Ari Daniel Fred Crittenden, 73, lost his sight to retinitis pigmentosa when he was 35 years old. Today he has no visual perception of light. "It's total darkness," he says. Still, he has cells in his eyes that use light to keep his internal clock ticking along nicely. Marta Iwanek for NPR Every baseball season, 73-year-old Fred Crittenden plants himself in front of his television in his small one-bedroom apartment an hour north of Toronto. "Oh, I love my sports — I love my Blue Jays," says Crittenden. "They need me to coach 'em — they'd be winning, I'll tell ya." He listens to the games in his apartment. He doesn't watch them, because he can't see. "I went blind," Crittenden recalls, when "I was 35 years young." Crittenden has retinitis pigmentosa, an inherited condition that led to the deterioration of his retinas. He lost all his rods (the cells that help us see in dim light) and all his cones (the cells that let us see color in brighter light). Within a single year, in 1985, Crittenden says he went from perfect vision to total blindness. Certain cells within Crittenden's retinas that contain melanopsin help his brain to detect light, even if what he sees is darkness. Among other things, these light-detecting cells help his body regulate his sleep cycles. Marta Iwanek for NPR "The last thing I saw clearly," he says, thinking back, "it was my daughter, Sarah. She was 5 years old then. I used to go in at night and just look at her when she was in the crib. And I could just barely still make her out — her little eyes or her nose or her lips or her chin, that kind of stuff. Even to this day it's hard." © 2022 npr

Keyword: Biological Rhythms; Vision
Link ID: 28598 - Posted: 12.17.2022

By Yasemin Saplakoglu Memory and perception seem like entirely distinct experiences, and neuroscientists used to be confident that the brain produced them differently, too. But in the 1990s neuroimaging studies revealed that parts of the brain that were thought to be active only during sensory perception are also active during the recall of memories. “It started to raise the question of whether a memory representation is actually different from a perceptual representation at all,” said Sam Ling, an associate professor of neuroscience and director of the Visual Neuroscience Lab at Boston University. Could our memory of a beautiful forest glade, for example, be just a re-creation of the neural activity that previously enabled us to see it? “The argument has swung from being this debate over whether there’s even any involvement of sensory cortices to saying ‘Oh, wait a minute, is there any difference?’” said Christopher Baker, an investigator at the National Institute of Mental Health who runs the learning and plasticity unit. “The pendulum has swung from one side to the other, but it’s swung too far.” Even if there is a very strong neurological similarity between memories and experiences, we know that they can’t be exactly the same. “People don’t get confused between them,” said Serra Favila, a postdoctoral scientist at Columbia University and the lead author of a recent Nature Communications study. Her team’s work has identified at least one of the ways in which memories and perceptions of images are assembled differently at the neurological level. When we look at the world, visual information about it streams through the photoreceptors of the retina and into the visual cortex, where it is processed sequentially in different groups of neurons. Each group adds new levels of complexity to the image: Simple dots of light turn into lines and edges, then contours, then shapes, then complete scenes that embody what we’re seeing. Simons Foundation © 2022

Keyword: Attention; Vision
Link ID: 28597 - Posted: 12.15.2022

ByElizabeth Pennisi Willpower might be key to getting off the couch to exercise, but bacteria may lend a helping hand. Studies in mice reported today in Nature suggest microbes in the gut may be behind differences in the desire to work out. A research team has homed in on specific microbial molecules that stimulate a rodent’s desire to run—and keep running. By revealing exactly how these molecules talk to the brain, this group has set the stage for finding out whether similar signals help keep humans active. The work “establishes just how critical the microbiome is for exercise and goes incredibly deep in providing a new gut-brain [connection],” says Aleksandar Kostic, a microbiologist at Harvard Medical School who is co-founder of FitBiomics, a company developing probiotics to improve fitness. Kostic, who wasn’t involved in the research, and others speculate that exercise-inducing commands from the microbes might one day be packaged into pills people could take. To explore why some people like to exercise and others don’t, University of Pennsylvania microbiologist Christoph Thaiss studied mice bred to have a lot of genetic and behavioral variation. His team found more than a fivefold difference in how far the mice ran on wheels in their cages—some covered more than 30 kilometers in 48 hours, whereas others rarely moved in their wheels. The active and lazy mice didn’t show any significant differences in their genetics or biochemistry. But the researchers did notice one clue: When treated with antibiotics, mice that were normally highly energetic tended to exercise less. Follow-up studies showed the antibiotic treatment affected the brains of the formerly active mice. The activity of certain brain genes declined, along with levels of dopamine, a neurotransmitter that has been linked to “runner’s high”—that sense of wellbeing that comes with prolonged exercise.

Keyword: Obesity
Link ID: 28596 - Posted: 12.15.2022

By Yasemin Saplakoglu It’s often subtle at first. A lost phone. A forgotten word. A missed appointment. By the time a person walks into a doctor’s office, worried about signs of forgetfulness or failing cognition, the changes to their brain have been long underway — changes that we don’t yet know how to stop or reverse. Alzheimer’s disease, the most common form of dementia, has no cure. “There’s not much you can do. There are no effective treatments. There’s no medicine,” said Riddhi Patira, a behavioral neurologist in Pennsylvania who specializes in neurodegenerative diseases. That’s not how the story was supposed to go. Three decades ago, scientists thought they had cracked the medical mystery of what causes Alzheimer’s disease with an idea known as the amyloid cascade hypothesis. It accused a protein called amyloid-beta of forming sticky, toxic plaques between neurons, killing them and triggering a series of events that made the brain waste away. The amyloid cascade hypothesis was simple and “seductively compelling,” said Scott Small, the director of the Alzheimer’s Disease Research Center at Columbia University. And the idea of aiming drugs at the amyloid plaques to stop or prevent the progression of the disease took the field by storm. Decades of work and billions of dollars went into funding clinical trials of dozens of drug compounds that targeted amyloid plaques. Yet almost none of the trials showed meaningful benefits to patients with the disease. That is, until September, when the pharmaceutical giants Biogen and Eisai announced that in a phase 3 clinical trial, patients taking the anti-amyloid drug lecanemab showed 27% less decline in their cognitive health than patients taking a placebo did. Last week, the companies revealed the data, now published in the New England Journal of Medicine, to an excited audience at a meeting in San Francisco. Simons Foundation © 2022

Keyword: Alzheimers
Link ID: 28595 - Posted: 12.15.2022

By Jake Buehler Female snakes have clitorises too, a new study finds. The research raises the possibility that the sex lives of snakes are more complicated and diverse than previously understood, researchers report December 14 in Proceedings of the Royal Society B. Clitorises are found in a wide range of vertebrate life, from crocodiles to dolphins (SN: 1/10/22). One exception is birds, which lost their clitorises over the course of their evolution. Female snakes appeared to have lost the sex organ too, which was puzzling, since their close lizard relatives possess paired clitorises, called hemiclitorises. Male lizards and snakes have accompanying paired phalli, or hemipenises.  This element of female snakes’ sexual anatomy went unexamined in detail for so long partly because hemiclitorises can be fragile and easy to miss, but also because female genitalia have historically been considered “quite taboo,” says evolutionary biologist Megan Folwell of the University of Adelaide in Australia. “Even in humans, the proper function and significance of the human clitoris was still being discussed in 2006,” she says. Conflicting accounts of snake hemiclitorises in some scientific papers led Folwell to take a detailed look. She first examined a euthanized female common death adder (Acanthophis antarcticus). “I just started with dissecting the tail and going into it with a really open mind of what I might find,” she says. She was “pleasantly surprised” to find dual organs within that were completely different from the hemipenises found in male snakes. Also, unlike lizard hemiclitorises, the snake’s couldn’t turn out externally. © Society for Science & the Public 2000–2022.

Keyword: Sexual Behavior; Evolution
Link ID: 28594 - Posted: 12.15.2022

By Ellen Barry BETHESDA, Md. — The psychiatrist E. Fuller Torrey is 85 years old and has Parkinson’s disease, the tremors at times so strong that his hand beats like a drum on the table. Still, every morning when he reads the newspapers, he looks for accounts of violent behavior by people with severe mental illness, to add to an archive he has maintained since the 1980s. His records include reports of people who, in the grip of psychosis, assaulted political figures or pushed strangers into the path of subway trains; parents who, while delusional, killed their children by smothering, drowning or beating them; adult children who, while off medication, killed their parents with swords, axes or hammers. Dr. Torrey, who has done pioneering research into the biological basis of schizophrenia, has used these stories in service of an argument: that it was a mistake for the United States to shut down its public psychiatric hospitals without adequate follow-up care. And that to remedy this, the government should create systems to compel seriously mentally ill people in the community to get treatment. For much of his career, Dr. Torrey was a lonely voice on this issue, disavowed by patient advocacy groups and by organized psychiatry. But his ideas are now animating major policy shifts, including the announcement by Mayor Eric Adams of New York last month that city officials would send people with untreated mental illnesses to hospitals, even if they posed no threat to others. Dr. Torrey’s influence on New York City’s policy is profound. The mayor’s adviser on this matter is Brian Stettin, who was thrust into mental health policy in 1999 when, as a lawyer in the office of Attorney General Eliot Spitzer of New York, he was asked to draft Kendra’s Law, named for a woman who was pushed in front of a subway train by a man with schizophrenia. The law allows a court to order a person with mental illness to comply with an outpatient treatment plan, risking involuntary commitment if the person refuses. © 2022 The New York Times Company

Keyword: Schizophrenia
Link ID: 28593 - Posted: 12.13.2022

By Allison Gasparini Are you drinking enough water? The question seems like it should have a straightforward answer — a specific amount of water you need to drink daily to combat dehydration.      But the rate and way in which the human body takes in and excretes water is not as universal as you might expect. By studying more than 5,000 people living in 23 countries and ranging in age from 8 days to 96 years, researchers have found that the turnover of water in a person’s body varies widely depending on the individual’s physical and environmental factors. The results, published in the Nov. 24 Science, suggest that the idea that a person should ideally consume eight 8-ounce glasses of water a day is not a one-size-fits-all solution to peak hydration.     Even within the calculations, “individual variabilities could be huge,” says biomedical engineer Kong Chen, director of the metabolic research program at the National Institutes of Health’s Clinical Center. Yosuke Yamada, a physiologist at the National Institute of Biomedical Innovation, Health and Nutrition in Japan, and colleagues used a stable isotope of hydrogen known as deuterium to track the movement of water through people’s bodies. Drinking water accounts for only half of the total water intake by humans, with the rest coming from food. Simply measuring the amount of water that a person drinks in a day is not enough to accurately gauge water turnover or the amount of water used by the body daily. © Society for Science & the Public 2000–2022.

Keyword: Obesity
Link ID: 28592 - Posted: 12.13.2022

By Christina Jewett and Cade Metz A jumble of cords and two devices the size of soda cans protrude from Austin Beggin’s head when he undergoes testing with a team of researchers studying brain implants that are meant to restore function to those who are paralyzed. Despite the cumbersome equipment, it is also when Mr. Beggin feels the most free. He was paralyzed from the shoulders down after a diving accident eight years ago, and the brain device picks up the electrical surges that his brain generates as he envisions moving his arm. It converts those signals to cuffs on the major nerves in his arm. They allow him to do things he had not done on his own since the accident, like lift a pretzel to his mouth. “This is like the first time I’ve ever gotten the opportunity or I’ve ever been privileged and blessed enough to think, ‘When I want to open my hand, I open it,’” Mr. Beggin, 30, said. Days like that are always “a special day.” The work at the Cleveland Functional Electrical Stimulation Center represents some of the most cutting-age research in the brain-computer interface field, with the team connecting the brain to the arm to restore motion. It’s a field that Elon Musk wants to advance, announcing in a recent presentation that brain implants from his company Neuralink would someday help restore sight to the blind or return people like Mr. Beggin to “full-body functionality.” Mr. Musk also said the Neuralink device could allow anyone to use phones and other machines with new levels of speed and efficiency. Neuroscientists and Mr. Beggin alike see such giant advances as decades away, though. Scientists who have approval to test such devices in humans are inching toward restoring normal function in typing, speaking and limited movements. Researchers caution that the goal is much harder and more dangerous than it may seem. And they warn that Mr. Musk’s goals may never be possible — if it is even worth doing in the first place. © 2022 The New York Times Company

Keyword: Robotics
Link ID: 28591 - Posted: 12.13.2022

Kristine Zengeler Many neurodegenerative diseases, or conditions that result from the loss of function or death of brain cells, remain largely untreatable. Most available treatments target just one of the multiple processes that can lead to neurodegeneration, which may not be effective in completely addressing disease symptoms or progress, if at all. But what if researchers harnessed the brain’s inherent capabilities to cleanse and heal itself? My colleagues and I in the Lukens Lab at the University of Virginia believe that the brain’s own immune system may hold the key to neurodegenerative disease treatment. In our research, we found a protein that could possibly be leveraged to help the brain’s immune cells, or microglia, stave off Alzheimer’s disease. No available treatments for neurodegenerative diseases stop ongoing neurodegeneration while also helping affected areas in the body heal and recuperate. In terms of failed treatments, Alzheimer’s disease is perhaps the most infamous of neurodegenerative diseases. Affecting more than 1 in 9 U.S. adults 65 and older, Alzheimer’s results from brain atrophy with the death of neurons and loss of the connections between them. These casualties contribute to memory and cognitive decline. Billions of dollars have been funneled into researching treatments for Alzheimer’s, but nearly every drug tested to date has failed in clinical trials.

Keyword: Alzheimers; Neuroimmunology
Link ID: 28590 - Posted: 12.13.2022

By Emily Anthes In creating modern dog breeds, humans sculpted canines into physical specimens perfectly suited for a wide variety of tasks. Bernese mountain dogs have solid, muscular bodies capable of pulling heavy loads, while greyhounds have lean, aerodynamic frames, ideal for chasing down deer. The compact Jack Russell terrier can easily shimmy into fox or badger dens. Now, a large study, published in Cell on Thursday, suggests that behavior, not just appearance, has helped qualify these dogs for their jobs. Breeds that were created for similar roles — whether rounding up sheep or flushing birds into the air — tend to cluster into distinct genetic lineages, which can be characterized by different combinations of behavioral tendencies, the researchers found. “Much of modern breeding has been focused predominantly on what dogs look like,” Evan MacLean, an expert on canine cognition at the University of Arizona who was not involved in the study, said in an email. But, he emphasized, “Long before we were breeding dogs for their appearances, we were breeding them for behavioral traits.” The study also found that many of the genetic variants that set these lineages apart from each other appear to regulate brain development, and many seem to predate modern breeds. Together, the results suggest that people may have created today’s stunning assortment of breeds, in part, by harnessing and preserving desirable behavioral traits that already existed in ancient dogs, the researchers said. “Dogs have fundamentally the same blueprint, but now you’ve got to emphasize certain things to get particular tasks done,” said Elaine Ostrander, a dog genomics expert at the National Human Genome Research Institute and the senior author of the study. “You’re going to tweak a gene up, you’re going to tweak it down.” In an email, Bridgett vonHoldt, an evolutionary biologist at Princeton University who was not involved in the research, called the new paper “a major landmark in the field of dog genomics and behavior. We know it is complicated. This study not only gives us hope, it will be viewed as an inspiration for all in the field.” © 2022 The New York Times Company

Keyword: Genes & Behavior; Evolution
Link ID: 28589 - Posted: 12.10.2022

By Bonnie Berkowitz and  William Neff Creating a physique that can win at the highest level of professional bodybuilding requires superhuman self-discipline, intense training and genetic good fortune. Increasingly, say the people familiar with the culture and its consequences, it cannot be done without illicit drugs and a willingness to push a body to — or past — its limits. More than a dozen scientists, trainers, judges and competitors interviewed for this report said that just earning a pro card, an amateur’s ticket to the pro ranks, is very difficult without anabolic steroids. Winning a marquee title drug-free? Several people laughed at the question. “Impossible,” said Harrison Pope, one of the country’s leading anabolic-steroid researchers. The behemoths who win the best-known and most lucrative titles barely resemble the iconic, classically muscled champions of the past, such as Arnold Schwarzenegger, who won the sport’s premiere title, Mr. Olympia, seven times between 1970 and 1980. “Arnold Schwarzenegger would not win today,” said Brad Schoenfeld, a professor at Lehman College in New York and author of several books on bodybuilding and muscle growth. “He would not even get a pro card.” Although bodybuilders spend years lifting weights and honing each muscle, they don’t need to demonstrate strength for the judges beyond the ability to hold poses onstage. They only need to look strong. Some competitors — and a growing legion of young, mostly male admirers — chase that look by diving into a reckless pharmacological game of whack-a-mole that insiders say has grown more intense and dangerous as sheer size has trumped the “Greek god” ideal of previous generations.

Keyword: Hormones & Behavior; Drug Abuse
Link ID: 28588 - Posted: 12.10.2022

Miryam Naddaf More than 3,500 genetic variations that potentially affect smoking and drinking behaviour have been identified in a study involving almost 3.4 million people with African, American, East Asian and European ancestry. The findings, published in Nature on 7 December1, highlight how increasing the sample size and ethnic diversity improves the power of such genome-screening analyses — called genome-wide association studies (GWASs) — to reveal how various traits are linked to genes, combinations of genes or mutations. Smoking and drinking are important risk factors for several physical and mental illnesses, including cardiovascular diseases and psychiatric disorders. Although both behaviours are influenced by environmental and social factors, there is evidence that genetics can affect tobacco and alcohol consumption. “We’re at a stage where genetic discoveries are being translated into clinical [applications],” says study co-author Dajiang Liu, a statistical geneticist at Penn State College of Medicine in Hershey, Pennsylvania. “If we can forecast someone's risk of developing nicotine or alcohol dependence using this information, we can intervene early and potentially prevent a lot of deaths.” Scientists use GWASs to find genetic ties to diseases or behaviours by comparing genetic sequences in large numbers of people. But so far, most of these studies have focused on European populations. Liu and his colleagues constructed a model that incorporated the genomic data of 3,383,199 people, 21% of whom had non-European ancestry. They identified 3,823 genetic variants that were associated with smoking or drinking behaviours. Thirty-nine of these were linked with the age at which individuals started smoking, 243 with the number of cigarettes smoked per day and 849 with the number of alcoholic drinks consumed per week.

Keyword: Drug Abuse; Genes & Behavior
Link ID: 28587 - Posted: 12.10.2022

By Ingrid Wickelgren  Recurrent intrusive memories lie at the heart of certain mental illnesses, including post-traumatic stress disorder and obsessive-compulsive disorder. Clinicians often treat these conditions with “exposure therapy.” They gradually and gently re-expose patients to feared stimuli or simulations—from reminders of active combat to germs on a toilet—teaching the brain to become accustomed to the stimuli and to decouple them from danger. But exposure therapy has drawbacks. “Facing these traumatic memories is painful to patients,” says Yingying Wang, a cognitive psychologist at Zhejiang University in China. “These treatments suffer from a very high dropout rate.” Wang and her colleagues have taken a first step toward developing a more benign way to dim traumatic memories. Their proof-of-concept study involves subliminal exposure to cues to those memories after putting the brain in a state in which it is likely to forget. The new findings present a new spin on a form of active forgetting in which people learn to suppress memories by practicing not thinking about them in the presence of reminders. In various studies, participants have memorized pairs of words such as needle-doctor or jogger-collie and then practiced either thinking or not thinking about the second word when the first word (the reminder) appears. Practicing not thinking about the second word has led to forgetting. The mechanism for this effect centers on the brain’s main memory hub, the hippocampus. Psychologists have discovered that suppressing memory retrieval puts the hippocampus in a degraded functional state. This state lasts for a small window of time—at least 10 seconds but potentially much longer—casting what researchers have dubbed an “amnesic shadow” that leads to poor memory for other things that happen within it. So when people suppress neutral word pairs, they put their brain into a state in which they are likely to forget new experiences. © 2022 Scientific American,

Keyword: Stress; Learning & Memory
Link ID: 28586 - Posted: 12.10.2022

ByDennis Normile Smoking kills. Ayesha Verrall has seen it up close. As a young resident physician in New Zealand’s public hospitals in the 2000s, Verrall watched smokers come into the emergency ward every night, struggling to breathe with their damaged lungs. Later, as an infectious disease specialist, she saw how smoking exacerbated illness in individuals diagnosed with tuberculosis and HIV/AIDS. She would tell them: “The best thing you can do to promote your health, other than take the pills, is to quit smoking.” Verrall is still urging citizens to give up cigarettes—no longer just one by one, but by the thousands. As New Zealand’s associate minister for health, she has led the development of the Smokefree Aotearoa 2025 Action Plan, which could make New Zealand the first country in the world to achieve smoke-free status—typically defined as an adult smoking rate of no more than 5%. (Aotearoa, loosely “Land of the Long White Cloud,” is a traditional Māori name for the country.) New Zealand’s Parliament is about to vote on the plan, which Chris Bostic, Washington, D.C.–based policy director at Action on Smoking & Health (ASH), calls “a huge deal. This will be the most comprehensive antitobacco policy in history.” Unveiled in December 2021, the plan features three radical interventions. One, called the smoke-free generation strategy, will make it illegal to ever sell combustible tobacco products to those born in 2009 or later. The goal is to create an ever-growing cohort that never picks up the smoking habit. A second provision calls for reducing the number of tobacco retailers by as much as 95%, to make cigarettes harder to get. The boldest proposal in the eyes of experts is reducing cigarettes’ nicotine content to below addictive levels. This “cuts right at the heart of why people smoke in the first place,” says Geoffrey Fong, head of the International Tobacco Control Policy Evaluation Project at the University of Waterloo. It’s potentially a “true game changer in the battle against smoking.”

Keyword: Drug Abuse
Link ID: 28585 - Posted: 12.10.2022

Heidi Ledford Severe COVID-19 is linked to changes in the brain that mirror those seen in old age, according to an analysis of dozens of post-mortem brain samples1. The analysis revealed brain changes in gene activity that were more extensive in people who had severe SARS-CoV-2 infections than in uninfected people who had been in an intensive care unit (ICU) or had been put on ventilators to assist their breathing — treatments used in many people with serious COVID-19. The study, published on 5 December in Nature Aging, joins a bevy of publications cataloguing the effects of COVID-19 on the brain. “It opens a plethora of questions that are important, not only for understanding the disease, but to prepare society for what the consequences of the pandemic might be,” says neuropathologist Marianna Bugiani at Amsterdam University Medical Centers. “And these consequences might not be clear for years.” Maria Mavrikaki, a neurobiologist at the Beth Israel Deaconess Medical Center in Boston, Massachusetts, embarked on the study about two years ago, after seeing a preprint, later published as a paper2, that described cognitive decline after COVID-19. She decided to follow up to see whether she could find changes in the brain that might trigger the effects. She and her colleagues studied samples taken from the frontal cortex — a region of the brain closely tied to cognition — of 21 people who had severe COVID-19 when they died and one person with an asymptomatic SARS-CoV-2 infection at death. The team compared these with samples from 22 people with no known history of SARS-CoV-2 infection. Another control group comprised nine people who had no known history of infection but had spent time on a ventilator or in an ICU — interventions that can cause serious side effects. The team found that genes associated with inflammation and stress were more active in the brains of people who had had severe COVID-19 than in the brains of people in the control group. Conversely, genes linked to cognition and the formation of connections between brain cells were less active. © 2022 Springer Nature Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 28584 - Posted: 12.06.2022

ByErik Stokstad Toxoplasma gondii is sometimes called the “mind control” parasite: It can infect the brains of animals and mess with their behavior in ways that may kill the host but help ensure the parasite’s spread. But now, researchers have found that infected wolves may actually benefit from those mind-altering tricks. A Toxoplasma infection, they found, makes wolves bolder and more likely to become pack leaders or disperse into other habitats, giving them more opportunity to reproduce. "We’ve really underestimated some of the consequences this parasite has,” says Eben Gering, a biologist at Nova Southeastern University who was not involved in the work. “The findings probably represent the tip of the iceberg concerning the parasite’s significance to the dynamics of wild ecosystems.” T. gondii, a single-celled parasite, only reproduces in domesticated cats and other felids. Infected cats excrete spore-packed oocysts in their feces, which can survive on plants or in soil or water. They can also persist in undercooked meat of livestock or game. When a host—humans included—consumes an oocyst, the spores are released and spread into the brain and muscles, forming new cysts. Worldwide, about one in four people is infected. Usually, the immune system keeps the parasite in check, but it can cause spontaneous abortion and other serious problems during pregnancy. It's long been known that rodents infected with Toxoplasma lose their fear of predators. Cysts in the brain somehow increase dopamine and testosterone, boosting boldness and risk-taking and increasing the chance the host will be eaten by cats. "These parasites are using some generic mind control or personality control that helps them fulfill their lifecycle," says Jaap de Roode, a biologist at Emory University who was not involved in the new study. "And that has all sorts of interesting consequences that we may not even have thought of before.” The consequences aren’t limited to rodents. In 2016, researchers in Gabon found that Toxoplasma-infected captive chimpanzees lost their aversion to leopard urine. And last year, another team described how Toxoplasma-infected hyena cubs in Kenya venture closer to lions, making them more likely to be killed.

Keyword: Aggression; Emotions
Link ID: 28583 - Posted: 12.06.2022

By Bruce Bower An ancient hominid dubbed Homo naledi may have lit controlled fires in the pitch-dark chambers of an underground cave system, new discoveries hint. Researchers have found remnants of small fireplaces and sooty wall and ceiling smudges in passages and chambers throughout South Africa’s Rising Star cave complex, paleoanthropologist Lee Berger announced in a December 1 lecture hosted by the Carnegie Institution of Science in Washington, D.C. “Signs of fire use are everywhere in this cave system,” said Berger, of the University of the Witwatersrand, Johannesburg. H. naledi presumably lit the blazes in the caves since remains of no other hominids have turned up there, the team says. But the researchers have yet to date the age of the fire remains. And researchers outside Berger’s group have yet to evaluate the new finds. H. naledi fossils date to between 335,000 and 236,000 years ago (SN: 5/9/17), around the time Homo sapiens originated (SN: 6/7/17). Many researchers suspect that regular use of fire by hominids for light, warmth and cooking began roughly 400,000 years ago (SN: 4/2/12). Such behavior has not been attributed to H. naledi before, largely because of its small brain. But it’s now clear that a brain roughly one-third the size of human brains today still enabled H. naledi to achieve control of fire, Berger contends. Last August, Berger climbed down a narrow shaft and examined two underground chambers where H. naledi fossils had been found. He noticed stalactites and thin rock sheets that had partly grown over older ceiling surfaces. Those surfaces displayed blackened, burned areas and were also dotted by what appeared to be soot particles, Berger said. © Society for Science & the Public 2000–2022.

Keyword: Evolution
Link ID: 28582 - Posted: 12.06.2022

By Roni Caryn Rabin Deaths due to substance abuse, particularly of alcohol and opioids, rose sharply among older Americans in 2020, the first year of the coronavirus pandemic, as lockdowns disrupted routines and isolation and fear spread, federal health researchers reported on Wednesday. Alcohol and opioid deaths remained far less common among older people than among those middled-aged and younger, and rates had been rising in all groups for years. But the pronounced uptick — another data point in the long list of pandemic miseries — surprised government researchers. Deaths from opioids increased among Americans aged 65 and older by 53 percent in 2020 over the previous year, the National Center for Health Statistics found. Alcohol-related deaths, which had already been rising for a decade in this age group, rose by 18 percent. “The rate of alcohol deaths in older people is much lower than for younger adults, but the change caught our eye,” said Ellen Kramarow, a health statistician at the center and the lead author of the report, which analyzed death certificate data. Overdose deaths from synthetic opioids account for fewer than 1 percent of deaths in people over 65, Dr. Kramarow noted. “But the shape of the curve jumped out at us,” she said. Physiological changes that occur with aging leave older adults more vulnerable to the ill effects of alcohol and drugs, as metabolism and excretion of substances slow down, increasing the risk of toxicity. Smaller amounts have bigger effects, researchers have found. Alcohol and opioids can interact poorly with prescription medications that many older adults take for common conditions like hypertension, diabetes and mood disorders. Misuse can lead to falls and injuries, exacerbate underlying medical conditions and worsen declines in cognition. © 2022 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 28581 - Posted: 12.06.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28580 - Posted: 12.03.2022

By Dino Grandoni The shrew scampered across the sand, zipping its tiny, velvety body right, left, right, left. In just a few seconds it found the prize concealed in the sandbox: a tasty mixture of earthworms, mealworms and other meat. To quickly solve the puzzle in Dina Dechmann’s lab, the shrew didn’t just need to learn where its meal was hidden. Something else astounding happened in its head. It had to regrow its own brain. “It’s a crazy animal,” said Dechmann, a behavioral ecologist at the Max Planck Institute of Animal Behavior in Germany. “We can learn a lot from the shrews.” To prepare for the depths of winter when food is scarce, many animals slow down, sleep through the cold or migrate to warmer locales. Not the common shrew. To survive the colder months, the animal eats away at its own brain, reducing the organ by as much as a fourth, only to regrow much of brain matter in the spring. The process of shrinking and expanding the brain and other organs with seasons — dubbed Dehnel’s phenomenon — allows animals to reduce calorie-consuming tissue when temperatures drop. Researchers have discovered seasonal shrinkage in the skulls of other small, high-metabolism mammals, including weasels and, most recently, moles. The shrew’s incredible shrinking brain is more than just a biological curiosity. Understanding how these animals are able to restore their brain power may help doctors treat Alzheimer’s, multiple sclerosis and other neurodegenerative diseases in humans. “In the beginning, I couldn’t quite grasp it,” said John Dirk Nieland, an associate professor of health science and technology who is now researching drugs designed to mimic shrews’ brain-altering chemistry in humans.

Keyword: Biological Rhythms; Multiple Sclerosis
Link ID: 28579 - Posted: 12.03.2022