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

By Stephen L. Macknik The year 2015 will go down in the annals of vision research history as a watershed moment. in which the internet discovered an entirely new visual phenomenon—a dress that half of the world saw as black/blue and the other half as white/gold. Had it not been for social media and its particular way of framing conversations around shared crowd-sourced images, this peculiar visual puzzle might have remained unknown. The idea that an object could look one color under one set of lighting conditions, and another color under another set of lighting conditions, was not new. What was unique about The Dress was that the same image, under the same exact viewing conditions, looked very different to different people. The color ambiguity only became evident when half of the viewers disagreed with the other half, which is probably why social media was so pivotal in its discovery. Vision scientists went bananas. Was it an artifact of different device screens? Did it have to do with gender, culture, education, or some other categorization of brain and persona? How many people—exactly—saw the image one way or the other? This was a dress that sailed a thousand ships. The vision science field eventually verified that the phenomenon was definitely real and not an artifact of viewing conditions. Though the precise underlying mechanisms remain unknown, even now. Similarly ambiguous color images followed the dress, but a main obstacle to figuring out how and why such effects existed was that all of the images were flukes. They were accidental happy snaps created by internet picture-posters. Scientists could not intentionally create new and carefully controlled examples for deep study in the lab. Until now. © 2020 Scientific American

Keyword: Vision
Link ID: 26996 - Posted: 01.27.2020

By Jane E. Brody My husband and I were psychological opposites. I’ve always seen the glass as half-full; to him it was half-empty. That difference, research findings suggest, is likely why I pursue good health habits with a vengeance while he was far less inclined to follow the health-promoting lifestyle I advocated. I’m no cockeyed optimist, but I’ve long believed that how I eat and exercise, as well as how I view the world, can benefit my mental and physical well-being. An increasing number of recent long-term studies have linked greater optimism to a lower risk of developing cardiovascular disease and other chronic ailments and to fostering “exceptional longevity,” a category one team of researchers used for people who live to 85 and beyond. Admittedly, the relationship between optimism and better health and a longer life is still only a correlation that doesn’t prove cause and effect. But there is also now biological evidence to suggest that optimism can have a direct impact on health, which should encourage both the medical profession and individuals to do more to foster optimism as a potential health benefit. According to Dr. Alan Rozanski, one of the field’s primary researchers, “It’s never too early and it’s never too late to foster optimism. From teenagers to people in their 90s, all have better outcomes if they’re optimistic.” Dr. Rozanski is a cardiologist at Mount Sinai St. Luke’s Hospital in New York who became interested in optimism while working in a cardiac rehabilitation program early in his career. In an interview, he explained, “Many heart-attack patients who had long been sedentary would come into the gym and say ‘I can’t do that!’ But I would put them on the treadmill, start off slowly and gradually build them up. Their attitude improved, they became more confident. One woman in her 70s said her heart attack may have been the best thing that had happened to her because it transformed what she thought she could do.” © 2020 The New York Times Company

Keyword: Emotions; Neuroimmunology
Link ID: 26995 - Posted: 01.27.2020

By Megan Schmidt Scientists say they’ve figured out what causes essential tremor, a common neurological disorder characterized by involuntary, rhythmic trembling that typically occurs in the hands. In a paper published in Science Translational Medicine this week, researchers at National Taiwan University and Columbia University Irving Medical Center discovered that people with essential tremor have abnormal connections among the neurons in their cerebellum, a region in the back of the brain that’s involved in the coordination of voluntary movement. Researchers say people with these abnormalities tend to generate overactive brain waves, or too much electrical activity, in this region of the brain, which is what fuels the tremors. In addition to pinpointing the roots of the disorder, the researchers say their work uncovered some new approaches that could potentially treat and diagnose essential tremor more effectively. Essential tremor is often mistaken for Parkinson’s disease, but there are some key distinctions that set these movement disorders apart. Parkinson’s, which is less common than essential tremor, is caused by the progressive loss of dopamine neurons in the midbrain, a small region of the brain that plays an important role in motor function. Essential tremor, as this new research reveals, is linked to abnormalities in the hindbrain — specifically, the cerebellum. © 2020 Kalmbach Media Co.

Keyword: Movement Disorders
Link ID: 26994 - Posted: 01.25.2020

Children as young as 6 years old who underwent fetal surgery to repair a common birth defect of the spine are more likely to walk independently and have fewer follow-up surgeries, compared to those who had traditional corrective surgery after birth, according to researchers funded by the National Institutes of Health. The study appears in Pediatrics. The procedure corrects myelomeningocele, the most serious form of spina bifida, a condition in which the spinal column fails to close around the spinal cord. With myelomeningocele, the spinal cord protrudes through an opening in the spine and may block the flow of spinal fluid and pull the brain into the base of the skull, a condition known as hindbrain herniation. In 2011, the Management of Myelomeningocele study, funded by NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), found that by 12 months of age, children who had fetal surgery required fewer surgical procedures to divert, or shunt, fluid away from the brain. By 30 months, the fetal surgery group was more likely to walk without crutches or other devices. For the current study, NICHD-funded researchers re-evaluated children from the original trial when they were 6 to 10 years old. Of the 161 children who took part in the follow-up study, 79 had been assigned to prenatal surgery and 82 had been assigned to traditional surgery. Children in the prenatal surgery group walked independently more often than those in the traditional surgery group (93% vs. 80%). Those in the prenatal surgery group also had fewer shunt placements for hydrocephalus, or fluid buildup in the brain (49% vs. 85%), and fewer shunt replacements (47% vs. 70%). The group also scored higher on a measure of motor skills. The two groups did not differ significantly in a test measuring communication ability, daily living skills, and social interaction skills.

Keyword: Development of the Brain
Link ID: 26993 - Posted: 01.25.2020

John Henning Schumann As the owner of a yellow lab named Gus, author Maria Goodavage has had many occasions to bathe her pooch when he rolls around in smelly muck at the park. Nevertheless, her appreciation for his keen sense of smell has inspired her write best-selling books about dogs with special assignments in the military and the U.S. Secret Service. Her latest, Doctor Dogs: How Our Best Friends Are Becoming Our Best Medicine, highlights a vast array of special medical tasks that dogs can perform — from the laboratory to the bedside, and everywhere else a dog can tag along and sniff. Canines' incredible olfactory capacity — they can sniff in parts per trillion — primes them to detect disease, and their genius for observing our behavior helps them guide us physically and emotionally. Goodavage spoke with NPR contributor John Henning Schumann, a doctor and host of Public Radio Tulsa's #MedicalMonday about what she has learned about dogs in medicine What led you to look into dogs in medicine? I've been reading and writing about military dogs and Secret Service dogs for many years now, and it was sort of a natural next step. These are dogs on the cutting edge of medicine. They're either working in research or right beside someone to save their life every day. And really, doctor dogs are, for the most part, using their incredible sense of smell to detect diseases. And if they're paired with a person, they bond with that person to tell them something that will save their life. © 2020 npr

Keyword: Chemical Senses (Smell & Taste)
Link ID: 26992 - Posted: 01.25.2020

By Simon Makin Knowing how the human brain develops is critical to understanding how things can go awry in neurodevelopmental disorders, from intellectual disability and epilepsy to schizophrenia and autism. But between the fact that researchers cannot poke around inside growing human brains and the inadequacies of animal models, scientists currently do not fully understand the process. “We know a bit about the early stages because [the situation is] very similar to what happens in rodents,” says psychiatrist Sergiu Paşca of Stanford University. “But everything beyond the second trimester [of pregnancy] and soon after birth is poorly understood.” Enter the invention of brain “organoids”: cells grown in 3-D clusters in the lab and designed to mimic the composition of the organ’s tissue. The technology recently reached the point where specific brain regions can be modelled for sufficiently long periods to allow researchers to study their development. Paşca and his colleagues have now used organoid models of parts of the human forebrain—the seat of higher cognitive abilities such as complex thought, perception and voluntary movement—to peer into how gene activity drives brain development. “The work brings new understanding of how, as the brain is formed, distinct regulatory regions of the genome are used to execute specific tasks—for example, the generation of specific types of neurons,” says neuroscientist Paola Arlotta of Harvard University, who was not involved in the new study. The researchers used their findings to map genes associated with certain disorders to specific cell types at specific stages, giving insight into the origins of conditions such as autism and schizophrenia. © 2020 Scientific American,

Keyword: Development of the Brain
Link ID: 26991 - Posted: 01.25.2020

Abby Olena Understanding the array of neural signals that occur as an organism makes a decision is a challenge. To tackle it, the authors of a study published last week (January 16) in Cell imaged large swaths of the larval zebrafish brain as the animals decided which way to move their tails to avoid an undesirable situation. Finding patterns in the data, they were then able to use imaging to predict—10 seconds in advance—the timing and direction of the fish’s movement. “In a lot of other model systems it’s really difficult to actually . . . record something that’s happening throughout the whole brain with a high level of precision,” says Kristen Severi, a biologist at the New Jersey Institute of Technology who was not involved in the study. “When you have something like a larval zebrafish where you have access to the entire brain with single-cell resolution in a transparent vertebrate, it’s a great place to start to try to look for activity patterns that might be distributed and might be hard to connect.” Even if an animal has learned to do something, it doesn’t execute the exact same motor responses every time, says biophysicist Alipasha Vaziri of the Rockefeller University. He adds that common approaches to studying the neural basis of decision-making may not tell the whole story. For instance, monitoring a handful of neurons and then extrapolating from their activity what’s happening brain-wide means that researchers might miss the big picture. Likewise, recording across the whole brain and then averaging results across trials risks losing details essential to understanding how the brain encodes this behavior. © 1986–2020 The Scientist

Keyword: Brain imaging
Link ID: 26990 - Posted: 01.24.2020

Katarina Zimmer Around 30 years ago, researchers in the UK discovered DNA strands of herpes simplex virus 1 in postmortem brain samples of Alzheimer’s patients at much higher levels than in healthy brains, hinting that viral infection could be somehow involved in the disease. Since then, a string of studies has bolstered the association between Alzheimer’s disease and HSV1, as well as other pathogens, particularly the herpesviruses HHV6A and HHV6B, yet proving causality has remained elusive. Now, in an extensive screen of hundreds of diseased brains from three separate cohorts, a collaboration of US-based researchers reports no evidence for increased RNA or DNA levels of HHV6A or HHV6B in tissue from people with Alzheimer’s disease relative to that from healthy individuals, contradicting the results of some previous results. The scientists also failed to find an association between transcripts of other viruses that have been linked to Alzheimer’s, such as Epstein-Barr virus and cytomegalovirus, and Alzheimer’s, they report today (January 23) in Neuron. “I’m very surprised,” Ruth Itzhaki, an Alzheimer’s disease researcher currently at the University of Oxford who was among those who first associated HSV1, and later HHV6, with the disease, writes to The Scientist in an email. “If their findings are correct, absence of HHV6 would make any involvement in Alzheimer’s disease unlikely,” although not impossible, she notes. Several groups have reported the presence of HHV6 viruses in the brains of Alzheimer’s patients, most notably in a 2018 Neuron study. In that investigation, researchers had found higher levels of HHV6A in patients than in healthy controls, largely based on RNA and DNA sequencing data. © 1986–2020 The Scientist

Keyword: Alzheimers; Neuroimmunology
Link ID: 26989 - Posted: 01.24.2020

By Nicholas Bakalar People with depression are at increased risk for dementia, researchers report, and the risk may persist for decades. Using the Swedish National Patient Register, scientists identified 119,386 people over 50 with depression and matched them with an equal number of people without that diagnosis. Dementia developed in 5.7 percent of those with depression, compared to only 2.6 percent of those without depression, over an average follow-up of more than 10 years. Those with depression were more than 15 times as likely to develop dementia in the first six months after their depression diagnosis as their peers who were not depressed. That rate decreased rapidly but was still evident after 20 years. The researchers also studied 25,322 sibling pairs older than 50 in which one sibling had depression and the other did not. A sibling with a depression diagnosis was more than 20 times as likely as his brother or sister without depression to be diagnosed with dementia in the first six months after the diagnosis. Again, the risk declined over time, but persisted for more than 20 years. The study is in PLOS Medicine. “This is an observational study that does not prove causation,” said the lead author, Peter Nordstrom, a professor of geriatrics at Umea University in Sweden. “If you are diagnosed with depression, that doesn’t mean that you are bound to have dementia.” © 2020 The New York Times Company

Keyword: Depression; Alzheimers
Link ID: 26988 - Posted: 01.24.2020

By Knvul Sheikh There is some truth to the longstanding anecdote that your locks can lose color when you’re stressed. A team of researchers has found that in mice, stressful events trigger damage the stem cells that are responsible for producing pigment in hair. These stem cells, found near the base of each hair follicle, differentiate to form more specialized cells called melanocytes, which generate the brown, black, red and yellow hues in hair and skin. Stress makes the stem cells differentiate faster, exhausting their number and resulting in strands that are more likely to be transparent — gray. The study, published Wednesday in Nature, also found that the sympathetic nervous system, which prepares the body to respond to threats, plays an important role in the graying process. “Normally, the sympathetic nervous system is an emergency system for fight or flight, and it is supposed to be very beneficial or, at the very least, its effects are supposed to be transient and reversible,” said Ya-Chieh Hsu, a stem cell biologist at Harvard University who led the study. The sympathetic nervous system helps mobilize many biological responses, including increasing the flow of blood to muscles and sharpening mental focus. But the researchers found that in some cases the same system of nerves permanently depleted the stem cell population in hair follicles. The findings provide the first scientific link between stress and hair graying, Dr. Hsu said. Stress affects the whole body, so the researchers had to do some sleuthing to figure out which physiological system was conveying its effects to hair follicles. At first, the team hypothesized that stress might cause an immune attack on melanocyte stem cells. They exposed mice to acute stress by injecting the animals with an analogue of capsaicin, the chemical in chili peppers that causes irritation. But even mice that lacked immune cells ended up with gray hair. Next, the scientists looked at the effects of the stress hormone cortisol. Mice that had their adrenal glands removed so they couldn’t produce cortisol still had hair that turned gray under stress. © 2020 The New York Times Company

Keyword: Stress
Link ID: 26987 - Posted: 01.23.2020

By Will Hobson In 2017, Bennet Omalu traveled the globe to accept a series of honors and promote his autobiography, “Truth Doesn’t Have A Side.” In a visit to an Irish medical school, he told students he was a “nobody” who “discovered a disease in America’s most popular sport.” In an appearance on a religious cable TV show, he said he named the disease chronic traumatic encephalopathy, or CTE, because “it sounded intellectually sophisticated, with a very good acronym.” And since his discovery, Omalu told Sports Illustrated, researchers have uncovered evidence that shows adolescents who participate in football, hockey, wrestling and mixed martial arts are more likely to drop out of school, become addicted to drugs, struggle with mental illness, commit violent crimes and kill themselves. A Ni­ger­ian American pathologist portrayed by Will Smith in the 2015 film, “Concussion,” Omalu is partly responsible for the most important sports story of the 21st century. Since 2005, when Omalu first reported finding widespread brain damage in a former NFL player, concerns about CTE have inspired a global revolution in concussion safety and fueled an ongoing existential crisis for America’s most popular sport. Omalu’s discovery — initially ignored and then attacked by NFL-allied doctors — inspired an avalanche of scientific research that forced the league to acknowledge a link between football and brain disease. Nearly 15 years later, Omalu has withdrawn from the CTE research community and remade himself as an evangelist, traveling the world selling his frightening version of what scientists know about CTE and contact sports. In paid speaking engagements, expert witness testimony and in several books he has authored, Omalu portrays CTE as an epidemic and himself as a crusader, fighting against not just the NFL but also the medical science community, which he claims is too corrupted to acknowledge clear-cut evidence that contact sports destroy lives.

Keyword: Brain Injury/Concussion
Link ID: 26986 - Posted: 01.23.2020

By Karen Weintraub A small injury to a nerve outside the brain and spinal cord is relatively easy to repair just by stretching it, but a major gap in such a peripheral nerve poses problems. Usually, another nerve is taken from elsewhere in the body, and it causes an extra injury and returns only limited movement. Now researchers at the University of Pittsburgh have found an effective way to bridge such a gap—at least in mice and monkeys—by inserting a biodegradable tube that releases a protein called a growth factor for several months. In a study published Wednesday in Science Translational Medicine, the team showed that the tube works as a guide for the nerve to grow along the proper path, and the naturally occurring protein induces the nerve to grow faster. Kacey Marra, a professor at the university’s departments of plastic surgery and bioengineering, says she’s been working for a dozen years on the device, which she particularly hopes will help soldiers injured in combat. More than half of injured soldiers suffer nerve injuries, she says. And as the daughter and granddaughter of military men, she considers it her mission to help their successors. Combat gear does a good job of protecting a soldier’s chest and head, but arms and legs are often exposed, which is why peripheral nerve injuries are so common, Marra says. Car crashes and accidents involving machinery such as snowblowers can also damage nerves involved in hand, arm, leg and foot control. In the U.S., there are about 600,000 nerve injuries every year, she says, though she is unsure how many are severe enough to require the relocation of a second nerve because that information is not tracked yet. When the injuries are severe, the only current treatment is to take a nerve from somewhere else on the body, Marra says. But patients recover just about 50 to 60 percent of function in the damaged nerve. © 2020 Scientific American,

Keyword: Regeneration
Link ID: 26985 - Posted: 01.23.2020

Janelia and Google scientists have constructed the most complete map of the fly brain ever created, pinpointing millions of connections between 25,000 neurons. Now, a wiring diagram of the entire brain is within reach. In a darkened room in Ashburn, Virginia, rows of scientists sit at computer screens displaying vivid 3-D shapes. With a click of a mouse, they spin each shape to examine it from all sides. The scientists are working inside a concrete building at the Howard Hughes Medical Institute’s Janelia Research Campus, just off a street called Helix Drive. But their minds are somewhere else entirely – inside the brain of a fly. Each shape on the scientists’ screens represents part of a fruit fly neuron. These researchers and others at Janelia are tackling a goal that once seemed out of reach: outlining each of the fly brain’s roughly 100,000 neurons and pinpointing the millions of places they connect. Such a wiring diagram, or connectome, reveals the complete circuitry of different brain areas and how they're linked. The work could help unlock networks involved in memory formation, for example, or neural pathways that underlie movements. Gerry Rubin, vice president of HHMI and executive director of Janelia, has championed this project for more than a decade. It’s a necessary step in understanding how the brain works, he says. When the project began, Rubin estimated that with available methods, tracing the connections between every fly neuron by hand would take 250 people working for two decades – what he refers to as “a 5,000 person-year problem.”

Keyword: Brain imaging
Link ID: 26984 - Posted: 01.23.2020

Kayt Sukel Since its inception, the field of neuroscience has relied on animal models, from fruit flies to macaque monkeys, to better understand the behavior and inner workings of neurons. But while these models have led to remarkable insights about the brain in both health and in disease, they do have limitations. The very genetic differences that place us in different species also make the translation of neurobiological findings in animals to humans challenging—if not outright impossible. “We’ve now cured Alzheimer’s disease a dozen times over in mice, but we haven’t cured it in human patients,” said Matthew Blurton-James, Ph.D., a neurobiologist at the University of California, Irvine. “There’s clearly a big species difference in how this disease develops, which means our current animal models can’t get us the answers we’re searching for.” In the past few years, however, advances in technology have led to the development of innovative models to study the activity of human neurons—and how they communicate with one another. Such models, which include ex vivo tissue harvested from living human donors, organoids, and chimeric models (animal tissue modified with human genes or cells), are enabling scientists to investigate processes in ways that were previously unthinkable. “These new technologies, including those that use induced pluripotent stem cells (iPSCs), are really quite striking,” said Walter Koroshetz, M.D., director of the National Institute of Neurological Disorders and Stroke. “And the real advantage of these is that they offer us a new way to study human brain cells, particularly when it comes to developmental processes, that is incredibly valuable.” © 2020 The Dana Foundation

Keyword: Development of the Brain
Link ID: 26983 - Posted: 01.23.2020

Nicola Davis When Mount Vesuvius erupted in AD79, the damage wreaked in nearby towns was catastrophic. Now it appears the heat was so immense it turned one victim’s brain to glass – thought to be the first time this has been seen. Experts say they have discovered that splatters of a shiny, solid black material found inside the skull of a victim at Herculaneum appear to be the remains of human brain tissue transformed by heat. They say the find is remarkable since brain tissue is rarely preserved at all due to decomposition, and where it is found it has typically turned to soap. “To date, vitrified remains of the brain have never been found,” said Dr Pier Paolo Petrone, a forensic anthropologist at the University of Naples Federico II and a co-author of the study. Writing in the New England Journal of Medicine, Petrone and colleagues reveal that the glassy brains belonged to a man of about 25 who was found in the 1960s lying face-down on a wooden bed under a pile of volcanic ash – a pose that suggests he was asleep when disaster struck the town. The bed was in a small room that was part of the Collegium Augustalium, a building relating to an imperial cult that worshipped the former emperor Augustus. The victim, according to Petrone, is believed to have been the caretaker. Petrone said it was when he recently focused his research on human remains found at the college that he noticed the black fragments in the caretaker’s skull. “I noticed something shining inside the head ,” he told the Guardian. “This material was preserved exclusively in the victim’s skull, thus it had to be the vitrified remains of the brain. But it had to be proved beyond any reasonable doubt.” © 2020 Guardian News & Media Limited

Keyword: Brain imaging
Link ID: 26982 - Posted: 01.23.2020

Liz Fuller-Wright, Office of Communications Barry L. Jacobs, an emeritus professor of psychology and neuroscience who became internationally known for his research on serotonin, sleep and depression, died Friday, Jan. 10, in Princeton. He was 77 years old. Jacobs joined the Princeton faculty in 1972 and transferred to emeritus status in 2017. Among his roles at the University, he served as director of the neuroscience graduate program from 1988 to 2000. “Barry Jacobs was a truly wonderful colleague — brilliant, knowledgeable, interesting, generous, and always upbeat and friendly,” said Ronald Comer, an emeritus member of Princeton’s psychology faculty. “Deeply committed to his work and to all of neuroscience, he was just as interested in and curious about the work of his other psychology colleagues, including those of us in social and clinical psychology. As a result of his special accomplishments in neuroscience, multiple interests, extraordinary skills as a teacher and communicator, and contagious passion for science, Barry was able to develop and teach, for decades, one of the University’s most successful and popular courses, ‘The Brain: A User’s Guide’ — a course that brought the wonders of neuroscience to life for University students of all concentrations and interests.” Jacobs was born Feb. 26, 1942, in Chicago. He received his B.S. in economics from the University of Illinois-Chicago, in 1966, and his doctorate in psychology from the University of California-Los Angeles in 1971. He was a postdoctoral fellow in the psychiatry department at Stanford University Medical School before coming to Princeton. © 2020 The Trustees of Princeton University

Keyword: Drug Abuse
Link ID: 26981 - Posted: 01.23.2020