Amber Dance A mouse finds itself in a box it’s never seen before. The walls are striped on one side, dotted on the other. The orange-like odor of acetophenone wafts from one end of the box, the spiced smell of carvone from the other. The mouse remembers that the orange smell is associated with something good. Although it may not recall the exact nature of the reward, the mouse heads toward the scent. Except this mouse has never smelled acetophenone in its life. Rather, the animal is responding to a false memory, implanted in its brain by neuroscientists at the Hospital for Sick Children in Toronto. Sheena Josselyn, a coauthor on a 2019 Nature Neuroscience study reporting the results of the project, says the goal was not to confuse the rodent, but for the scientists to confirm their understanding of mouse memory. “If we really understand memory, we should be able to trick the brain into remembering something that never happened at all,” she explains. By simultaneously activating the neurons that sense acetophenone and those associated with reward, the researchers created the “memory” that the orange-y scent heralded good things. Thanks to optogenetics, which uses a pulse of light to activate or deactivate neurons, Josselyn and other scientists are manipulating animal memories in all kinds of ways. Even before the Toronto team implanted false memories into mice, researchers were making rodents forget or recall an event with the flick of a molecular light switch. With every flash of light, they test their hypotheses about how these animals—and by extension, people—collect, store, and access past experiences. Scientists are also examining how memory formation and retrieval change with age, how those processes are altered in animal models of Alzheimer’s disease, and how accessing memories can influence an animal’s emotional state. © 1986–2020 The Scientist.

Keyword: Learning & Memory; Alzheimers
Link ID: 27228 - Posted: 05.02.2020

By Dennis Normile Scientists studying brains and other organs and cancerous tumors have long tried to get detailed 3D views of their insides—down to the level of blood vessel and cell type. But producing such images is time-consuming and difficult. Now, dramatic improvements to a 3D imaging technique can reveal the internal components of entire organs or even animals in a simple procedure, researchers report this week. The new tissue staining protocol allows cellular level analyses in unprecedented detail; it could aid research efforts in neuroscience, developmental and evolutionary biology, and immunology, and it could prove useful in diagnosing some cancers and studying damaged brain tissue after death. To image biological samples in 3D, researchers basically have two main options: They can slice tissues into thin sections and use computer software to reconstruct the whole sample, or they can render biological tissue transparent using special chemicals, which lets researchers view its interior with an optical microscope. To distinguish different cell types, researchers typically stain tissues by soaking them in a cocktail of dyes and chemicals. But getting staining dyes to penetrate organs and large samples has proved difficult. To tackle this problem, researchers at the RIKEN Center for Biosystems Dynamics Research identified a gel that closely mimics the physicochemical properties of organs that have undergone the tissue clearing process. Starting with computer simulations and following up with laboratory tests, the team optimized the soaking solution temperature, dye and antibody concentrations, chemical additives, and electrical properties to produce the best staining and imaging results. They then tested their method with more than two dozen commonly used dyes and antibodies on mouse and marmoset brains. © 2020 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 27227 - Posted: 05.02.2020

Ruth Williams Scientists have created a light-responsive opsin so sensitive that even when engineered into cells deep within tissue it can respond to an external light stimulus, according to a report in Neuron yesterday (April 30). Experiments in mice and macaques showed that shining blue light on the surface of the skull or brain was sufficient to activate opsin-expressing neurons six millimeters deep. “I was pretty blown away that this was even possible,” says Gregory Corder, who studies the neurological basis of pain and addiction at the University of Pennsylvania and who was not involved with the work. At that sort of depth, he continues, “essentially no part of the rodent brain is off-limits now for doing this non-invasive [technique]. . . . It’s pretty impressive.” “This development will help to extend the use of optogenetics in non-human primate models, and bring the techniques closer to clinical application in humans,” adds neurological disease expert Adriana Galvan of Yerkes National Primate Research Center in an email to The Scientist. Galvan was not a member of the research team. Optogenetics is a technique whereby excitable cells, such as neurons, can be controlled at will by light. To do this, cells are genetically engineered to produce ion channels called opsins that sit in the cells’ membranes and open in response to a certain wavelength of light. Switching on the light, then, floods the cells with ions, causing them to fire. Because light doesn’t penetrate tissue easily, to activate opsin-producing neurons deep in the brain of a living animal, researchers insert fiber optic cables. This is “highly invasive,” says Galvan, explaining that “the brain tissue can be damaged.” © 1986–2020 The Scientist.

Keyword: Brain imaging
Link ID: 27226 - Posted: 05.02.2020

Diana Kwon As rodents scuttle through a maze, scientists can observe the activity of their brains’ “inner GPS,” neurons that manage spatial orientation and navigation. This positioning system was revealed through two different discoveries, decades apart. In 1971, neuroscientist John O’Keefe found place cells, neurons that are consistently activated when rats are in a specific location, while observing the animals as they ran around an enclosure. More than thirty years later, neuroscientists May-Britt and Edvard Moser used a similar method to identify grid cells, neurons that fire at regular intervals as animals move, enabling them to keep track of navigational cues. It was the early 2010s when neuroscientist Elizabeth Buffalo and her team at Emory University’s Yerkes National Primate Research Center in Atlanta started investigating what the brain’s GPS looks like in primates. While conducting memory tests by tracking the eye movements of primates viewing either familiar or unfamiliar images, the researchers began to wonder: Was this system also active in stationary animals? “They were moving their eyes as they were forming a memory of these pictures,” Buffalo says. “So we thought that maybe this eye movement exploration was something that primates do in an analogous way to how rodents explore as they move around a physical environment.” One of Buffalo’s graduate students, Nathaniel Killian, put this hypothesis to the test. Working with monkeys, he placed electrodes into the entorhinal cortex—the brain region where grid cells are found in rodents—and recoded brain activity while the animals viewed images on a screen. One day, Killian came into a lab meeting with an announcement: he had found grid cells in the primate brain. Although it took many more months to complete additional experiments to validate the results, Buffalo remembers thinking during that meeting, “Wow, we’re seeing something really new.” © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27225 - Posted: 05.02.2020

By Lisa Sanders, M.D. “Honey” — the woman could hear fear tightening her husband’s voice as he called out to her — “I think your mother just died.” She ran into the living room. Her 78-year-old mother sat rigid in a chair, her skin gray and lifeless. Her eyes were open but all white, as if she were trying to see the back of her own skull. Then her arms started to make little jerking movements; her lips parted as saliva seeped out the corner of her mouth onto her chin. Then her body slumped. She seemed awake but confused after this seizure-like episode. Should I call an ambulance? the husband asked. No, his wife responded. Her mother had a complicated medical history, including a kidney transplant 12 years before and an autoimmune disease. An ambulance would want to take her to the nearby Hartford Hospital. But her doctors were at Yale New Haven Hospital — some 30 miles from their home in Cromwell, Conn. They helped the woman into the car. It was only a half-hour drive to the hospital that March 10 evening, but it seemed to last forever. Would her mother make it? Her eyes were closed, and she looked very pale. Her other daughter worked at the hospital and was waiting with a wheelchair when they arrived. The daughters made sure that the doctors and nurses knew that their mother took two medications to keep her immune system from killing her transplanted kidney. Because of those immune-suppressing drugs, she’d had many infections over the years. Six months earlier, she nearly lost her kidney to a particularly aggressive bacterium. She’d been well since then, until a few days earlier when she came down with a cold. It was just a sore throat and a runny nose, but the couple were worried enough to move her into their home to keep an eye on her. She didn’t want to eat because of the pain in her throat, but otherwise she seemed to be doing well. © 2020 The New York Times Company

Keyword: Epilepsy
Link ID: 27224 - Posted: 04.30.2020

By Emily Willingham Professional burnout is all too familiar: Go at something too hard for too long, and the motivational tank empties. But burnout for an autistic person isn’t always about overwork, Dora Raymaker, an autistic systems scientist at Portland State University (PSU), found in a study of autistic workers. Instead, the need to mask autistic behaviors through a workday with nonautistic people can cause chronic exhaustion, reduced ability to tolerate stimuli like light or sound, and loss of skills, the study showed through interviews and a survey of social media comments. The work, which Raymaker’s team published last month, highlights a new trend in autism research. Raymaker and colleagues are part of a small but growing number of research teams with autistic members. These groups are shifting the focus in autism research from cause and cure to practical steps, including ones that help autistic people in settings such as the workplace. And they’re publishing some of their findings in a new journal, Autism in Adulthood, which is dedicated to including the perspectives of autistic people in what it publishes. Interest in those perspectives is “skyrocketing,” says Christina Nicolaidis, a co-author on the burnout study. Nicolaidis, a professor in the School of Social Work at PSU, has an adult son who is autistic. Although much research on autism has focused on children, autistic adults who came of age in the 1990s and early 2000s are joining the field and bringing a focus on their own experience. One member of that cohort is TC Waisman, a doctoral candidate at the University of Calgary studying how faculty and staff can improve autistic students’ college experiences. Waisman says she sees researchers increasingly “respecting us as our own self-determined culture and foregrounding our needs in studies.” © 2020 American Association for the Advancement of Science

Keyword: Autism
Link ID: 27223 - Posted: 04.30.2020

By Tanya Lewis In March 2019 biotechnology giant Biogen stopped two big trials of its experimental Alzheimer's disease drug aducanumab because it did not appear to improve memory in declining patients. Then, in a surprise reversal several months later, the company and its partner, Japanese drugmaker Eisai, said they would ask the U.S. Food and Drug Administration to approve the treatment. A new analysis, Biogen said, showed that a subset of people on the highest doses in one trial did benefit from the compound, which dissolves clumps of a protein called beta-amyloid within the brain. The back-and-forth decisions, along with the failure of a slew of other amyloid-clearing compounds, have left experts divided about whether treating amyloid buildup—long thought to be the best target for an Alzheimer's therapy—is still a promising approach. Some of the scientists rethinking the so-called amyloid hypothesis helped to generate it in the first place. “I would say it has legs, but it's limping,” says geneticist John Hardy, who co-authored the genetic studies that pioneered the idea more than two decades ago. According to Hardy, who runs a molecular neuroscience program at University College London's Institute of Neurology, “the [concept] we drew in 1998 is cartoonishly oversimplistic. There were lots of question marks. We thought those questions would be filled in within a couple of years. And yet 20 years later they are not filled in.” Other experts, though, still contend that the amyloid hypothesis is a strong explanation and that treatments targeting the protein are the right way to go. © 2020 Scientific American

Keyword: Alzheimers
Link ID: 27222 - Posted: 04.30.2020

By Jennifer Couzin-Frankel Science's COVID-19 reporting is supported by the Pulitzer Center. Among the many surprises of the new coronavirus is one that seems to defy basic biology: infected patients with extraordinarily low blood-oxygen levels, or hypoxia, scrolling on their phones, chatting with doctors, and generally describing themselves as comfortable. Clinicians call them happy hypoxics. “There is a mismatch [between] what we see on the monitor and what the patient looks like in front of us,” says Reuben Strayer, an emergency physician at Maimonides Medical Center in New York City. Speaking from home while recovering from COVID-19 himself, Strayer says he was first struck by the phenomenon in March as patients streamed into his emergency room. He and other doctors are keen to understand this hypoxia, and when and how to treat it. A normal blood-oxygen saturation is at least 95%. In most lung diseases, such as pneumonia, falling saturations accompany other changes, including stiff or fluid-filled lungs, or rising levels of carbon dioxide because the lungs can’t expel it efficiently. It’s these features that leave us feeling short of breath—not, counterintuitively, low oxygen saturation itself, says Paul Davenport, a respiratory physiologist at the University of Florida. “The brain is tuned to monitoring the carbon dioxide with various sensors,” Davenport explains. “We don’t sense our oxygen levels.” In serious cases of COVID-19, patients struggle to breathe with damaged lungs, but early in the disease, low saturation isn’t always coupled with obvious respiratory difficulties. Carbon dioxide levels can be normal and breathing deeply is comfortable—“the lung is inflating so they feel OK,” says Elnara Marcia Negri, a pulmonologist at Hospital Sírio-Libanês in São Paulo. But oxygen saturation, measured by a device clipped to a finger and in many cases confirmed with blood tests, can be in the 70s, 60s, or 50s. Or even lower. Although mountain climbers can have similar readings, here the slide downward, some doctors believe, is potentially “ominous,” says Nicholas Caputo, an emergency physician at New York City Health + Hospitals/Lincoln. © 2020 American Association for the Advancement of Science.

Keyword: Emotions
Link ID: 27221 - Posted: 04.29.2020

By Asher Elbein Rufous treepies, birds in the crow family native to South and Southeast Asia, usually eat insects, seeds or fruits. But some of them have learned to eat fire. Well, not exactly, but close. At a small temple in the Indian state of Gujarat, the caretakers regularly set out small votive candles made with clarified butter. The birds flit down to steal the candles, extinguish the butter-soaked wicks with a quick shake of their heads and then gulp them down. This willingness to experiment with new foods and ways of foraging is an indicator of behavioral flexibility, and some scientists think it is evidence that certain species of birds might be less vulnerable to extinction. “The idea is that if a species has individuals that are capable of these novel behaviors, they’ll respond with changes in their behavior more easily than individuals from species that do not tend to produce novel behaviors like that,” said Louis Lefebvre, a professor at McGill University in Montreal and an author on the study. “The idea is pretty simple. The problem was to be able to test it in a convincing way.” A team of researchers, led by Simon Ducatez of Spain’s Center for Research on Ecology and Forestry Applications and including Dr. Lefebvre, combed through 204 ornithological journals for mentions of novel behaviors and feeding innovations, comparing the number of sightings in each species with their risk of extinction. Their results were published this month in Nature Ecology & Evolution. Dr. Lefebvre said the approach provided backup to earlier cognition experiments he had led with wild-caught birds, such as testing their ability to figure out how to open boxes full of food. © 2020 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 27220 - Posted: 04.29.2020

African Americans with severe sleep apnea and other adverse sleep patterns are much more likely to have high blood glucose levels — a risk factor for diabetes — than those without these patterns, according to a new study funded in part by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health. The findings suggest that better sleep habits may lead to better blood glucose control and prove beneficial for type 2 diabetes prevention and diabetes management in African Americans, who are at higher risk for type 2 diabetes than other groups. They also point to the importance of screening for sleep apnea to help fight the potential for uncontrolled blood sugar in this high-risk group, the researchers said. Previous studies have linked disturbed sleep patterns, including sleep apnea, to increased blood glucose levels in white and Asian populations. But this new study is one of the few to use objective measurements to link these disturbed sleep patterns to increased blood glucose levels in black men and women, the researchers said. Their findings appear online on April 28 in the Journal of the American Heart Association. “The study underscores the importance of developing interventions to promote regular sleep schedules, particularly in those with diabetes,” said Yuichiro Yano, M.D., Ph.D., the lead study author and a researcher in the Department of Family Medicine and Community Health at Duke University. “It also reaffirms the need to improve the screening and diagnosis of sleep apnea, both in African Americans and other groups.”

Keyword: Sleep
Link ID: 27219 - Posted: 04.29.2020

By Neil Genzlinger Mel Baggs, whose forthright writings and films about being a nonverbal person with autism made an impact in the fields of neurodiversity and disability rights, died on April 11 in Burlington, Vt., at age 39. Anna Baggs, Mx. Baggs’s mother, said the cause was believed to be respiratory failure, though numerous health problems may also have played a part. Mx. Baggs, a vigorous blogger, used the term “genderless” as a self-description. “I like that it just means lack of gender, and has no spoken or unspoken secondary meaning,” read a 2018 entry on the blog “Cussin’ and Discussin’: Mel being human in a world that says I’m not.” Many friends and admirers posting about Mx. Baggs’s death on social media used gender-neutral pronouns, while others used the traditional feminine ones. Gender issues, though, were not Mx. Baggs’s major concern. Of more urgency was conveying that people who think and communicate in nontraditional ways are fully human, and that humanness is a spectrum, not something that can be reduced to a normal/abnormal dichotomy. Many people were introduced to these ideas through Mx. Baggs’s short film “In My Language,” posted on the internet in 2007 and given wide exposure through coverage on CNN. For three minutes it shows Mx. Baggs fiddling with the knob on a dresser drawer, rubbing against a book and more. Then it offers “a translation,” as the film puts it. “The previous part of this video was in my native language,” a synthesized voice says. “Many people have assumed that when I talk about this being my language, that means that each part of the video must have a particular symbolic message within it designed for the human mind to interpret. But my language is not about designing words or even visual symbols for people to interpret. It is about being in a constant conversation with every aspect of my environment.” By the time “In My Language” was posted, Mx. Baggs had already drawn considerable attention in the autism world for creating the website “Getting the Truth Out,” a response to an awareness campaign by the Autism Society of America called “Getting the Word Out,” which Mx. Baggs thought made autistic people objects of pity. Part of that attention was skepticism about Mx. Baggs’s claims. Autism online forums can be caustic, with sharp divisions among various factions, and the harshest detractors have accused Mx. Baggs of being a fake. © 2020 The New York Times Company

Keyword: Autism
Link ID: 27218 - Posted: 04.29.2020

Kerry Grens Several hospitals in the US have observed strokes in a number of patients being treating for coronavirus, leading to concern that the infection may be causing devastating blockages in the brain. For at least two facilities, these events account for a spike in stroke cases among middle-aged patients. “Our report shows a seven-fold increase in incidence of sudden stroke in young patients during the past two weeks,” Thomas Oxley, a neurosurgeon at Mount Sinai Health System in New York who describes five of his patients in an upcoming paper in the New England Journal of Medicine, tells CNN. “Most of these patients have no past medical history and were at home with either mild symptoms (or in two cases, no symptoms) of Covid.” Although the numbers of stroke incidents among coronavirus patients remains low, The Washington Post notes that three medical centers in the US will be publishing reports on dozens of COVID-19 patients who experienced strokes. And these appear to be the most serious kind of stroke, called a large vessel occlusion, which might account for the surge in the number of people who have died at home during the pandemic, but this cannot be confirmed. Thomas Jefferson University Hospitals and NYU Langone Health found that 40 percent of the 12 people treated for large vessel blockage who also tested positive for SARS-CoV-2 were under age 50, according to the Post. “We are used to thinking of 60 as a young patient when it comes to large vessel occlusions,” Eytan Raz of NYU Langone tells the newspaper. “We have never seen so many in their 50s, 40s and late 30s.” © 1986–2020 The Scientist.

Keyword: Stroke
Link ID: 27217 - Posted: 04.29.2020

Sandra G. Boodman First she toppled off a ladder. Then Carol Hardy-Fanta tripped on a step outside her western Massachusetts home while gazing at her cellphone. Next she fell three times during a five-mile hike after catching her left foot on a rock or tree root. At first, Hardy-Fanta thought her repeated stumbles had a simple cause: She was distracted. But when she racked up more than 30 falls in a three-year period — some for no apparent reason — she repeatedly asked her doctors whether an undiagnosed medical problem might be causing her to “drop like a log.” The 10 doctors she consulted between 2016 and 2019 — four orthopedists, three neurologists, a rheumatologist, a podiatrist and her internist — reached disparate conclusions. One suggested she was clumsy. Others suspected her problem was primarily orthopedic or could find no clear explanation. It wasn't until September 2019 that a scan revealed what Hardy-Fanta had come to suspect — a diagnosis she said several of her doctors had brushed off. “These are the smartest people,” said Hardy-Fanta, now 71, whose husband is a Boston physician. “They really wanted to help” but appeared to be misled by her symptoms. “If someone’s falling that much, they should really pay attention.” The falls started in 2016, shortly after Hardy-Fanta and her husband sold their house in a Boston suburb and began splitting their time between a condo in the city and what she described as their “dream home” in the Berkshires. Hardy-Fanta had retired as director of a university think tank. Her fourth book on women and politics had just been published. She was in excellent health, which she regarded as a legacy from her mother, who remained mentally sharp and physically able until shortly before her death at age 100. Hardy-Fanta said she was looking forward to traveling with her husband and taking long bike rides along the scenic rural roads that snake through the Berkshires.

Keyword: Parkinsons
Link ID: 27216 - Posted: 04.27.2020

by Peter Hess The mood-stabilizing drug lithium eases repetitive behaviors seen in mice missing SHANK3, an autism gene, according to a new study1. The findings suggest lithium merits further study as a treatment for some people with autism, even though the drug has troublesome side effects, including tremors and impaired memory. “Lithium is, of course, a rather difficult, non-ideal treatment,” says lead investigator Gina Turrigiano, professor of vision science at Brandeis University in Waltham, Massachusetts. “It’s really hard to get people on a lithium regimen that they can tolerate well.” But understanding why lithium works may set the stage for better treatments, she says. About 1 percent of people with autism have mutations in SHANK3. Deletion or mutation of the gene can also lead to Phelan-McDermid syndrome, which is characterized by intellectual disability, delayed speech and, often, autism. Case studies of people with Phelan-McDermid syndrome also suggest that lithium eases behavior problems associated with the condition2. Previous work has shown that SHANK3 helps stabilize neuronal circuits by adjusting excitatory and inhibitory signaling like a thermostat. This process, called homeostatic plasticity, allows neurons to respond to changes in sensory input. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27215 - Posted: 04.27.2020

By Sam Roberts Donald Kennedy, a neurobiologist who headed the Food and Drug Administration before becoming president of Stanford University, where he oversaw major expansions of its campus and curriculum and weathered a crisis over research spending, died on April 21 in Redwood City, Calif. He was 88. His death, at a residential care facility, was caused by complications of the new coronavirus, his wife, Robin Kennedy, said. He had suffered a severe stroke in 2015. Stanford had been Dr. Kennedy’s life since 1960, when, not yet 30, he joined its faculty as an assistant professor of biology. And except for a stint in the late 1970s as head of the F.D.A. under President Jimmy Carter, he remained wedded to the university, becoming provost and then president in 1980, beginning an 11-year tenure. It was a productive one. During his presidency the university opened the Stanford Humanities Center and campuses in Oxford, England; Kyoto, Japan; and Washington; diversified the Western culture curriculum; and raised $1.2 billion in a five-year centennial campaign, although by the end of the decade the university was facing deficits. His tenure also coincided with fiery debates over antiwar protests and academic freedom by both professors and students, divestiture of the university’s holdings in companys doing business in South Africa, and $160 million in damage inflicted by the Loma Prieta Earthquake in 1989. A would-be writer who had become a neurobiologist in college adventitiously, Dr. Kennedy found his leadership under the microscope in the early 1990s, when the university was accused — and later cleared — of improperly billing the Navy for research expenses. The accusations were aired by federal auditors and Representative John D. Dingell Jr., a tenacious Michigan Democrat, who said that Stanford may have billed the government for as much as $200 million in improper expenses on research contracts for over a decade. © 2020 The New York Times Company

Keyword: Miscellaneous
Link ID: 27214 - Posted: 04.27.2020

By E. Ray Dorsey, Todd Sherer, Michael S. Okun, Bastiaan R. Bloem The number of people with Parkinson’s disease more than doubled from 1990 to 2015 and could double again by 2040. An aging population alone does not account for this rise. Air pollution, metal production, certain industrial chemicals, and some synthetic pesticides are linked to Parkinson’s. Yet we are doing little to manage known risk factors. Neither our increased awareness of the disease nor our lengthening life spans can fully account for the upsurge in diagnoses that we now face. Our knowledge of another neurological disorder, multiple sclerosis, has increased too, and we have improved diagnostic tools for it. Rates for multiple sclerosis have indeed gone up, but that increase is nothing like the exponential rise of Parkinson’s (see figure below). As for aging, more people are, of course, living longer. For example, from 1900 to 2014, the number of individuals over age 65 in the United Kingdom increased about sixfold. However, over that same period, the number of deaths due to Parkinson’s disease increased almost three times faster. Parkinson’s disease is characterized by tremors, slowness in movement, stiffness, and difficulties with balance and walking. It can also cause a wide range of symptoms that are not visible—loss of smell, constipation, sleep disorders, and depression. Most people with Parkinson’s are diagnosed in their fifties or later. But it is not just a disease of the elderly. Up to 10 percent of those with the condition develop the disease in their forties or younger. © 2020 Sigma Xi, The Scientific Research Honor Society

Keyword: Parkinsons; Neurotoxins
Link ID: 27213 - Posted: 04.24.2020

by Lauren Schenkman Mice with mutations in a gene called DLG2 are anxious and asocial; they also sleep poorly and overgroom themselves, according to a new study1. These characteristics resemble those seen in some people with autism. The results offer the first evidence that mutations in DLG2 may account for some of the condition’s behavioral traits. “This study is a baby step indicating DLG2’s implication in [autism’s] core behavioral symptoms,” says lead investigator Soo Young Kim, assistant professor of pharmacy at Yeungnam University in Gyeongsan, South Korea. A 2013 study reported that mice and people with DLG2 mutations have differences in learning, attention and other cognitive processes2. Last year, a study of nearly 500 families with two or more autistic children identified DLG2 as a candidate gene for autism3. The new work offers “a more full picture” of DLG2’s effect on behavior, says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland. Grant led the 2013 work but was not involved in the new study. “It’s a useful contribution.” Kim and her colleagues bred male mice that have two mutant copies of DLG2. The animals lack the corresponding protein, which forms part of a neuron’s scaffolding. DLG4, another gene implicated in autism, has a similar role. © 2020 Simons Foundation

Keyword: Autism; Schizophrenia
Link ID: 27212 - Posted: 04.24.2020

By Ann Gibbons If you think you got your freckles, red hair, or even narcolepsy from a Neanderthal in your family tree, think again. People around the world do carry traces of Neanderthals in their genomes. But a study of tens of thousands of Icelanders finds their Neanderthal legacy had little or no impact on most of their physical traits or disease risk. Paleogeneticists realized about 10 years ago that most Europeans and Asians inherited 1% to 2% of their genomes from Neanderthals. And Melanesians and Australian Aboriginals get another 3% to 6% of their DNA from Denisovans, Neanderthal cousins who ranged across Asia 50,000 to 200,000 years ago or so. A steady stream of studies suggested gene variants from these archaic peoples might raise the risk of depression, blood clotting, diabetes, and other disorders in living people. The archaic DNA may also be altering the shape of our skulls; boosting our immune systems; and influencing our eye color, hair color, and sensitivity to the Sun, according to scans of genomic and health data in biobanks and medical databases. But the new study, which looked for archaic DNA in living Icelanders, challenges many of those claims. Researchers from Aarhus University in Denmark scanned the full genomes of 27,566 Icelanders in a database at deCODE Genetics in Iceland, seeking unusual archaic gene variants. The researchers ended up with a large catalog of 56,000 to 112,000 potentially archaic variants—and a few surprises. They found, for example, that Icelanders had inherited 3.3% of their archaic DNA from Denisovans and 12.2% from unknown sources. (84.5% came from close relatives of the reference Neanderthals.) © 2020 American Association for the Advancement of Science.

Keyword: Evolution; Genes & Behavior
Link ID: 27211 - Posted: 04.24.2020

Christie Wilcox Sex might be biology’s most difficult enigma. The downsides of relying on sex to reproduce are undeniable: It takes two individuals, each of whom gets to pass on only part of their genome. Because these individuals generally have to get fairly intimate, they make themselves vulnerable to physical harm or infections from their partner. Asexual reproduction, or self-cloning, has none of these disadvantages. Clones can be made anywhere and anytime, and they receive the full complement of an individual’s genes. Yet despite all its benefits, asexual reproduction is the exception, not the norm, among organisms that have compartmentalized cells (eukaryotes). In plants, for example — which are somewhat known for their genetic flexibility — less than 1% of species are thought to reproduce asexually often. Among animals, only one out of every thousand known species is exclusively asexual. For centuries, biologists have pondered this apparent paradox. In 1932, the geneticist Hermann Muller, whose work on radiation-induced mutations would eventually garner a Nobel Prize, believed he had the answer. “Genetics has finally solved the age-old problem of the reason for the existence (i.e., the function) of sexuality and sex,” he boasted in The American Naturalist. He went on to explain, “Sexuality, through recombination, is a means for making the fullest use of the possibilities of gene mutations.” All Rights Reserved © 2020

Keyword: Sexual Behavior; Evolution
Link ID: 27210 - Posted: 04.24.2020

By Benjamin Powers On the 10th floor of a nondescript building at Columbia University, test subjects with electrodes attached to their heads watch a driver’s view of a car going down a street through a virtual reality headset. All the while, images of pianos and sailboats pop up to the left and right of each test subject’s field of vision, drawing their attention. The experiment, headed by Paul Sajda, a biomedical engineer and the director of Columbia’s Laboratory for Intelligent Imaging and Neural Computing, monitors the subjects’ brain activity through electroencephalography technology (EEG), while the VR headset tracks their eye movement to see where they’re looking — a setup in which a computer interacts directly with brain waves, called a brain computer interface (BCI). In the Columbia experiment, the goal is to use the information from the brain to train artificial intelligence in self-driving cars, so they can monitor when, or if, drivers are paying attention. BCIs are popping up in a range of fields, from soldiers piloting a swarm of drones at the Defense Advanced Research Projects Agency (DARPA) to a Chinese school monitoring students’ attention. The devices are also used in medicine, including versions that let people who have been paralyzed operate a tablet with their mind or that give epileptic patients advance warning of a seizure. And in July 2019, Elon Musk, the CEO and founder of Tesla and other technology companies, showed off the work of his venture Neuralink, which could implant BCIs in people’s brains to achieve “a symbiosis with artificial intelligence.”

Keyword: Robotics; Brain imaging
Link ID: 27209 - Posted: 04.22.2020