4, could tell when Biden repeated (“I-I-I-I-I”) or blocked (“…”) on certain sounds. The article went viral, putting Hendrickson in the position of being invited to go on television — a “nightmare,” he said on MSNBC at the time, though it did lead to a flood of letters from fellow stutterers, a number of whom he interviewed for this book. “Life on Delay” traces an arc from frustration and isolation to acceptance and community, recounting a lifetime of bullying and well-meaning but ineffectual interventions and what Hendrickson calls “hundreds of awful first impressions.” When he depicts scenes from his childhood it’s often in a real-time present tense, putting us in the room with the boy he was, more than two decades before. Hendrickson also interviews people: experts, therapists, stutterers, his own parents. He calls up his kindergarten teacher, his childhood best friend and the actress Emily Blunt. He reaches out to others who have published personal accounts of stuttering, including The New Yorker’s Nathan Heller and Katharine Preston, the author of a memoir titled “Out With It.” We learn that it’s only been since the turn of the millennium or so that stuttering has been understood as a neurological disorder; that for 75 percent of children who stutter, “the issue won’t follow them to adulthood”; that there’s still disagreement over whether “disfluency” is a matter of language or motor control, because “the research is still a bit of a mess.” © 2023 The New York Times Company

Keyword: Language; Attention
Link ID: 28643 - Posted: 01.27.2023

By Diana Kwon Alan Alda was running for his life. The actor, best known for his role on the television series M*A*S*H, wasn’t on a set. This threat was real—or at least it felt that way. So when he saw a bag of potatoes in front of him, he grabbed it and threw it at his attacker. Suddenly, the scene shifted. He was in his bedroom, having lurched out of sleep, and the sack of potatoes was a pillow he’d just chucked at his wife. Acting out dreams marks a disorder that occurs during the rapid eye movement (REM) phase of sleep. Called RBD, for REM sleep behavior disorder, it affects an estimated 0.5 to 1.25 percent of the general population and is more commonly reported in older adults, particularly men. Apart from being hazardous to dreamers and their partners, RBD may foreshadow neurodegenerative disease, primarily synucleinopathies—conditions in which the protein α-synuclein (or alpha-synuclein) forms toxic clumps in the brain. Not all nocturnal behaviors are RBD. Sleepwalking and sleep talking, which occur more often during childhood and adolescence, take place during non-REM sleep. This difference is clearly distinguishable in a sleep laboratory, where clinicians can monitor stages of sleep to see when a person moves. Nor is RBD always associated with a synucleinopathy: it can also be triggered by certain drugs such as antidepressants or caused by other underlying conditions such as narcolepsy or a brain stem tumor. When RBD occurs in the absence of these alternative explanations, the chance of future disease is high. Some epidemiological studies suggest that enacted dreaming predicts a more than 80 percent chance of developing a neurodegenerative disease within the patient’s lifetime. It may also be the first sign of neurodegenerative disease, which on average shows up within 10 to 15 years after onset of the dream disorder. One of the most common RBD-linked ailments is Parkinson’s disease, characterized mainly by progressive loss of motor control. Another is Lewy body dementia, in which small clusters of α-synuclein called Lewy bodies build up in the brain, disrupting movement and cognition. A third type of synucleinopathy, multiple system atrophy, interferes with both movement and involuntary functions such as digestion. RBD is one of the strongest harbingers of future synucleinopathy, more predictive than other early markers such as chronic constipation and a diminished sense of smell.

Keyword: Parkinsons; Sleep
Link ID: 28642 - Posted: 01.25.2023

Hannah Devlin Science correspondent Widely used antidepressants cause “emotional blunting”, according to research that offers new insights into how the drugs may work and their possible side-effects. The study found that healthy volunteers became less responsive to positive and negative feedback after taking a selective serotonin reuptake inhibitor (SSRI) drug for three weeks. The “blunting” of negative emotions could be part of how the drugs help people recover from depression, but could also explain a common side-effect. The work’s senior author, Prof Barbara Sahakian of the University of Cambridge, said: “In a way, this may be in part how they work. They take away some of the emotional pain that people who experience depression feel, but unfortunately it seems that they also take away some of the enjoyment.” The findings could help patients make better informed choices about their medication, she said, but added “there is no doubt that antidepressants are beneficial” for many patients. According to the NHS more than 8.3 million patients in England received an antidepressant drug in 2021-22. SSRIs are among the most widely used, and are effective for the majority of, although not all, patients. Some people on the medication report feeling emotionally dull or no longer finding things as pleasurable, with one study suggesting this applied to 40-60% of people taking the drug. However, it has been unclear whether this symptom is a drug side-effect or a symptom of depression. The latest work suggests that the drug alone can produce emotional blunting. In the study, published in the journal Neuropsychopharmacology, 66 volunteers were given either the SSRI drug, escitalopram, or a placebo for at least 21 days before doing a set of cognitive tests. © 2023 Guardian News & Media Limited

Keyword: Depression; Emotions
Link ID: 28641 - Posted: 01.25.2023

By Darren Incorvaia The great apes do not have spoken language, but they share many gestures. Can humans like you understand those gestures too? Watch this short video and test your ability to read chimpanzee body language. What is this chimpanzee (the one scratching its arm) asking the other one to do? © 2023 The New York Times Company

Keyword: Animal Communication; Evolution
Link ID: 28640 - Posted: 01.25.2023