By Sam Roberts Chris Pendergast, a Long Island teacher who defied the odds by surviving 27 years with Lou Gehrig’s disease, leading marathon “rides for life” for hundreds of miles from his motorized wheelchair to publicize the plight of fellow patients and raise $10 million for research, died on Oct. 14 at his home in Miller Place, N.Y. He was 71. His wife, Christine Pendergast, said the cause was complications of amyotrophic lateral sclerosis, the medical term for the disease that ended the career of Gehrig, the Yankee first baseman who, after playing in 2,130 consecutive games, proclaimed himself “the luckiest man on the face of the earth.” Gehrig died two years later, shortly before his 38th birthday. Mr. Pendergast was a 44-year-old teacher of gifted students at Dickinson Avenue elementary school in East Northport, on Long Island, when his eyes and hands began twitching and he started getting muscle spasms. On Oct. 13, 1993, he received the diagnosis: He had A.L.S., a degenerative disease, which diminishes muscle function and eventually the ability to breathe. The prognosis: He had three to five years to live. But Mr. Pendergast proved to be indomitable. He recast himself as the disease’s self-described squeaky wheel — “Since there’s no surviving constituency for A.L.S., there’s no squeaky wheel,” he told The New York Times in 2008. He founded the A.L.S. Ride for Life in 1997. The following year it mounted a 350-mile, two-week cavalcade from Yankee Stadium in the Bronx to Washington, with Mr. Pendergast leading it from his wheelchair. Subsequent annual rides went from Long Island’s East End to Manhattan with a small group of fellow patients. “We are dying men riding for life,” he told The Baltimore Sun in 2000. © 2020 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 27557 - Posted: 10.31.2020

By Abby Goodnough PHILADELPHIA — Steven Kelty had been addicted to crack cocaine for 32 years when he tried a different kind of treatment last year, one so basic in concept that he was skeptical. He would come to a clinic twice a week to provide a urine sample, and if it was free of drugs, he would get to draw a slip of paper out of a fishbowl. Half contained encouraging messages — typically, “Good job!” — but the other half were vouchers for prizes worth between $1 and $100. “I’ve been to a lot of rehabs, and there were no incentives except for the idea of being clean after you finished,” said Mr. Kelty, 61, of Winfield, Pa. “Some of us need something to motivate us — even if it’s a small thing — to live a better life.” The treatment is called contingency management, because the rewards are contingent on staying abstinent. A number of clinical trials have found it highly effective in getting people addicted to stimulants like cocaine and methamphetamine to stay in treatment and to stop using the drugs. But outside the research arena and the Department of Veterans Affairs, where Mr. Kelty is a patient, it is nearly impossible to find programs that offer such treatment — even as overdose deaths involving meth, in particular, have soared. There were more than 16,500 such deaths last year, according to preliminary data, more than twice as many as in 2016. Early data suggests that overdoses have increased even more during the coronavirus pandemic, which has forced most treatment programs to move online. Researchers say that one of the biggest obstacles to contingency management is a moral objection to the idea of rewarding someone for staying off drugs. That is one reason publicly funded programs like Medicaid, which provides health coverage for the poor, do not cover the treatment. Some treatment providers are also wary of giving prizes that they say patients could sell or trade for drugs. Greg Delaney, a pastor and the outreach coordinator at Woodhaven, a residential treatment center in Ohio, said, “Until you’re at the point where you can say, ‘I can make a good decision with this $50,’ it’s counterproductive.” © 2020 The New York Times Company

Keyword: Drug Abuse; Learning & Memory
Link ID: 27556 - Posted: 10.28.2020

R. Douglas Fields As I opened my copy of Science at home one night, an unfamiliar word in the title of a new study caught my eye: dopaminylation. The term refers to the brain chemical dopamine’s ability, in addition to transmitting signals across synapses, to enter a cell’s nucleus and control specific genes. As I read the paper, I realized that it completely upends our understanding of genetics and drug addiction. The intense craving for addictive drugs like alcohol and cocaine may be caused by dopamine controlling genes that alter the brain circuitry underlying addiction. Intriguingly, the results also suggest an answer to why drugs that treat major depression must typically be taken for weeks before they’re effective. I was shocked by the dramatic discovery, but to really understand it, I first had to unlearn some things. “Half of what you learned in college is wrong,” my biology professor, David Lange, once said. “Problem is, we don’t know which half.” How right he was. I was taught to scoff at Jean-Baptiste Lamarck and his theory that traits acquired through life experience could be passed on to the next generation. The silly traditional example is the mama giraffe stretching her neck to reach food high in trees, resulting in baby giraffes with extra-long necks. Then biologists discovered we really can inherit traits our parents acquired in life, without any change to the DNA sequence of our genes. It’s all thanks to a process called epigenetics — a form of gene expression that can be inherited but isn’t actually part of the genetic code. This is where it turns out that brain chemicals like dopamine play a role. All genetic information is encoded in the DNA sequence of our genes, and traits are passed on in the random swapping of genes between egg and sperm that sparks a new life. Genetic information and instructions are coded in a sequence of four different molecules (nucleotides abbreviated A, T, G and C) on the long double-helix strand of DNA. The linear code is quite lengthy (about 6 feet long per human cell), so it’s stored neatly wound around protein bobbins, similar to how magnetic tape is wound around spools in cassette tapes. All Rights Reserved © 2020

Keyword: Drug Abuse; Epigenetics
Link ID: 27555 - Posted: 10.28.2020

By Elizabeth Pennisi When Ian Ausprey outfitted dozens of birds with photosensor-containing backpacks, the University of Florida graduate student was hoping to learn how light affected their behavior. The unusual study, which tracked 15 species in Peru’s cloud forest, has now found that eye size can help predict where birds breed and feed—the bigger the eye, the smaller the prey or the darker the environment. The study also suggests birds with big eyes are especially at risk as humans convert forests into farmland. The study reveals a “fascinating new area of sensory biology,” says Richard Prum, an evolutionary biologist at Yale University who was not involved in the new work. It also shows the size of a bird’s eye says a lot about its owner, adds Matthew Walsh, an evolutionary ecologist at the University of Texas, Arlington, also not involved with the work. Light matters—not just for plants, but also for animals. Large eyes have long been associated with the need to see in dim conditions, but very little research has looked in depth at light’s impact on behavior. Recently, scientists have shown that the relative size of frogs’ eyes corresponds to where they live, hunt, and breed. And several studies published in the past 3 years suggest the eyes of killifish and water fleas vary in size depending on the presence of predators. With no predators, even slightly larger eyes offer a potential survival advantage. To find out how eye size might matter for birds, Ausprey and his adviser, Scott Robinson, an ecologist at the Florida Museum of Natural History, turned to the 240 species they had identified in one of Peru’s many cloud forests. The study area included a range of habitats—dense stands of trees, farms with fencerows, shrubby areas, and open ground. Because light can vary considerably by height—for example, in the tropics, the forest floor can have just 1% of the light at the tops of the trees—they included species living from the ground to the treetops. © 2020 American Association for the Advancement of Science.

Keyword: Vision; Evolution
Link ID: 27554 - Posted: 10.28.2020

By Lisa Sanders, M.D. The 61-year-old woman put on her reading glasses to try to decipher the tiny black squiggles on the back of the package of instant pudding. Was it two cups of milk? Or three? The glasses didn’t seem to help. The fuzzy, faded marks refused to become letters. The right side of her head throbbed — as it had for weeks. The constant aggravation of the headache made everything harder, and it certainly wasn’t helping her read this label. She rubbed her forehead, then brought her hand down to cover her right eye. The box disappeared into darkness. She could see only the upper-left corner of the instructions. Everything else was black. She quickly moved her hand to cover her left eye. The tiny letters sprang into focus. She moved back to the right: blackness. Over to the left: light and letters. That scared her. For the past few months, she’d had one of the worst headaches she had ever experienced in her lifetime of headaches. One that wouldn’t go away no matter how much ibuprofen she took. One that persisted through all the different medications she was given for her migraines. Was this terrible headache now affecting her vision? The neurologists she saw over the years always asked her about visual changes. She’d never had them, until now. “Should I take you to the hospital?” her husband asked anxiously when she told him about her nearly sightless left eye. “This could be serious.” She thought for a moment. No, tomorrow was Monday; her neurologist’s office would be open, and the doctor would see her right away. She was always reliable that way. The patient had bad headaches for most of her adult life. They were always on the right side. They were always throbbing. They could last for days, or weeks, or sometimes months. Loud noises were always bothersome. With really bad headaches, her eye would water and her nose would run, just on that side. Bending over was agony. For the past few weeks, her headache had been so severe that if she dropped something on the floor, she had to leave it there. When she bent down, the pounding was excruciating. © 2020 The New York Times Company

Keyword: Pain & Touch; Vision
Link ID: 27553 - Posted: 10.28.2020

Sara Reardon In Alysson Muotri’s laboratory, hundreds of miniature human brains, the size of sesame seeds, float in Petri dishes, sparking with electrical activity. These tiny structures, known as brain organoids, are grown from human stem cells and have become a familiar fixture in many labs that study the properties of the brain. Muotri, a neuroscientist at the University of California, San Diego (UCSD), has found some unusual ways to deploy his. He has connected organoids to walking robots, modified their genomes with Neanderthal genes, launched them into orbit aboard the International Space Station, and used them as models to develop more human-like artificial-intelligence systems. Like many scientists, Muotri has temporarily pivoted to studying COVID-19, using brain organoids to test how drugs perform against the SARS-CoV-2 coronavirus. But one experiment has drawn more scrutiny than the others. In August 2019, Muotri’s group published a paper in Cell Stem Cell reporting the creation of human brain organoids that produced coordinated waves of activity, resembling those seen in premature babies1. The waves continued for months before the team shut the experiment down. This type of brain-wide, coordinated electrical activity is one of the properties of a conscious brain. The team’s finding led ethicists and scientists to raise a host of moral and philosophical questions about whether organoids should be allowed to reach this level of advanced development, whether ‘conscious’ organoids might be entitled to special treatment and rights not afforded to other clumps of cells and the possibility that consciousness could be created from scratch. The idea of bodiless, self-aware brains was already on the minds of many neuroscientists and bioethicists. Just a few months earlier, a team at Yale University in New Haven, Connecticut, announced that it had at least partially restored life to the brains of pigs that had been killed hours earlier. By removing the brains from the pigs’ skulls and infusing them with a chemical cocktail, the researchers revived the neurons’ cellular functions and their ability to transmit electrical signals2.

Keyword: Consciousness; Development of the Brain
Link ID: 27552 - Posted: 10.28.2020

By Nicholas Bakalar Long-term exposure to noise may be linked to an increased risk for Alzheimer’s disease and other forms of dementia. Researchers did periodic interviews with 5,227 people 65 and older participating in a study on aging. They assessed them with standard tests of orientation, memory and language, and tracked average daytime noise levels in their neighborhoods for the five years preceding the cognitive assessments. About 11 percent had Alzheimer’s disease, and 30 percent had mild cognitive impairment, which often progresses to full-blown dementia. Residential noise levels varied widely, from 51 to 78 decibels, or from the level of a relatively quiet suburban neighborhood to that of an urban setting near a busy highway. The study is in Alzheimer’s & Dementia. After controlling for education, race, smoking, alcohol consumption, neighborhood air pollution levels and other factors, they found that each 10 decibel increase in community noise level was associated with a 36 percent higher likelihood of mild cognitive impairment, and a 29 percent increased risk for Alzheimer’s disease. The associations were strongest in poorer neighborhoods, which also had higher noise levels. The reasons for the connection are unknown, but the lead author, Jennifer Weuve, an associate professor of epidemiology at Boston University, suggested that excessive noise can cause sleep deprivation, hearing loss, increased heart rate, constriction of the blood vessels and elevated blood pressure, all of which are associated with an increased risk for dementia. © 2020 The New York Times Company

Keyword: Alzheimers; Hearing
Link ID: 27551 - Posted: 10.28.2020

By Jane E. Brody Do you have the heart to safely smoke pot? Maybe not, a growing body of medical reports suggests. Currently, increased smoking of marijuana in public, even in cities like New York where recreational use remains illegal (though no longer prosecuted), has reinforced a popular belief that this practice is safe, even health-promoting. “Many people think that they have a free pass to smoke marijuana,” Dr. Salomeh Keyhani, professor of medicine at the University of California, San Francisco, told me. “I even heard a suggestion on public radio that tobacco companies should switch to marijuana because then they’d be selling life instead of selling death.” But if you already are a regular user of recreational marijuana or about to become one, it would be wise to consider medical evidence that contradicts this view, especially for people with underlying cardiovascular diseases. Well: Get the best of Well, with the latest on health, fitness and nutrition. Compared with tobacco, marijuana smoking causes a fivefold greater impairment of the blood’s oxygen-carrying capacity, Dr. Keyhani and colleagues reported. In a review of medical evidence, published in January in the Journal of the American College of Cardiology, researchers described a broad range of risks to the heart and blood vessels associated with the use of marijuana. The authors, led by Dr. Muthiah Vaduganathan, cardiologist at Brigham and Women’s Hospital in Boston, point out that “marijuana is becoming increasingly potent, and smoking marijuana carries many of the same cardiovascular health hazards as smoking tobacco.” Edible forms of marijuana have also been implicated as a possible cause of a heart attack, especially when high doses of the active ingredient THC are consumed. © 2020 The New York Times Company

Keyword: Drug Abuse
Link ID: 27550 - Posted: 10.26.2020

By Scott Barry Kaufman Do you get excited and energized by the possibility of learning something new and complex? Do you get turned on by nuance? Do you get really stimulated by new ideas and imaginative scenarios? If so, you may have an influx of dopamine in your synapses, but not where we traditionally think of this neurotransmitter flowing. In general, the potential for growth from disorder has been encoded deeply into our DNA. We didn’t only evolve the capacity to regulate our defensive and destructive impulses, but we also evolved the capacity to make sense of the unknown. Engaging in exploration allows us to integrate novel or unexpected events with existing knowledge and experiences, a process necessary for growth. Dopamine production is essential for growth. But there are so many misconceptions about the role of dopamine in cognition and behavior. Dopamine is often labeled the “feel-good molecule,” but this is a gross mischaracterization of this neurotransmitter. As personality neuroscientist Colin DeYoung (a close colleague of mine) notes, dopamine is actually the “neuromodulator of exploration.” Dopamine’s primary role is to make us want things, not necessarily like things. We get the biggest rush of dopamine coursing through our brains at the possibility of reward, but this rush is no guarantee that we’ll actually like or even enjoy the thing once we get it. Dopamine is a huge energizing force in our lives, driving our motivation to explore and facilitating the cognitive and behavioral processes that allow us to extract the most delights from the unknown. If dopamine is not all about feeling good, then why does the feel-good myth persist in the public imagination? I think it’s because so much research on dopamine has been conducted with regard to its role in motivating exploration toward our more primal “appetitive” rewards, such as chocolate, social attention, social status, sexual partners, gambling or drugs like cocaine. © 2020 Scientific American

Keyword: Attention; Drug Abuse
Link ID: 27549 - Posted: 10.26.2020

By Perri Klass, M.D. In a new report on pediatric pain in the British medical journal The Lancet, a commission of experts, including scientists, doctors, psychologists, parents and patients, challenged those who take care of children to end what they described as the common undertreatment of pain in children, starting at birth. Isabel Jordan, of Squamish, British Columbia, took part as a parent partner, along with her son Zachary, 19, who has a genetic condition, and lives with chronic pain. “Pain matters with every child and at every intersection with the health care system,” she said. But for her son, “it didn’t matter with many providers, doctors, nurses, phlebotomists, and that made for worse outcomes.” “The professionals had a wealth of knowledge and experience, but what they lacked was the knowledge of what was really impacting patients in day-to-day life, they didn’t know how impactful poorly managed procedural pain was to patients,” especially children like her son who have ongoing medical issues, Ms. Jordan said. “He’s got a rare disease and has had a lifetime of chronic pain and also procedure pain.” Although we often pride ourselves, in pediatrics, on taking a kinder and gentler approach to our patients, pain experts feel that children’s pain is often taken for granted, and that simple and reliable strategies to mitigate it are disregarded; such as, for example, the 2015 World Health Organization recommendations that infants should be held by parents and perhaps breastfed during immunizations, and that distraction techniques should be used with older children. Christopher Eccleston, a professor of pain science and medical psychology at the University of Bath, where he directs the Centre for Pain Research, was the lead author on the report. He became interested in pediatric pain through working with adults with chronic pain, he said, and realizing that many of them had pain going back into adolescence, which had not been treated. © 2020 The New York Times Company

Keyword: Pain & Touch
Link ID: 27548 - Posted: 10.26.2020

By Stephani Sutherland Many of the symptoms experienced by people infected with SARS-CoV-2 involve the nervous system. Patients complain of headaches, muscle and joint pain, fatigue and “brain fog,” or loss of taste and smell—all of which can last from weeks to months after infection. In severe cases, COVID-19 can also lead to encephalitis or stroke. The virus has undeniable neurological effects. But the way it actually affects nerve cells still remains a bit of a mystery. Can immune system activation alone produce symptoms? Or does the novel coronavirus directly attack the nervous system? Some studies—including a recent preprint paper examining mouse and human brain tissue—show evidence that SARS-CoV-2 can get into nerve cells and the brain. The question remains as to whether it does so routinely or only in the most severe cases. Once the immune system kicks into overdrive, the effects can be far-ranging, even leading immune cells to invade the brain, where they can wreak havoc. Some neurological symptoms are far less serious yet seem, if anything, more perplexing. One symptom—or set of symptoms—that illustrates this puzzle and has gained increasing attention is an imprecise diagnosis called “brain fog.” Even after their main symptoms have abated, it is not uncommon for COVID-19 patients to experience memory loss, confusion and other mental fuzziness. What underlies these experiences is still unclear, although they may also stem from the body-wide inflammation that can go along with COVID-19. Many people, however, develop fatigue and brain fog that lasts for months even after a mild case that does not spur the immune system to rage out of control. Another widespread symptom called anosmia, or loss of smell, might also originate from changes that happen without nerves themselves getting infected. Olfactory neurons, the cells that transmit odors to the brain, lack the primary docking site, or receptor, for SARS-CoV-2, and they do not seem to get infected. Researchers are still investigating how loss of smell might result from an interaction between the virus and another receptor on the olfactory neurons or from its contact with nonnerve cells that line the nose. © 2020 Scientific American,

Keyword: Learning & Memory; Chemical Senses (Smell & Taste)
Link ID: 27547 - Posted: 10.24.2020

The plant compound apigenin improved the cognitive and memory deficits usually seen in a mouse model of Down syndrome, according to a study by researchers at the National Institutes of Health and other institutions. Apigenin is found in chamomile flowers, parsley, celery, peppermint and citrus fruits. The researchers fed the compound to pregnant mice carrying fetuses with Down syndrome characteristics and then to the animals after they were born and as they matured. The findings raise the possibility that a treatment to lessen the cognitive deficits seen in Down syndrome could one day be offered to pregnant women whose fetuses have been diagnosed with Down syndrome through prenatal testing. The study appears in the American Journal of Human Genetics. Down syndrome is a set of symptoms resulting from an extra copy or piece of chromosome 21. The intellectual and developmental disabilities accompanying the condition are believed to result from decreased brain growth caused by increased inflammation in the fetal brain. Apigenin is not known to have any toxic effects, and previous studies have indicated that it is an antioxidant that reduces inflammation. Unlike many compounds, it is absorbed through the placenta and the blood brain barrier, the cellular layer that prevents potentially harmful substances from entering the brain. Compared to mice with Down symptoms whose mothers were not fed apigenin, those exposed to the compound showed improvements in tests of developmental milestones and had improvements in spatial and olfactory memory. Tests of gene activity and protein levels showed the apigenin-treated mice had less inflammation and increased blood vessel and nervous system growth. Guedj, F. et al. Apigenin as a candidate prenatal treatment for Trisomy 21: effects in human amniocytes and the Ts1Cje mouse model. American Journal of Human Genetics. 2020.

Keyword: Development of the Brain; Genes & Behavior
Link ID: 27546 - Posted: 10.24.2020

Jon Hamilton Medical research was an early casualty of the COVID-19 pandemic. After cases began emerging worldwide, thousands of clinical trials unrelated to COVID-19 were paused or canceled amid fears that participants would be infected. But now some researchers are finding ways to carry on in spite of the coronavirus. "It's been a struggle of course," says Joshua Grill, who directs the Institute for Memory Impairments and Neurological Disorders at the University of California, Irvine. "But I think there's an imperative for us to find ways to move forward." Grill got a close-up view of the challenge in July when COVID-19 cases were spiking nationwide as he was trying to launch a study. UC Irvine and dozens of other research centers had just begun enrolling participants in the AHEAD study, a global effort that will test whether an investigational drug can slow down the earliest brain changes associated with Alzheimer's disease. Finding individuals willing and able to sign up for this sort of research is difficult even without a pandemic, says Grill, who also co-directs recruitment for the Alzheimer's Clinicals Trial Consortium, funded by the National Institute on Aging. "We're asking people do a lot, including enroll in long studies that require numerous visits," he says, "and in the AHEAD study, taking an investigational drug or placebo that's injected into a vein." Participants will receive either a placebo or a drug called BAN2401, made by Eisai, which is meant to reduce levels of amyloid, a toxic protein associated with Alzheimer's. People in the study will also have positron emission tomography, or PET, scans of their brains to measure changes in amyloid and another toxic protein called tau. © 2020 npr

Keyword: Alzheimers
Link ID: 27545 - Posted: 10.24.2020

By Jeremy Hsu Artificial intelligence could soon help screen for Alzheimer’s disease by analyzing writing. A team from IBM and Pfizer says it has trained AI models to spot early signs of the notoriously stealthy illness by looking at linguistic patterns in word usage. Other researchers have already trained various models to look for signs of cognitive impairments, including Alzheimer’s, by using different types of data, such as brain scans and clinical test results. But the latest work stands out because it used historical information from the multigenerational Framingham Heart Study, which has been tracking the health of more than 14,000 people from three generations since 1948. If the new models’ ability to pick up trends in such data holds up in forward-looking studies of bigger and more diverse populations, researchers say they could predict the development of Alzheimer’s a number of years before symptoms become severe enough for typical diagnostic methods to pick up. And such a screening tool would not require invasive tests or scans. The results of the Pfizer-funded and IBM-run study were published on Thursday in EClinicalMedicine. The new AI models provide “an augmentation to expert practitioners in how you would see some subtle changes earlier in time, before the clinical diagnosis has been achieved,” says Ajay Royyuru, vice president of health care and life sciences research at IBM. “It might actually alert you to some changes that [indicate] you ought to then go do a more complete exam.” To train these models, the researchers used digital transcriptions of handwritten responses from Framingham Heart Study participants who were asked to describe a picture of a woman who is apparently preoccupied with washing dishes while two kids raid a cookie jar behind her back. These descriptions did not preserve the handwriting from the original responses, says Rhoda Au, director of neuropsychology at the Framingham study and a professor at Boston University. © 2020 Scientific American,

Keyword: Alzheimers; Language
Link ID: 27544 - Posted: 10.24.2020

By Bruce Bower A type of bone tool generally thought to have been invented by Stone Age humans got its start among hominids that lived hundreds of thousands of years before Homo sapiens evolved, a new study concludes. A set of 52 previously excavated but little-studied animal bones from East Africa’s Olduvai Gorge includes the world’s oldest known barbed bone point, an implement probably crafted by now-extinct Homo erectus at least 800,000 years ago, researchers say. Made from a piece of a large animal’s rib, the artifact features three curved barbs and a carved tip, the team reports in the November Journal of Human Evolution. Among the Olduvai bones, biological anthropologist Michael Pante of Colorado State University in Fort Collins and colleagues identified five other tools from more than 800,000 years ago as probable choppers, hammering tools or hammering platforms. The previous oldest barbed bone points were from a central African site and dated to around 90,000 years ago (SN: 4/29/95), and were assumed to reflect a toolmaking ingenuity exclusive to Homo sapiens. Those implements include carved rings around the base of the tools where wooden shafts were presumably attached. Barbed bone points found at H. sapiens sites were likely used to catch fish and perhaps to hunt large land prey. The Olduvai Gorge barbed bone point, which had not been completed, shows no signs of having been attached to a handle or shaft. Ways in which H. erectus used the implement are unclear, Pante and his colleagues say. © Society for Science & the Public 2000–2020.

Keyword: Evolution; Learning & Memory
Link ID: 27543 - Posted: 10.24.2020

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

By Meagan Cantwell Although bird brains are tiny, they’re packed with neurons, especially in areas responsible for higher level thinking. Two studies published last month in Science explore the structure and function of avian brains—revealing they are organized similarly to mammals’ and are capable of conscious thought. © 2020 American Association for the Advancement of Science.

Keyword: Evolution; Learning & Memory
Link ID: 27541 - 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

By Jake Buehler Naked mole-rats — with their subterranean societies made up of a single breeding pair and an army of workers — seem like mammals trying their hardest to live like insects. Nearly 300 of the bald, bucktoothed, nearly blind rodents can scoot along a colony’s labyrinth of tunnels. New research suggests there’s brute power in those numbers: Like ants or termites, the mole-rats go to battle with rival colonies to conquer their lands. Wild naked mole-rats (Heterocephalus glaber) will invade nearby colonies to expand their territory, sometimes abducting pups to incorporate them into their own ranks, researchers report September 28 in the Journal of Zoology. This behavior may put smaller, less cohesive colonies at a disadvantage, potentially supporting the evolution of bigger colonies. Researchers stumbled across this phenomenon by accident while monitoring naked mole-rat colonies in Kenya’s Meru National Park. The team was studying the social structure of this extreme form of group living among mammals (SN: 6/20/06). Over more than a decade, the team trapped and marked thousands of mole-rats from dozens of colonies by either implanting small radio-frequency transponder chips under their skin, or clipping their toes. One day in 1994, while marking mole-rats in a new colony, researchers were surprised to find in its tunnels mole-rats from a neighboring colony that had already been marked. The queen in the new colony had wounds on her face from the ravages of battle. It looked like a war was playing out down in the soil. © Society for Science & the Public 2000–2020.

Keyword: Evolution; Sexual Behavior
Link ID: 27538 - Posted: 10.21.2020