Alison Abbott Researchers studying the biological basis of mental illness have conducted the first genomic analysis of schizophrenia in an African population, and have identified multiple rare mutations that occur more frequently in people with the condition. The mutations are mainly in genes that are important for brain development and the brain’s synapses, tiny structures that coordinate communication between neurons. The genes match those identified in other similar studies of schizophrenia — but nearly all previous research has been conducted in European or Asian populations. The latest work was published1 in Science on 31 January. This research is particularly important because Africa has represented a big gap in the populations that geneticists have studied, says psychiatric geneticist Andreas Meyer-Lindenberg, director of the Central Institute of Mental Health in Mannheim, Germany. He says that the work lends support to current hypotheses about the biological origins of schizophrenia, which can cause a range of symptoms including hallucinations, delusions and disordered thinking. Researchers think that each mutation might contribute a small amount to the overall risk of developing the condition, and that disruption to synapses could be crucial to the disease’s development. Over the past decade, as studies that use genome sequencing to identify the genetic basis of diseases have flourished, geneticists have come under increasing fire for failing to sample diverse populations, largely neglecting African people. Around 80% of participants in genetic studies are of European descent, and less than 3% are of African descent. © 2020 Springer Nature Limited

Keyword: Schizophrenia; Genes & Behavior
Link ID: 27016 - Posted: 02.04.2020

By Nicholas Bakalar Flavonols, a large class of compounds found in most fruits and vegetables, may be associated with a reduced risk for Alzheimer’s disease. Flavonols are known to have antioxidant and anti-inflammatory effects, and animal studies have suggested they may improve memory and learning. A study in Neurology involved 921 men and women, average age 81 and free of dementia, who reported their diet using well-validated food questionnaires. During an average follow-up of six years, 220 developed Alzheimer’s disease. People with the highest levels of flavonol intake tended to have higher levels of education and were more physically active. But after controlling for these factors plus age, sex, the Apo E4 gene (which increases the risk for dementia) and late-life cognitive activity, the scientists found that compared with those in the lowest one-fifth for flavonol intake, those in the highest one-fifth had a 48 percent reduced risk for Alzheimer’s disease. The study covered four types of flavonols: kaempferol, quercetin, isorhamnetin and myricetin. All except quercetin showed a strong association with Alzheimer’s risk reduction. These flavonols are available as supplements, but the lead author, Dr. Thomas M. Holland, a professor of medicine at Rush Medical College in Chicago, said that foods are a better source. “You get a broader intake of vitamins, minerals and bioactives in food than in the supplements,” he said. © 2020 The New York Times Company

Keyword: Alzheimers
Link ID: 27015 - Posted: 02.04.2020

Joanna McKittrick, Jae-Young Jung Slamming a beak against the trunk of a tree would seem like an activity that would cause headaches, jaw aches and serious neck and brain injuries. Yet woodpeckers can do this 20 times per second and suffer no ill effects. Woodpeckers are found in forested areas worldwide, except in Australia. These birds have the unusual ability to use their beaks to hammer into the trunks of trees to make holes to extract insects and sap. Even more impressive they do this without hurting themselves. We are materials scientists who study biological substances like bones, skins, feathers and shells found in nature. We are interested in the skull and tongue bone structure of woodpeckers, because we think their unusual anatomy could yield insights that could help researchers develop better protective head gear for humans. Concussions in people Woodpeckers endure many high impact shocks to their heads as they peck. They have strong tail feathers and claws that help them keep their balance as their head moves toward the tree trunk at 7 meters – 23 feet – per second. Then, when their beak strikes, their heads slow down at about 1,200 times the force of gravity (g). All of this occurs without the woodpecker sustaining concussions or brain damage. A concussion is a form of traumatic brain injury caused by repeated blows to the head. It is a common occurrence and happens frequently during contact sports like football or hockey. Repeated traumatic brain injury eventually causes a progressive brain disorder, chronic traumatic encephalopathy (CTE), which is irreversible and results in symptoms such as memory loss, depression, impulsivity, aggressiveness and suicidal behavior. The National Football League says concussions in football players occur at 80 g. So how do woodpeckers survive repeated 1,200 g impacts without harming their brain? © 2010–2020, The Conversation US, Inc.

Keyword: Brain Injury/Concussion; Evolution
Link ID: 27014 - Posted: 02.01.2020

Timothy Bella The headaches had become so splitting for Gerardo Moctezuma that the pain caused him to vomit violently. The drowsiness that came with it had intensified for months. But it wasn’t until Moctezuma, 40, fainted without explanation at a soccer match in Central Texas last year that he decided to figure out what was going on. When Jordan Amadio looked down at his MRI results, the neurosurgeon recognized — but almost couldn’t believe — what looked to be lodged in Moctezuma’s brain. As he opened up Moctezuma’s skull during an emergency surgery in May 2019, he was able to confirm what it was that had uncomfortably set up shop next to the man’s brain stem: a tapeworm measuring about an inch-and-a-half. “It’s very intense, very strong, because it made me sweat too, sweat from the pain,” Moctezuma said to KXAN. The clear and white parasite came from tapeworm larva that Amadio believes Moctezuma, who moved from Mexico to the U.S. 14 years before his diagnosis, might have had in his brain for more than a decade undetected. His neurological symptoms had intensified due to his neurocysticercosis, which was the direct result of the tapeworm living in his brain. The cyst would trigger hydrocephalus, an accumulation of cerebrospinal fluid that increased pressure to the skull to the point that the blockage and pain had become life-threatening. “It’s a remarkable case where a patient came in and, if he had not been treated urgently, he would have died from tremendous pressure in the brain,” Amadio, attending neurosurgeon at the Ascension Seton Brain and Spine Institute in Austin, told The Washington Post on Thursday night.

Keyword: Development of the Brain
Link ID: 27013 - Posted: 02.01.2020

By Elizabeth Pennisi It’s been a bad couple of weeks for behavioral ecologist Jonathan Pruitt—the holder of one of the prestigious Canada 150 Research Chairs—and it may get a lot worse. What began with questions about data in one of Pruitt’s papers has flared into a social media–fueled scandal in the small field of animal personality research, with dozens of papers on spiders and other invertebrates being scrutinized by scores of students, postdocs, and other co-authors for problematic data. Already, two papers co-authored by Pruitt, now at McMaster University, have been retracted for data anomalies; Biology Letters is expected to expunge a third within days. And the more Pruitt’s co-authors look, the more potential data problems they find. All papers using data collected or curated by Pruitt, a highly productive researcher who specialized in social spiders, are coming under scrutiny and those in his field predict there will be many retractions. The furor has even earned a Twitter hashtag—#PruittData. Yet even one of the researchers who initially probed Pruitt’s data cautions that what has happened remains unclear. “There is no hard evidence that [Pruitt’s] data are fabricated,” says behavioral ecologists Niels Dingemanse of Ludwig Maximilian University of Munich (LMU). © 2019 American Association for the Advancement of Science.

Keyword: Emotions; Evolution
Link ID: 27012 - Posted: 02.01.2020

Madeline Andrews, Aparna Bhaduri, Arnold Kriegstein What was going on with our brain organoids? As neuroscientists, we use these three-dimensional clusters of cells grown in petri dishes to learn more about how the human brain works. Researchers culture various kinds of organoids from stem cells – cells that have the potential to become one of many different cell types found throughout the body. We use chemical signals to direct stem cells to produce brain-like cells that together resemble certain structural aspects of a real brain. While they are not “brains in a dish” – organoids cannot function or think independently – the idea is that organoid models let scientists see developmental processes that may yield insights into how the human brain works. If researchers better understand normal development, we may be able to understand when and how things go wrong in diseases. When we recently compared our lab’s organoid cells to normal brain cells, we were surprised to find that they didn’t look as similar as we’d expected. Our brain organoids, each the size of a few millimeters, were stressed out. Our investigation into why has important implications for this popular new method since many labs are using it to study brain function and neurological disease. Without accurate models of the brain, scientists will not be able to work toward disease treatments. Our lab is particularly interested in the human cerebral cortex – the brain’s bumpy exterior – because it is so different in human beings than it is in any other species. The human cortex is proportionally bigger than in our closest living relatives, the great apes, containing more and different types of cells. It’s the source of many unique human abilities, including our cognitive capacity. © 2010–2020, The Conversation US, Inc.

Keyword: Development of the Brain
Link ID: 27011 - Posted: 01.31.2020

By Leah Shaffer Football’s concussion crisis has been part of the NFL for almost two decades. But the pros aren’t the only ones reevaluating their relationship with the game. Now, studies are finding that parents of younger children are increasingly concerned about the long-term impacts of playing football. A national survey from 2015 found that 25 percent of parents do not let their kids play contact sports due to fear of concussions, while an Aspen Institute report recently found that participation in tackle football declined by 12 percent among children ages 6 to 12 between 2016 and 2017. The research into the risks of youth football is still coming into shape, and there’s disagreement about just how universal and severe the risks are. Some researchers think football is dangerous for everybody; others are finding evidence that some kids might be more predisposed to health consequences than others. In the last two years, some researchers have shown that head hits in youth sports increase the risk of developing chronic traumatic encephalopathy, or CTE, an untreatable degenerative brain disease with symptoms ranging from memory loss to progressive dementia. Other studies have shown that the longer a person plays football, the higher the risk they have for developing symptoms associated with CTE. So, case closed, right? No — football is not the only risk factor in developing symptoms of CTE. The same study that found an association between repetitive head impact and dementia in CTE also found that cardiovascular disease and dementia in CTE were correlated. And a separate study of some 10,000 people found no association between participation in contact sports and later cognitive decline or increase in symptoms of depression. © 2020 ABC News Internet Ventures

Keyword: Brain Injury/Concussion; Development of the Brain
Link ID: 27010 - Posted: 01.31.2020

By Neuroskeptic A new neuroscience paper bears the remarkable title of Life without a brain. Although the title is somewhat misleading, this is still a rather interesting report about a unique rat who functioned extremely well despite having a highly abnormal brain. This case sheds new light on a number of famous examples of humans born with similar abnormalities. According to the authors of the new paper, Ferris et al., the rat in question was called R222 and it was discovered unexpectedly during testing as part of a batch of rats taking part in an experiment. R222 didn't actually have no brain, but it had a highly abnormal brain anatomy. Its brain was actually twice the size of a normal rat's, but much of it consisted of empty, fluid-filled space. The cerebral cortex was limited to a thin sheet surrounding the fluid spaces, although the total cortical volume was - surprisingly given the images shown above - only slightly less than normal - 575 μL vs. the normal ~615 μL. Despite the grossly abnormal appearance of R222's brain, the rat seemed to suffer no major impairments. Ferris et al. say that "R222’s general health, appearance and body weight were no different from the other rats in the cohort." The rodent's motor skills and memory function were within the normal range, although it did seem to be highly anxious. © 2020 Kalmbach Media Co.

Keyword: Development of the Brain
Link ID: 27009 - Posted: 01.31.2020

By Veronique Greenwood You might mistake jewel wings for their colorful cousins, dragonflies. New research shows that these two predators share something more profound than their appearance, however. In a paper published this month in Current Biology, Dr. Gonzalez-Bellido and colleagues reveal that the neural systems behind jewel wings’ vision are shared with dragonflies, with whom they have a common ancestor that lived before the dinosaurs. But over the eons, this brain wiring has adapted itself in different ways in each creature, enabling radically different hunting strategies. For flying creatures, instantaneous, highly accurate vision is crucial to survival. Recent research showed that birds of prey that fly faster also see changes in their field of vision more quickly, demonstrating the link between speed on the wing and speed in the brain. But the group of insects that includes jewel wings and dragonflies took to the air long before birds were even on the evolutionary horizon, and their vision is swifter than any vertebrate’s studied thus far, said Dr. Gonzalez-Bellido. Researchers looking to understand how their vision, flight and hunting abilities are connected are thus particularly interested in the neurons that send visual information to the wings. But recordings made in the lab by Dr. Gonzalez-Bellido and her colleagues confirmed that dragonflies rise up in a straight line to seize unsuspecting insects from below, almost like their prey had stepped on a land mine. This eerie climb may contribute to their startling success rate: Dragonflies snag their prey 97 percent of the time. The difference in hunting behavior may be linked to the placement of the insects’ eyes. Jewel wings’ eyes are on either side of the head, facing forward. The eyes of these dragonflies — the species Sympetrum vulgatum, also known as the vagrant darter — encase the top of the insect’s head in an iridescent dome, with a thin line running down the middle the only visible reminder that they may have once been separate. © 2020 The New York Times Company

Keyword: Vision; Evolution
Link ID: 27008 - Posted: 01.29.2020

Jordana Cepelewicz Part of the brain’s allure for scientists is that it is so deeply personal — arguably the core of who we are and what makes us human. But that fact also renders a large share of imaginable experiments on it monstrous, no matter how well intended. Neuroscientists have often had to swallow their frustration and settle for studying the brains of experimental animals or isolated human neurons kept alive in flat dishes — substitutes that come with their own ethical, practical and conceptual limitations. A new world of possibilities opened in 2008, however, when researchers learned how to create cerebral organoids — tiny blobs grown from human stem cells that self-organize into brainlike structures with electrically active neurons. Though no bigger than a pea, organoids hold enormous promise for improving our understanding of the brain: They can replicate aspects of human development and disease once thought impossible to observe in the laboratory. Scientists have already used organoids to make discoveries about schizophrenia, autism spectrum disorders and the microcephaly caused by the Zika virus. Yet the study of brain organoids can also be fraught with ethical dilemmas. “In order for it to be a good model, you want it to be as human as possible,” said Hank Greely, a law professor at Stanford University who specializes in ethical and legal issues in the biosciences. “But the more human it gets, the more you’re backing into the same sorts of ethics questions that are the reasons why you can’t just use living humans.” In the popular imagination, fueled by over-the-top descriptions of organoids as “mini-brains,” these questions often center on whether the tissue might become conscious and experience its unnatural existence as torture. The more immediate, realistic concerns that trouble experts are less sensational but still significant. It also doesn’t help that the study of organoids falls into an odd gap between other areas of research, complicating formal ethical oversight. Still, no one wants to see brain organoids’ potential discarded lightly. All Rights Reserved © 2020

Keyword: Development of the Brain
Link ID: 27007 - Posted: 01.29.2020

By Theodor Schaarschmidt A 51-year-old man I will call “Mr. Pinocchio” had a strange problem. When he tried to tell a lie, he often passed out and had convulsions. In essence, he became a kind of Pinocchio, the fictional puppet whose nose grew with every fib. For the patient, the consequences were all too real: he was a high-ranking official in the European Economic Community (since replaced by the European Union), and his negotiating partners could tell immediately when he was bending the truth. His condition, a symptom of a rare form of epilepsy, was not only dangerous, it was bad for his career. Doctors at the University Hospitals of Strasbourg in France discovered that the root of the problem was a tumor about the size of a walnut. The tumor was probably increasing the excitability of a brain region involved in emotions; when Mr. Pinocchio lied, this excitability caused a structure called the amygdala to trigger seizures. Once the tumor was removed, the fits stopped, and he was able to resume his duties. The doctors, who described the case in 1993, dubbed the condition the “Pinocchio syndrome.” Mr. Pinocchio’s plight demonstrates the far-reaching consequences of even minor changes in the structure of the brain. But perhaps just as important, it shows that lying is a major component of the human behavioral repertoire; without it, we would have a hard time coping. When people speak unvarnished truth all the time—as can happen when Parkinson’s disease or certain injuries to the brain’s frontal lobe disrupt people’s ability to lie—they tend to be judged tactless and hurtful. In everyday life, we tell little white lies all the time, if only out of politeness: Your homemade pie is awesome (it’s awful). No, Grandma, you’re not interrupting anything (she is). A little bit of pretense seems to smooth out human relationships without doing lasting harm. © 2020 Scientific American

Keyword: Emotions
Link ID: 27006 - Posted: 01.29.2020

Rhitu Chatterjee One in seven women experiences depression during or after pregnancy. The good news is that perinatal depression is treatable. Here are five things to know about perinatal depression, its symptoms and treatment options. Loveis Wise for NPR Shortly after she gave birth to her son last May, Meghan Reddick, 36, began to struggle with depression. "The second I had a chance where I wasn't holding [my son], I would go to my room and cry," says Reddick, who lives with her son and husband. "And I probably couldn't count how many hours a day I cried." Reddick is among the many women who suffer from depression during pregnancy and after childbirth. "There's this kind of myth that women couldn't possibly be depressed during pregnancy, [that] this is such a happy time," says Jennifer Payne, a psychiatrist and the director of the Women's Mood Disorders Center at Johns Hopkins University. "The reality is that a lot of women struggle with anxiety and depression during pregnancy as well as during the postpartum period." An estimated one in seven women experiences depression during or after pregnancy. Among some groups, such as teenage moms and women with a history of trauma, the rate can be even higher. Left untreated, depression during this time can have serious consequences on the health of the mother, the baby and the entire family. © 2020 npr

Keyword: Depression; Sexual Behavior
Link ID: 27005 - Posted: 01.29.2020

A fast acting ketamine-like anti-depressant spray that can lift mood within hours has been rejected by the NHS healthcare watchdog. The National Institute for Health and Care and Excellence (NICE) says there are too many uncertainties about the correlation between the price and clinical benefits of esketamine. It is licensed as a therapy for people with hard-to-treat depression. But it costs about £10,000 per patient for a single course of treatment. Mixed reactions Some people already prescribed it - as part of a trial, for example - will be able to continue on the treatment if their doctor says it is appropriate to do so, the NICE's draft recommendation for England and Wales says. Scotland is yet to issue guidance. Experts have expressed mixed reactions to NICE's decision. Dr Sameer Jauhar, at the Institute of Psychiatry, Psychology and Neuroscience, King's College London, said NICE had made the call because there was not yet enough long-term evidence to support the use of nasal esketamine alongside another anti-depressant. Consultant psychiatrist Dr Paul Keedwell, at Cardiff University, said patients would be disappointed by a decision based largely on cost rather than lack of effectiveness. Marjorie Wallace, chief executive of mental health charity Sane, said: "People with depression are currently relying on medications that are 30 years old. "Although these drugs can be life-saving for some people, they can have unpleasant side-effects and do not work for everyone. "It is therefore deeply disappointing that the first new compound that works in a fundamentally different way on the brain should not have passed this hurdle. "This is especially so because people can take as much as six to eight weeks to feel the full effects of most anti-depressants. "We hope this setback will serve only to inspire pharmaceutical companies, researchers and others to discover new ways of treating serious depression." Recreational misuse Ketamine is used in medicine to numb the body or induce sleep and sometimes prescribed for depression. © 2020 BBC.

Keyword: Depression; Drug Abuse
Link ID: 27004 - Posted: 01.29.2020

By Laura Sanders After taking a compound found in magic mushrooms, people with cancer had less anxiety and depression, even years later, a new study suggests. The evidence isn’t strong enough yet to pin these lasting improvements on the hallucinatory episode itself, as opposed to other life changes. But the findings leave open the possibility that the compound, called psilocybin, may be able to profoundly reshape how people handle distress and fear (SN: 9/26/06). Research published in 2016 suggested that a dose of psilocybin in combination with therapy could quickly ease anxiety and depression in people with cancer. But scientists wanted to know whether these effects lasted. Surveys conducted about three and 4½ years after the psilocybin dose showed that a majority of the 15 people still had fewer signs of anxiety and depression compared with before they took the compound, the team reports January 28 in the Journal of Psychopharmacology. (By the second follow-up, about a third of the participants still had active cancer; the rest were in partial or complete remission.) All the participants said they had “moderate,” “strong” or “extreme” positive changes in their behavior that they attribute to their experience, which many described as one of the most personally meaningful events of their lives. © Society for Science & the Public 2000–2020

Keyword: Depression; Drug Abuse
Link ID: 27003 - Posted: 01.29.2020

Elena Renken The sting of a paper cut or the throb of a dog bite is perceived through the skin, where cells react to mechanical forces and send an electrical message to the brain. These signals were believed to originate in the naked endings of neurons that extend into the skin. But a few months ago, scientists came to the surprising realization that some of the cells essential for sensing this type of pain aren’t neurons at all. It’s a previously overlooked type of specialized glial cell that intertwines with nerve endings to form a mesh in the outer layers of the skin. The information the glial cells send to neurons is what initiates the “ouch”: When researchers stimulated only the glial cells, mice pulled back their paws or guarded them while licking or shaking — responses specific to pain. This discovery is only one of many recent findings showing that glia, the motley collection of cells in the nervous system that aren’t neurons, are far more important than researchers expected. Glia were long presumed to be housekeepers that only nourished, protected and swept up after the neurons, whose more obvious role of channeling electric signals through the brain and body kept them in the spotlight for centuries. But over the last couple of decades, research into glia has increased dramatically. “In the human brain, glial cells are as abundant as neurons are. Yet we know orders of magnitude less about what they do than we know about the neurons,” said Shai Shaham, a professor of cell biology at the Rockefeller University who focuses on glia. As more scientists turn their attention to glia, findings have been piling up to reveal a family of diverse cells that are unexpectedly crucial to vital processes. All Rights Reserved © 2020

Keyword: Glia; Pain & Touch
Link ID: 27002 - Posted: 01.28.2020

Scott Grafton When people ask me about the “mind-body connection,” I typically suggest walking on an icy sidewalk. Skip the yoga, mindfulness, or meditation, and head to the corner on a cold, windy, snowy day. Every winter, much of North America becomes exceedingly slippery with ice. Emergency rooms across the continent see a sharp uptick in fractured limbs and hips as people confidently trudge outside in such conditions, unveiling a profound disconnection between what people believe and what they can actually do with their bodies. One might think that a person could call on experience from years past to adjust their movement or provide a little insight or caution. But the truth is that the body forgets what it takes to stay upright in these perilous conditions. Why is there so much forgetting and relearning on an annual basis? We remember how to ride a bike. Why can’t we remember how to walk on ice? I attempt to answer this and other questions concerning the connection (or lack thereof) between motion in the mind and motion by the body in my new book, Physical Intelligence: The Science of How the Body and the Mind Guide Each Other Through Life. Pantheon, January 2020 Falling on ice reveals a delicate tradeoff that the brain must reconcile as it pilots the body. On the one hand, it needs to build refined motor programs to execute skills such as walking, running, and throwing. On the other hand, those programs can’t be too specific. There is a constant need to tweak motor plans to account for dynamic conditions. When I throw a backpack on, my legs don’t walk in the same way as they do without the pack: my stance widens, my stride shortens. Often, the tweaking needs to happen in moments. As I pick the pack up, I need to lean in or I could tip myself over. Just as importantly, as soon as I put it down, I need to forget I ever held it in the first place. © 1986–2020 The Scientist

Keyword: Learning & Memory
Link ID: 27001 - Posted: 01.28.2020

By Gretchen Vogel A prominent neuroscientist whose German lab was targeted by animal rights activists is heading to China, where he says he will be freer to pursue his work on macaques and other monkeys. Nikos Logothetis, a director at the Max Planck Institute for Biological Cybernetics in Tübingen, Germany, told colleagues last week that the first members of his lab would move in the coming months to a new International Center for Primate Brain Research (ICPBR) in Shanghai, which he will co-direct with neuroscientist Poo Mu-Ming, scientific director of the Chinese Academy of Sciences’s Center for Excellence in Brain Science and Intelligence Technology. Logothetis says he will follow as soon as remaining lab members have finished their projects, likely by late 2020 or early 2021. The Chinese institute is building a new facility in Shanghai’s Songjiang district, which will house as many as 6000 nonhuman primates, including many transgenic monkeys. “Scientifically it’s incredible,” he says. “They have excellent groups working with CRISPR and genetic engineering.” And, he adds, the acceptance of nonhuman primate research by authorities and the public in China is much higher than in Europe. They “know that no other brain (besides that of humans themselves) can be a true help in making progress.” The move is another sign that China’s investment in neuroscience research, especially involving primates, is paying off, says Stefan Treue, a neuroscientist and director of the German Primate Center. “China has made incredible progress in an unbelievably short period of time. That is the positive side of a political system that is able to move very quickly,” he says. “The combination of political will and necessary resources mean that they have put together an impressive collection of neuroscientists.” © 2019 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 27000 - Posted: 01.28.2020

By Laura Sanders A cruel twist of genetic fate brought Alzheimer’s disease to a sprawling Colombian family. But thanks to a second twist, one member of the clan, a woman, managed to evade the symptoms for decades. Her escape may hold the key to halting, or even preventing, Alzheimer’s. The inherited version of Alzheimer’s disease erodes people’s memories early, starting around age 40. In this family and others, a mutation in a gene called presenilin 1 eventually leaves its carriers profoundly confused and unable to care for themselves. Locals around the Colombian city of Medellín have a name for the condition: la bobera, or “the foolishness.” The woman in the afflicted family who somehow fended off the disease carried the same mutation that usually guarantees dementia. And her brain was filled with plaques formed by a sticky protein called amyloid. Many scientists view that accumulation as one of the earliest signs of the disease. Yet she stayed sharp until her 70s. Researchers were stumped, until they discovered that the woman also carried another, extremely rare genetic mutation that seemed to be protecting her from the effects of the first one. This second mutation, in a different Alzheimer’s-related gene called APOE, seemed to slow the disease down by decades, says Joseph Arboleda-Velasquez, a cell biologist at Harvard Medical School. “There was this idea of inevitability,” he says. But the woman’s circumstances bring “a different perspective” — one in which amyloid buildup no longer guarantees problems. Arboleda-Velasquez and colleagues reported the details of the woman’s exceptional case November 4 in Nature Medicine, omitting the woman’s name and precise age to protect her privacy. © Society for Science & the Public 2000–2020

Keyword: Alzheimers
Link ID: 26999 - Posted: 01.27.2020

One day, a scientist in Craig Ferris’s lab was scanning the brains of very old rats when he found that one could see, hear, smell, and feel just like the other rats, but it was walking around with basically no brain—and likely had been since birth. This rat, named R222, did have a brain. But its brain, affected by a condition called hydrocephalus, had compressed and collapsed as it filled with fluid, and many of the functions that would ordinarily be carried out in the brain had relocalized to areas that weren’t taken over by fluid. This provided the tools for Ferris, a psychology professor at Northeastern, to investigate how powerful the brain remains, even when tight on space. This, he says, might even influence the ever-present goal of machine learning: How small can you be and still get the job done? Pretty small, it turns out, at least in R222’s case, but this efficient use of space is dependent on the brain’s capacity to reorganize. This ability, known as neuroplasticity, is a widely documented phenomenon, but such an extreme example was rare, says Ferris. In R222’s case, he says, the processing of visual input “was distributed over much of the remaining brain, and the same thing with smell and touch.” What at first the scans suggested to be a brainless rat was actually a rat with a brain that had been pushed out of the way and flattened like a pancake—and kept working. ©2020 Technology Networks

Keyword: Development of the Brain
Link ID: 26998 - Posted: 01.27.2020

By Aimee Cunningham A concussion diagnosis depends upon a careful assessment of symptoms. Now the largest study to date of sports-related concussion points to a potential medical assist when evaluating a college athlete for this injury. Certain proteins in the blood are elevated after a concussion, researchers report online January 24 in JAMA Network Open. That discovery may one day help with distinguishing athletes who have suffered this brain injury from those who haven’t. Researchers took blood samples pre- and post-injury from 264 college athletes who had concussions while playing football, rugby and other contact sports from 2015 to mid-2018. Blood levels for three proteins were higher than they were before the injury occurred, the researchers found. Each of the three proteins can serve as a sign that damage has occurred to a different type of brain cell, says Michael McCrea, a neuropsychologist at the Medical College of Wisconsin in Milwaukee. Glial fibrillary acidic protein is released in response to injury to glial cells, which provide support to nerve cells in the brain. Ubiquitin C-terminal hydrolase-L1 signals that nerve cells have been injured, and tau is a sign of damage to axons, which transmit nerve impulses. These proteins have been evaluated in past research as potential makers of more severe traumatic brain injury. McCrea’s team also measured these proteins in 138 athletes who played contact sports but were not concussed, and in 102 athletes who did not have the injury and played noncontact sports. The protein levels for these two groups remained steady throughout the study. If there had been large variability in the protein levels in non-concussed athletes, McCrea says, that would have undermined the association between the proteins and concussion. © Society for Science & the Public 2000–2020

Keyword: Brain Injury/Concussion
Link ID: 26997 - Posted: 01.27.2020