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Mercedes Burns An Asian water dragon hatched from an egg at the Smithsonian National Zoo, and her keepers were shocked. Why? Her mother had never been with a male water dragon. Through genetic testing, zoo scientists discovered the newly hatched female, born on Aug. 24, 2016, had been produced through a reproductive mode called parthenogenesis. Parthenogenesis is a Greek word meaning “virgin creation,” but specifically refers to female asexual reproduction. While many people may assume this behavior is the domain of science fiction or religious texts, parthenogenesis is surprisingly common throughout the tree of life and is found in a variety of organisms, including plants, insects, fish, reptiles and even birds. Because mammals, including human beings, require certain genes to come from sperm, mammals are incapable of parthenogenesis. Creating offspring without sperm Sexual reproduction involves a female and a male, each contributing genetic material in the form of eggs or sperm, to create a unique offspring. The vast majority of animal species reproduce sexually, but females of some species are able to produce eggs containing all the genetic material required for reproduction. Females of these species, which include some wasps, crustaceans and lizards, reproduce only through parthenogenesis and are called obligate parthenogens. A larger number of species experience spontaneous parthenogenesis, best documented in animals kept in zoo settings, like the Asian water dragon at the National Zoo or a blacktip shark at the Virginia Aquarium. Spontaneous parthenogens typically reproduce sexually, but may have occasional cycles that produce developmentally ready eggs. © 2010–2020, The Conversation US, Inc.

Keyword: Sexual Behavior
Link ID: 27630 - Posted: 12.19.2020

By Bruce Bower Bonobos display responsibility toward grooming partners akin to that of people working together on a task, a new study suggests. Until now, investigations have shown only that humans can work jointly toward a common goal presumed to require back-and-forth exchanges and an appreciation of being obligated to a partner (SN: 10/5/09). Primate biologist Raphaela Heesen of Durham University in England and colleagues studied 15 of the endangered great apes at a French zoological park. The researchers interrupted 85 instances of social grooming, in which one ape cleaned another’s fur, and 26 instances of self-grooming or solitary play. Interruptions consisted either of a keeper calling one bonobo in a grooming pair to come over for a food reward or a keeper rapidly opening and closing a sliding door to an indoor enclosure, which typically signaled mealtime and thus attracted both bonobos. Social grooming resumed, on average, 80 percent of the time after food rewards and 83 percent of the time after sliding-door disruptions, the researchers report December 18 in Science Advances. In contrast, self-grooming or playing alone was resumed only around 50 percent of the time, on average. © Society for Science & the Public 2000–2020

Keyword: Evolution; Emotions
Link ID: 27629 - Posted: 12.19.2020

By Matthew Hutson Somehow, even in a room full of loud conversations, our brains can focus on a single voice in something called the cocktail party effect. But the louder it gets—or the older you are—the harder it is to do. Now, researchers may have figured out how to fix that—with a machine learning technique called the cone of silence. Computer scientists trained a neural network, which roughly mimics the brain’s wiring, to locate and separate the voices of several people speaking in a room. The network did so in part by measuring how long it took for the sounds to hit a cluster of microphones in the room’s center. When the researchers tested their setup with extremely loud background noise, they found that the cone of silence located two voices to within 3.7º of their sources, they reported this month at the online-only Conference on Neural Information Processing Systems. That compares with a sensitivity of only 11.5º for the previous state-of-the-art technology. When the researchers trained their new system on additional voices, it managed the same trick with eight voices—to a sensitivity of 6.3º—even if it had never heard more than four at once. Such a system could one day be used in hearing aids, surveillance setups, speakerphones, or laptops. The new technology, which can also track moving voices, might even make your Zoom calls easier, by separating out and silencing background noise, from vacuum cleaners to rambunctious children. © 2020 American Association for the Advancement of Science.

Keyword: Hearing
Link ID: 27628 - Posted: 12.19.2020

Sophie Balisky, 26, says she struggled with anorexia and bulimia through most of her teens but got help three years ago and was doing great — until COVID hit and she lost her job as a flight attendant. She found herself reverting to old coping patterns in dealing with stressful and uncertain situations. "I was actually quite shocked, I was a bit taken aback, because I consider myself to be quite strong in my coping against my eating tendencies," said Balisky. Advocates for those who struggle with eating disorders say the pandemic is exacerbating the problem — prompting a greater need for community supports. Experts believe the problem is related to the stress, uncertainty and isolation that stems from the pandemic and related-restrictions and say it's not only a problem in the province but around the world. Some eating disorder support groups in Alberta who connect with people of all ages say they have seen a steady rise in demand since the pandemic hit. The Eating Disorder Support Network of Alberta is reporting a 5½ times increase in participants year-over-year between the period from March to the end of August. "So a huge surge through this," said Lauren Berlinguette, executive director of the support network. Another community-based agency that offers support to those who are struggling as well as their families, the Calgary Silver Linings Foundation, says it's experiencing a substantial increase in demand, too. The number of participants in all of its adult programs went from 37 to 64 participants, year-over-year. ©2020 CBC/Radio-Canada.

Keyword: Anorexia & Bulimia
Link ID: 27627 - Posted: 12.15.2020

By Paula Span By now, we were supposed to be swiftly approaching the day when we could walk into a CVS or Walgreens, a Best Buy or Walmart, and walk out with a pair of quality, affordable hearing aids approved by the Food and Drug Administration. Hearing aids, a widely needed but dauntingly expensive investment, cost on average $4,700 a pair. (Most people need two.) So in 2017, Congress passed legislation allowing the devices to be sold directly to consumers, without a prescription from an audiologist. The next step was for the F.D.A. to issue draft regulations to establish safety and effectiveness benchmarks for these over-the-counter devices. Its deadline: August 2020. A public comment period would follow, and then — right about now — the agency would be preparing its final rule, to take effect in May 2021. So by next summer, people with what is known as “perceived mild to moderate hearing loss” might need to spend only one-quarter of today’s price or less, maybe far less. And then we could have turned down the TV volume and stopped making dinner reservations for 5:30 p.m., when restaurants are mostly empty and conversations are still audible. “These regulations are going to help a lot of people,” said Dr. Vinay Rathi, an otolaryngologist at Massachusetts Eye and Ear. “There could be great potential for innovation.” So, where are the new rules? This long-sought alternative to the current state of hearing aid services has been delayed, perhaps one more victim of the pandemic. Of course, the agency has other crucial matters to address just now. Although the office charged with hearing aid regulations is not the one assessing Covid-19 vaccines, an F.D.A. spokesman said via email that it was dealing with “an unprecedented volume of emergency use authorizations” for diagnostics, ventilators and personal protective equipment. © 2020 The New York Times Company

Keyword: Hearing
Link ID: 27626 - Posted: 12.15.2020

Claudia Dreifus Questions like “why do men and women act differently?” are age-old, with tangled, deeply buried answers. But that is why Catherine Dulac, a Howard Hughes Medical Investigator and a professor of molecular and cellular biology at Harvard University, has become so well respected by her neuroscientist colleagues for the originality and creativity with which she has brought important answers to light. Though she is trained as a developmental biologist, Dulac takes her research into territory usually explored by social scientists by trying to discern the balance of genetic determination and environmental influence that shapes vital behaviors in mammals. Moreover, she deploys the genetic tools of modern biology to discover the mechanisms that activate these behaviors. Relatively early in her career, Dulac’s investigations into how animals detect pheromones changed our understanding of what those airborne chemicals may signify to the brain. More recently, her experiments identified how the brain circuitry that regulates crucial mating and parenting behaviors works — at least in her model animals, which are mice. She found astonishing evidence that although certain of these behaviors are often described as “male” or “female,” both types of circuitry are present and potentially active in both sexes. As a result, the right combination of triggers can switch an individual creature’s behavior to that of the opposite sex. Scientists are still exploring the full implications of her findings, but Dulac and others are hopeful that they might yield useful insights into conditions like postpartum behavioral disorders. Because of her work’s relevance, in September Dulac, just age 57, was awarded the $3 million Breakthrough Prize in Life Sciences, the richest single personal award in the scientific world. The citation for the prize hailed the success of her work, which connected behaviors to specific neural mechanisms and “overturned decades-old dogma in behavioral science.” Simons Foundation © 2020

Keyword: Sexual Behavior
Link ID: 27625 - Posted: 12.15.2020

By Cara Giaimo The rooms that make up the Bloomington Drosophila Stock Center at Indiana University are lined wall to wall with identical shelves. Each shelf is filled with uniform racks, and each rack with indistinguishable glass vials. The tens of thousands of fruit fly types within the vials, though, are each magnificently different. Some have eyes that fluoresce pink. Some jump when you shine a red light on them. Some have short bodies and iridescent curly wings, and look “like little ballerinas,” said Carol Sylvester, who helps care for them. Each variety doubles as a unique research tool, and it has taken decades to introduce the traits that make them useful. If left unattended, the flies would die in a matter of weeks, marooning entire scientific disciplines. Throughout the Covid-19 pandemic, workers across industries have held the world together, taking on great personal risk to care for sick patients, maintain supply chains and keep people fed. But other essential jobs are less well-known. At the Stock Center dozens of employees have come to work each day, through a lockdown and afterward, to minister to the flies that underpin scientific research. Tiny Bug, Huge Impact To most casual observers, fruit flies are little dots with wings that hang out near old bananas. But over the course of the last century, researchers have turned the insect — known to science as Drosophila melanogaster — into a sort of genetic switchboard. Biologists regularly develop new “strains” of flies, in which particular genes are turned on or off. Studying these slight mutants can reveal how those genes function — including in humans, because we share over half of our genes with Drosophila. For instance, researchers discovered what is now called the hippo gene — which helps regulate organ size in both fruit flies and vertebrates — after flies with a defect in it grew up to be unusually large and wrinkly. Further work with the gene has indicated that such defects may contribute to the unchecked cell growth that leads to cancer in people. © 2020 The New York Times Company

Keyword: Genes & Behavior; Development of the Brain
Link ID: 27624 - Posted: 12.15.2020

By Krystnell A. Storr Can you tell the difference between high – and low –thread-count sheets just by touching them? Thank usherin, a protein found in a mysterious structure in your fingertips. Usherin also helps us see and hear, suggesting a deep molecular connection among our most important senses. “The work is surprising,” says Ellen Lumpkin, a neuroscientist at the University of California (UC), Berkeley, who was not involved in the study. The study, she says, points to a single protein being used over and over again in distinct ways to help us monitor the outside world. Scientists already had some hints that usherin is important for our sense of touch. A mutation in the gene that codes for it, USH2A, causes Usher syndrome—a rare, inherited disease that leads to blindness, deafness, and an inability to feel faint vibrations in the fingertips. To further explore usherin’s role in touch, researchers recruited 13 patients with a form of Usher syndrome that specifically affects touch. The team—led by Gary Lewin, a neuroscientist at the Max Delbrück Center for Molecular Medicine—measured how well each person sensed pain, temperature changes, and tiny vibrations at 10 and 125 hertz (Hz), mimicking the sensation of moving a fingertip across a rough surface. The scientists then compared the patients’ results against those of 65 healthy volunteers. People with Usher syndrome did just as well as their counterparts at sensing temperature changes and mild pain, the team found. But they were four times less likely to pick up on the 125-Hz vibrations and 1.5 times less likely to detect the 10-Hz vibrations. © 2020 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 27623 - Posted: 12.12.2020

Sam Wollaston A single-storey building in a lonely rural business park, a few miles from Milton Keynes on a grey autumn day. It looks like a location for a bleak thriller: where a kidnap victim is held, perhaps, or the scene of a final shootout. Inside, though, something kind of cool is happening. In a brightly lit room, four inverted metal cups have been placed on the red carpet, each containing a small glass jar. One of these contains a smell: a “training odour”. Into the room bursts Billy, followed by Jess. Billy is a labrador, and Jess his human trainer. Billy bounces about the place, clearly super excited. He sniffs at everything – furniture, people, the cups – wagging ferociously. When he sniffs at the cup that contains the smell, another trainer, Jayde, indicates success with a clicking noise. Billy is rewarded with his favourite toy, a well-chewed rubber ball, and a chorus of “good boy”. So far, so unremarkable. Dogs have excellent noses, everyone knows that. They are estimated to be at least 10,000 times better than ours. It’s not immediately clear just how good Billy is. Did he really find the smell, or did Jayde just click when he sniffed the right cup? To be fair to Billy, he’s young, 18 months old, and this is only his second session. The trainers – Jess, Jayde and Mark – have high hopes for him. And after a couple more goes, it becomes clear that he is definitely finding the right cup, quickly. He is also clearly enjoying the game. What Billy lacks in refinement, he makes up for in youthful enthusiasm and exuberance, and he learns fast. Which is good news: this is just the first stage for Billy, who is on a fast-track training course to learn to sniff out Covid-19. He’s not working with the actual virus, of course, but a training sample, which will teach him to do that job. © 2020 Guardian News & Media Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27622 - Posted: 12.12.2020

Jon Hamilton Root extracts from the African shrub iboga have long been used in traditional healing rituals and more recently as an experimental treatment for depression and to reduce drug cravings in addiction. Scientists now are working on a version of the extract that doesn't cause heart attacks or hallucinations as side effects. Steeve Jordan/AFP via Getty Images A chemically tweaked version of the psychedelic drug ibogaine appears to relieve depression and addiction symptoms without producing hallucinations or other dangerous side effects. The results of a study in rodents suggest it may be possible to make psychedelic drugs safe enough to become mainstream treatments for psychiatric disorders, the authors report Wednesday in the journal Nature. "What we need is a medicine that is so safe that you can take it home and put it in your medicine cabinet just like you would aspirin," says David Olson, the paper's senior author and an assistant professor at the University of California, Davis. "And that's really what we were trying to achieve." The success with ibogaine is "a promising first step," says Gabriela Manzano, a postdoctoral fellow at Weill Cornell Medicine in New York and a co-author of a commentary on the study. "This provides a road map on how we could start tweaking these chemical compounds to make them very useful in the clinic," she says. "Keep the good parts, get rid of the bad parts." For decades, psychedelic drugs, including ketamine and psilocybin, have shown promise in treating people with mental health problems including addiction, depression and post-traumatic stress disorder. But doctors and researchers have been wary of using the drugs because of their side effects. © 2020 npr

Keyword: Drug Abuse; Depression
Link ID: 27621 - Posted: 12.12.2020

By Jennie Erin Smith MEDELLÍN, Colombia — Aliria Rosa Piedrahita de Villegas carried a rare genetic mutation that had all but guaranteed she would develop Alzheimer’s disease in her 40s. But only at age 72 did she experience the first symptoms of it. Her dementia was not terribly advanced when she died from cancer on Nov. 10, a month shy of her 78th birthday, in her daughter’s home on a hillside that overlooks the city. Neurology investigators at the University of Antioquia in Medellín, led by Dr. Francisco Lopera, have followed members of Ms. Piedrahita de Villegas’s vast extended family for more than 30 years, hoping to unlock the secrets of early-onset Alzheimer’s disease. In that time they encountered several outliers, people whose disease developed later than expected, in their 50s or even 60s. But none were as medically remarkable as the woman they all knew as doña Aliria. In recent years Aliria traveled to Boston, where investigators at Massachusetts General Hospital conducted nuclear imaging studies of her brain as part of an ongoing study of this Colombian family, the largest in the world with genetic early-onset Alzheimer’s. In Boston it was discovered that Aliria had exceptionally large quantities of one protein seen in Alzheimer’s — amyloid beta — without much tau, the toxic protein that spreads later in the disease cascade. Something had interrupted the usual degenerative process, leaving her day-to-day functioning relatively preserved. Last year, researchers at Harvard Medical School and the University of Antioquia published the surprise finding that while Aliria carried a well-known mutation, unique to Colombia, that causes early Alzheimer’s, she also carried two copies of another rare mutation that appear to have thwarted the activity of the first one. Since then, investigators worldwide have been studying what is known as the Christchurch mutation, a variant on a gene, APOE, that can affect a person’s risk of developing Alzheimer’s. Thus far, drugs targeting amyloid beta have disappointed in clinical trials. If the protective effect of Aliria’s double Christchurch mutation can be replicated, a new avenue for desperately needed therapies could open. © 2020 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 27620 - Posted: 12.12.2020

By Jason Castro To be an expectant mother, or the anxious partner of one, is to be keenly, even agonizingly aware of how chemicals affect a developing life. The basic advice is well known, and obsessively followed: Alcohol in strict moderation, and no nicotine at all. Don’t mess with mercury. Folic acid is your friend. More protein and less caffeine. Stay away from BPA, PBCs and PFA, and generally make an enemy of the unpronounceable. But, if we take the results of a provocative recent paper seriously, there may be another important, and deeply underappreciated chemical influence at work: a man’s odor. The research, by a team headed by Noam Sobel of the Weizmann Institute of Science, suggests that there is a relationship between women’s response to “social odors” contained in male sweat and the heartbreaking condition of unexplained repeated pregnancy loss (uRPL). Specifically, in blind smell-tests, these scientists observed that women who had experienced uRPL were significantly better at identifying their spouse’s odor than age-matched controls. Additionally, their brains responded differently to nonspouse odors and they displayed unique olfactory neuroanatomy. Taken in the context of a large body of literature on chemosignaling in nonhuman animals, these results make it conceivable that the human nose could also communicate with the womb and may even influence a pregnancy. So far, the results are strictly correlative, and in no way point to male odor as some kind of pheromonal smoking gun that explains pregnancy loss. Hypothetically, it could also be true that women experiencing uRPL have, on average, larger middle toes, larger whites of their eyes, thinner wrists and a proclivity for wearing purple socks. None of these would give one pause or prompt a serious search for some kind of causal link to pregnancy loss. Yet this particular link between smell and pregnancy loss is intriguing because of how prevalent and robust it is in other mammals, including primates. Many miscarriages still have unexplained causes, which makes any lead, correlative or not, a particularly interesting and worthwhile area of research. © 2020 Scientific American

Keyword: Chemical Senses (Smell & Taste); Sexual Behavior
Link ID: 27619 - Posted: 12.09.2020

David Cox Seven years ago, rhinology surgeon Peter Andrews found himself performing an operation that would go on to change the course of his career. Andrews was operating on a patient who had broken his nose many decades earlier after being struck by a cricket ball. The procedure was delicate: straightening the septum – the thin wall of cartilage that separates the nostrils – and in the process improving his breathing, which had become more laboured in later life. But it had a surprising outcome. As well being able to breathe more freely, Andrews’s patient found he could smell again for the first time in 40 years, a remarkable turn of events that provided the medical community with a new insight into our sense of smell, and its capacity to regenerate. Being able to smell is actually a result of a complex neurological process. Smell-specific nerve cells known as olfactory neurons, located high in the nasal cavity, detect molecules in the air such as those released by a perfume, or smoke particles from something burning. They then convey this information via a long nerve fibre running up through the skull, to a part of the brain that makes sense of it all. This network is one of the most adaptable in the entire central nervous system. To keep functioning, it completely regenerates every six weeks, shedding existing olfactory neurons, and creating new ones from scratch. “That’s quite a feat in itself, because those neurons then have to reconnect up into the brain tissue,” says Andrews. But sometimes things can happen that impair its ability to regenerate. An estimated 5% of the general population is believed to have anosmia, the medical term for temporary or permanent smell loss. Anosmia can occur as part of the ageing process, but also in those of all ages due to factors ranging from broken noses to viral infections. © 2020 Guardian News & Media Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 27618 - Posted: 12.09.2020

By Gretchen Reynolds Can exercise help us shed pounds? An interesting new study involving overweight men and women found that working out can help us lose weight, in part by remodeling appetite hormones. But to benefit, the study suggests, we most likely have to exercise a lot — burning at least 3,000 calories a week. In the study, that meant working out six days a week for up to an hour, or around 300 minutes a week. The relationship between working out and our waistlines is famously snarled. The process seems as if it should straightforward: We exercise, expend calories and, if life and metabolisms were just, develop an energy deficit. At that point, we would start to use stored fat to fuel our bodies’ continuing operations, leaving us leaner. But our bodies are not always cooperative. Primed by evolution to maintain energy stores in case of famine, our bodies tend to undermine our attempts to drop pounds. Start working out and your appetite rises, so you consume more calories, compensating for those lost. The upshot, according to many past studies of exercise and weight loss, is that most people who start a new exercise program without also strictly monitoring what they eat do not lose as much weight as they expect — and some pack on pounds. But Kyle Flack, an assistant professor of nutrition at the University of Kentucky, began to wonder a few years ago if this outcome was inevitable. Maybe, he speculated, there was a ceiling to people’s caloric compensations after exercise, meaning that if they upped their exercise hours, they would compensate for fewer of the lost calories and lose weight. © 2020 The New York Times Company

Keyword: Obesity
Link ID: 27617 - Posted: 12.09.2020

by Laura Dattaro In 1983, psychologist Christopher Gillberg posed a provocative question to the readers of the British Journal of Psychiatry: Could autism and anorexia nervosa share underlying causes? Gillberg’s curiosity came in part from his observations of three autistic boys whose female cousins all had the eating disorder, which is characterized by food restrictions, low body weight, an intense fear of gaining weight and a distorted body image. Gillberg, professor of child and adolescent psychiatry at the University of Gothenburg in Sweden, initially suggested that anorexia is the ‘female form of autism.’ Although that idea wasn’t entirely accurate, his suspicions that eating disorders and autism are linked have borne out: People with anorexia are more likely to be autistic than those without it, studies show. There are fewer data demonstrating that autistic people are at particularly high risk for eating disorders, but experts say it’s likely. How often do anorexia and autism overlap? Estimates vary, though most researchers agree that roughly 20 percent of people with anorexia are autistic. Both conditions are rare — about 1 percent of people are autistic and 0.3 percent have anorexia — and most research so far has examined the prevalence of autism in people with anorexia, not the reverse. Among 60 women receiving treatment for an eating disorder at a clinic in the United Kingdom, for example, 14 of them, or 23 percent, scored above the diagnostic cutoff on a test called the Autism Diagnostic Observation Schedule (ADOS). Similarly, about one-third of people with anorexia have been diagnosed with autism, according to a long-running study that has followed 51 people with anorexia and 51 controls in Sweden since the 1980s. © 2020 Simons Foundation

Keyword: Autism; Anorexia & Bulimia
Link ID: 27616 - Posted: 12.09.2020

Sarah Sloat Patience, you might have heard, is a virtue. That’s why so many Puritans named their daughters “Patience” in the 1600s. It is the ability to wait calmly in the face of frustration or adversity. Like Penelope weaving while waiting for Odysseus, patient people wait for their partners to finish a Netflix show they’re binging. Impatient people do not. But despite the societal framing of patience as a measurement of character, in its purest sense, patience is a chemically induced output of the brain. However, exactly what goes on in the brain that leads to patience isn’t well understood. A new study involving mice takes a step toward understanding patience by pointing to the role of serotonin, and how it interacts with different brain structures. Serotonin is a chemical and a neurotransmitter, meaning it sends messages throughout the brain. It influences many behaviors, including mood and sleep. In a paper recently released in the journal Science Advances, scientists argue that serotonin influences specific areas of the brain to promote patient behavior. But critically, this process only occurs if there’s already “high expectation or confidence” that being patient will lead to future rewards. First author Katsuhiko Miyazaki is a scientist at the Okinawa Institute of Science and Technology in Japan who researches the relationship between serotonergic neural activity and animal behavior. He tells me this study originated from an interest in revealing how projections of serotonin promote waiting for future rewards.

Keyword: Attention; Learning & Memory
Link ID: 27615 - Posted: 12.09.2020

Alison Abbott In October 2013, I attended the launch of the Human Brain Project in Lausanne, Switzerland, as correspondent for Nature. I hoped to leave with a better understanding of the exact mission of the baffling billion-euro enterprise, but I was frustrated. Things became clear the following year, when the project fell spectacularly, and very publicly, apart. Noah Hutton’s documentary In Silico captures a sense of what it was like behind the scenes of the project, which was supported with great fanfare by the European Commission. It had been hyped as a quantum leap in understanding how the human brain works. Instead, it left a trail of angry neuroscientists across Europe. Yet aspects of what went so expensively wrong still remain elusive. In Silico is more about the back story of the Human Brain Project (HBP). Hutton was 22 years old when he watched a 2009 talk by Henry Markram, the controversial figure who later became the first director of the HBP. Markham was speaking about the Blue Brain Project, a major initiative he had launched a few years before at one of Europe’s top universities, the Swiss Federal Institute of Technology in Lausanne, with generous funding from the Swiss government. He claimed that he would — with the help of a supercomputer related to the one that beat world chess champion Garry Kasparov in 1997 — simulate an entire rodent brain within a decade. He planned to build it from information about the brain’s tens of millions of individual neurons. © 2020 Springer Nature Limited

Keyword: Brain imaging
Link ID: 27614 - Posted: 12.09.2020

Carrie Arnold In her job as a physician at the Boston Medical Center in Massachusetts, Sondra Crosby treated some of the first people in her region to get COVID-19. So when she began feeling sick in April, Crosby wasn’t surprised to learn that she, too, had been infected. At first, her symptoms felt like those of a bad cold, but by the next day, she was too sick to get out of bed. She struggled to eat and depended on her husband to bring her sports drinks and fever-reducing medicine. Then she lost track of time completely. For five days, Crosby lay in a confused haze, unable to remember the simplest things, such as how to turn on her phone or what her address was. She began hallucinating, seeing lizards on her walls and smelling a repugnant reptilian odour. Only later did Crosby realize that she had had delirium, the formal medical term for her abrupt, severe disorientation. “I didn’t really start processing it until later when I started to come out of it,” she says. “I didn’t have the presence of mind to think that I was anything more than just sick and dehydrated.” Physicians treating people hospitalized with COVID-19 report that a large number experience delirium, and that the condition disproportionately affects older adults. An April 2020 study in Strasbourg, France, found that 65% of people who were severely ill with coronavirus had acute confusion — a symptom of delirium1. Data presented last month at the annual meeting of the American College of Chest Physicians by scientists at the Vanderbilt University Medical Center in Nashville, Tennessee, showed that 55% of the 2,000 people they tracked who were treated for COVID-19 in intensive-care units (ICUs) around the world had developed delirium. These numbers are much higher than doctors are used to: usually, about one-third of people who are critically ill develop delirium, according to a 2015 meta-analysis2 (see ‘How common is delirium?’). © 2020 Springer Nature Limited

Keyword: Alzheimers
Link ID: 27613 - Posted: 12.07.2020

By Jamie Talan After 20 years of marriage, after raising two kids, after building a farm in Kentucky and tending horses and dogs, Laura Prewitt knew this much about her husband: He was tenderhearted, fun-loving and never let stress land too long on his shoulders. But in 2014, old Ted somehow morphed into a new guy, one who is not so communicative. A guy who lost his social edge and seemed unable to read faces or feelings. Who is tired and withdrawn. “He’s just not the same guy,” she says. “I want him back.” At 59, the old Ted, the sensitive husband who cried during sad movies, is gone. A scan of Ted’s brain helps explain it: Discrete regions of the right temporal lobe that regulate emotion are getting smaller; the tissue is shrinking. Ted can still do some of the things he has done for decades. Until a few years ago, he was the president at a construction company. Lately, he’ll see someone he is supposed to know but forgets who they are. He sleeps a lot. And he can’t be left alone for too long or his wife may find him trying to eat a battery or a hammer. He’s agitated. He’s always putting things in his mouth. Ted Prewitt, who has behavioral variant frontotemporal dementia (bvFTD), is one of a growing number of people in midlife diagnosed with an atypical form of dementia. Unlike Alzheimer’s, which generally occurs in older people, these are rarer dementias — including bvFTD; another frontotemporal variant that leads to language disturbances called primary progressive aphasia; a visual and spatial dementia called posterior cortical atrophy; Lewy body dementia; and early-onset Alzheimer’s in people with no family history. These conditions show up in people in their 50s and 60s, sometimes even earlier and sometimes a bit later. No one knows whether these conditions are becoming more common or doctors are better at diagnosing them. © 1996-2020 The Washington Post

Keyword: Alzheimers
Link ID: 27612 - Posted: 12.07.2020

by Angie Voyles Askham Many people with mutations that disrupt a gene called NCKAP1 have autism or autism traits — along with speech and language problems, motor delays and learning difficulties — according to a new study. The results, from a large international team of researchers and clinicians, clarify how mutations in NCKAP1 affect people and solidify its position as a top autism gene. Sequencing studies over the past decade have turned up three autistic people with de novo, or non-inherited, variants that likely disrupt NCKAP1, putting it on a list of genes strongly tied to autism. Other work has shown that mice that do not express the gene have atypical brain development. But those reports contain little information about the outward characteristics of people with NCKAP1 mutations — which are challenging to study because variants in the gene are rare, says Hui Guo, associate professor of life sciences at Central South University in Changsha, China. In the new work, Guo teamed up with scientists and clinicians across the globe to identify and characterize 18 additional people with NCKAP1 mutations. “This study demonstrates that international cooperation among many institutions is becoming fundamental to advancing our understanding of rare variants,” says Abha Gupta, assistant professor of pediatrics at Yale University, who was not involved in the study. Painting a detailed picture of traits associated with NCKAP1 mutations can also improve a person’s chance of being diagnosed and provide guidance about expected outcomes, she says. Guo asked colleagues who collect genetic data for other research to sift through their records for people with NCKAP1 variants. He also used GeneMatcher, a site that connects researchers to clinicians interested in the same genetic variants. © 2020 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 27611 - Posted: 12.07.2020