By Aaron E. Carroll Even before the recent news that a group of researchers managed to get several ridiculous fake studies published in reputable academic journals, people have been aware of problems with peer review. Throwing out the system — which deems whether research is robust and worth being published — would do more harm than good. But it makes sense to be aware of peer review’s potential weaknesses. Reviewers may be overworked and underprepared. Although they’re experts in the subject they are reading about, they get no specific training to do peer review, and are rarely paid for it. With 2.5 million peer-reviewed papers published annually worldwide — and more that are reviewed but never published — it can be hard to find enough people to review all the work. There is evidence that reviewers are not always consistent. A 2010 paper describes a study in which two researchers selected 12 articles already accepted by highly regarded journals, swapped the real names and academic affiliations for false ones, and resubmitted the identical material to the same journals that had already accepted them in the previous 18 to 32 months. Only 8 percent of editors or reviewers noticed the duplication, and three papers were detected and pulled. Of the nine papers that continued through the review process, eight were turned down, with 89 percent of reviewers recommending rejection. Peer review may be inhibiting innovation. It takes significant reviewer agreement to have a paper accepted. One potential downside is that important research bucking a trend or overturning accepted wisdom may face challenges surviving peer review. In 2015, a study published in P.N.A.S. tracked more than 1,000 manuscripts submitted to three prestigious medical journals. Of the 808 that were published at some point, the 2 percent that were most frequently cited had been rejected by the journals. An even bigger issue is that peer review may be biased. Reviewers can usually see the names of the authors and their institutions, and multiple studies have shown that reviews preferentially accept or reject articles based on a number of demographic factors. In a study published in eLife last year, researchers created a database consisting of more than 9,000 editors, 43,000 reviewers and 126,000 authors whose work led to about 41,000 articles in 142 journals in a number of domains. They found that women made up only 26 percent of editors, 28 percent of reviewers and 37 percent of authors. Analyses showed that this was not because fewer women were available for each role. © 2018 The New York Times Compan

Keyword: Attention
Link ID: 25643 - Posted: 11.05.2018

By Ed Silverman, In a highly controversial move, the Food and Drug Administration approved an especially powerful opioid painkiller despite criticism that the medicine could be a “danger” to public health. And in doing so, the agency addressed wider regulatory thinking for endorsing such a medicine amid nationwide angst about overdoses and deaths attributed to opioids. The drug is called Dsuvia, which is a tablet version of an opioid marketed for intravenous delivery, but is administered under the tongue using a specially developed, single-dose applicator. These “unique features” make the medicine well-suited for the military and therefore was a priority for the Pentagon, a point that factored heavily into the decision, according to FDA Commissioner Scott Gottlieb. Although an FDA advisory committee last month recommended approval, the agency was urged by critics not to endorse the drug because it is 10 times more powerful than fentanyl, a highly addictive opioid. Among those who opposed approval were four U.S. senators and the FDA advisory panel chair, who could not attend the meeting, but took the rare step of later writing a letter to the agency. The objections included complaints that Dsuvia has no unique medical benefits and might be easily diverted by medical personnel, despite a risk mitigation plan the manufacturer, AcelRx Pharmaceuticals, must maintain. There was also criticism the FDA failed to convene the Drug Safety and Risk Management Advisory Committee, not just the Anesthetic and Analgesic Drug Products Advisory Committee. Last year, the FDA refused to approve the medicine over concerns about usage directions and a need for additional safety data. © 2018 Scientific American

Keyword: Drug Abuse; Pain & Touch
Link ID: 25642 - Posted: 11.03.2018

Allison Aubrey When it comes to turning back the clocks on our devices, technology has us covered. Our smartphones automatically adjust. But our internal clocks aren't as easy to re-program. And this means that the time shift to save daylight in the fall and again in the spring can influence our health in unexpected ways. "You might not think that a one hour change is a lot," says Fred Turek, who directs the Center for Sleep & Circadian Biology at Northwestern University. "But it turns out that the master clock in our brain is pretty hard-wired, " Turek explains. It's synchronized to the 24 hour light/dark cycle. Daylight is a primary cue to reset the body's clock each day. So, if daylight comes an hour earlier — as it will for many of us this weekend — it throws us off. "The internal clock has to catch up, and it takes a day or two to adjust to the new time," Turek says. Scientists have documented that the shift to daylight saving time in the spring, when we lose an hour of sleep, can increase the risk of heart attacks, strokes and traffic accidents. These studies are a reminder of just how sensitive we are to time and rhythm. Over the last 20 years, scientists have documented that, in addition to the master clock in our brains, every cell in our body has a time-keeping mechanism. These clocks help regulate important functions such as sleep and metabolism. And increasingly, there's evidence that when our habits — such as when we eat and sleep — are out of sync with our internal clocks, it can harm us. © 2018 npr

Keyword: Biological Rhythms
Link ID: 25641 - Posted: 11.03.2018

Ian Sample In daylight hours there is so little melatonin in the bloodstream that it is barely detectable. But when the sun goes down, the eyes sense the failing light, and part of the hippocampus signals the pineal gland, a pea-sized lump of tissue near the centre of the brain, to ramp up production of the sleep-promoting hormone. Levels of melatonin rise sharply from 9pm, inducing feelings of sleepiness, and remain high until the following morning. Much of the research on prescribing melatonin for children with sleep problems has focused on those with disorders such as autism, ADHD and intellectual disability (ID). For good reason too: sleeping difficulties are far more common and pronounced in children with neurodevelopmental or psychiatric disorders. For them, small doses of melatonin can be safe and effective. In one recent study, researchers from Southampton University monitored the sleep patterns of 45 children with autism, ADHD, or ID, and found that a third fell asleep faster, slept longer, and woke less frequently at night on low dose (2.5-3mg) melatonin. Above 6mg per night there was little extra benefit. A poor night’s sleep can be caused by any number of factors, but there is good evidence that screen time matters, whether it is TV, computer, tablet or mobile phone. A recent review of scientific papers on the issue found that 90% linked screen time to poor sleep in schoolchildren and adolescents. Part of the problem is obvious: being online at bedtime eats into the hours left for sleep, and it hardly helps people to wind down for the night. But glowing screens can affect sleep directly by suppressing the natural production of melatonin. Using an iPad on full brightness for two hours, for example, has been shown to suppress melatonin levels. © 2018 Guardian News and Media Limited

Keyword: Biological Rhythms; Hormones & Behavior
Link ID: 25640 - Posted: 11.03.2018

By David Grimm The number of monkeys used in U.S. biomedical research reached an all-time high last year, according to data released in late September by the United States Department of Agriculture (USDA). The uptick (see graph below)—to nearly 76,000 nonhuman primates in 2017—appears to reflect growing demand from scientists who believe nonhuman primates are more useful than other animals, such as mice or dogs, for testing drugs and studying diseases that also strike humans. “I think the numbers are trending up because these animals give us better data. … We need them more than ever,” says Jay Rappaport, director of the Tulane National Primate Research Center in Covington, Louisiana, which houses about 5000 monkeys. The increase also comes amidst a surge in funding from the National Institutes of Health (NIH), which supports much of the nonhuman primate research in the United States. The figures have surprised and disappointed groups seeking to reduce the use of lab animals. The biomedical community has said it is committed to reducing the use of research animals by finding replacements and using these animals more selectively, says Thomas Hartung, director of Johns Hopkins University’s Center for Alternatives to Animal Testing in Baltimore, Maryland. But the new numbers suggest “people are just blindly running toward the monkey model without critically evaluating how valuable it really is.” © 2018 American Association for the Advancement of Science

Keyword: Animal Rights
Link ID: 25639 - Posted: 11.03.2018

Researchers funded by the National Institutes of Health have reached a milestone in their quest to catalog the brain’s “parts list.” The NIH BRAIN Initiative Cell Census Network (BICCN) has issued its first data release. Posted on a public web portal (link is external) for researchers, it profiles molecular identities of more than 1.3 million mouse brain cells and anatomical data from 300 mouse brains – among the largest such characterizations to date. BICCN research teams (link is external) focused initially on a key area of the mouse motor cortex, an area of the brain that controls movement, as a first major step in the 5-year effort. Initiated in 2017, the BICCN projects aim to build comprehensive, three-dimensional common reference brain atlases that will ultimately integrate molecular, anatomical and functional data on cell types in mouse, human and non-human primate brains. To expedite scientific impact, they are making their data immediately available to the research community via the web portal. “No single research group could do this by themselves—they needed to leverage the power of a team,” explained Joshua Gordon, M.D., Ph.D., director of the National Institute of Mental Health (NIMH), which is helping to coordinate the BRAIN Initiative effort. “The BICCN is a product of nine different teams each bringing to bear their finely-honed tools to the same brain region at the same time. By doing so, they could compare results and create a unified resource for the community.” The new molecular fingerprints cover comprehensive information on gene transcription and epigenomic signature maps of the brain cells. Each type of cell is classified according to its molecular characteristics and identifiable by telltale marker genes.

Keyword: Sexual Behavior; Epigenetics
Link ID: 25638 - Posted: 11.02.2018

by Lena Simon Four limbs. Warm blood. A love for cheese. And a hatred for infidelity. Although this may sound characteristic of the average Wisconsinite, the previous is actually also true for the California mouse. A recent University of Wisconsin news release revealed research that shows California pair-bonded mice become increasingly vocal after infidelity experiences. Experiments were designed to test how communication changes after mice have been given the opportunity to be “unfaithful” to their bonded mate. The California deer mouse, or Peromyscus californicus, is part of only 3 to 5 percent of mammal species that practice any kind of monogamy, per research from the National Science Foundation. At UW, research on the California mouse is ongoing. Josh Pultorak, a biology instructor at Madison Area Technical College and UW’s Wisconsin Institute for Discovery, led this research. He and his collaborators identified several types of sounds that the California mouse makes, all of which are ultrasonic — unable to be heard by the human ear unless slowed down to about 5 percent of their original speed. These include chirps — or “sweeps,” which are usually more peaceful sounds — and barks, which indicate aggression. Microbes in your gut could hold cure to diabetesThere are millions of microbes living in your gut. They help you digest and access nutrients your own organs would Read… The Badger Herald, 1995 - 2018

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 25637 - Posted: 11.02.2018

Devika G. Bansal Tools that use light, drugs, or temperature to make neurons fire or rest on command have become a mainstay in neuroscience. Thermogenetics, which enables neurons to respond to temperature shifts, first took off with fruit flies about a decade ago, but is emerging as a new trick to manipulate the neural functioning of other model organisms. That’s due to some advantages it affords over optogenetics—the light-based technique that started it all. Genetic toolkits such as thermogenetics and optogenetics follow a basic recipe: scientists pick a receptor that responds to an external cue such as temperature or light, express the receptor in specific neurons as a switch that changes the cell’s voltage—triggering or inhibiting firing—and then use the cue to turn the neural switch on or off. Optogenetics revolutionized our understanding of how the brain’s wiring affects animal behavior. But it comes with drawbacks. For one, delivering light into the deepest regions of the brains of nontransparent animals is a challenge. In mice, this requires surgically inserting optical fibers into the brain, tethering the animal to the light source. Researchers working with adult fruit flies can cut a window through the head cuticle to access the brain. In both cases, the necessary experimental setups are invasive and often time and effort intensive. Additionally, the light intensity required for optogenetics tends to damage tissue. “You pump a lot of light through the optical fiber to activate neurons,” says Vsevolod Belousov, a biochemist at the Russian Academy of Sciences in Moscow who develops thermogenetic tools. “In general, this is not avoidable.” © 1986 - 2018 The Scientist

Keyword: Brain imaging
Link ID: 25636 - Posted: 11.02.2018

By Alycia Halladay Click-worthy health and science headlines are an essential currency in today’s media world. When they pertain to autism, they might include phrases like “groundbreaking trial,” “offer hope” or “game-changer.” But for people with autism and their families, these headlines and the research news stories they highlight often bring false hope, confusion—or worse. There is something about autism, a disorder that remains widely misunderstood, that seems to encourage the promulgation of news coverage about potential “breakthroughs” and unorthodox treatment approaches. A nearly constant stream of headlines touts promising new findings that supposedly help explain the origins of autism spectrum disorder (ASD), improve our understanding of its key features or reveal novel ways to treat the symptoms. This attention is a mixed blessing. It can encourage talented scientists to design research to better understand autism. It also generates support for advocacy efforts and research funding, and I have seen it motivate people to participate in research studies. However, there is a dark side to this almost insatiable interest in autism science news: it has created an environment that encourages media hype of early, preliminary findings, with headlines that are tantalizing but not always accurate. The hype machine also too often promotes mediocre or even bad science, which ultimately puts people with autism at risk. © 2018 Scientific American

Keyword: Autism
Link ID: 25635 - Posted: 11.02.2018

Ashley P. Taylor Two studies in mice published today (October 31) in Nature report the existence of several types of brain cells that had not been acknowledged before. These cell types are distinguished by their gene expression patterns, and within one cortical area, they perform distinct functions. For the gene expression study, led by the Allen Institute’s Hongkui Zeng, researchers performed single-cell RNA sequencing on more than 20,000 cells, most of which were neurons, in the visual cortex and the anterior lateral motor cortex of the mouse brain. Using this method, they identified 133 distinct cell types, both excitatory and inhibitory. They found that the various inhibitory neurons were present in both cortical areas but that the excitatory cell types kept to specific regions, as neuroscientists Aparna Bhaduri and Tomasz Nowakowski of the University of California, San Francisco, describe in an accompanying Nature commentary. “When we see not only cell types that people have identified before, but a number of new ones that are showing up in the data, it’s really exciting for us,” says Zeng in a press release. “It’s like we are able to put all the different pieces of the puzzle The other study, led by Karel Svoboda of the Janelia Research Campus of the Howard Hughes Medical Institute, examined the functions of two subtypes identified through the gene-expression study. These are excitatory cells called pyramidal tract neurons that reside within layer five of the anterior lateral motor cortex in mice. The researchers used optogenetics to activate either one neuronal subtype or the other in mice and at the same time monitored the activity of the two types of neurons during movement. They found that pyramidal tract neurons in the upper part of layer five seem to be involved in preparing for movement, whereas those in the lower part of layer five help execute it. © 1986 - 2018 The Scientist

Keyword: Brain imaging
Link ID: 25634 - Posted: 11.02.2018

Ian Sample Science editor Two men who were paralysed in separate accidents more than six years ago can stand and walk short distances on crutches after their spinal cords were treated with electrical stimulation. David Mzee, 28, and Gert-Jan Oskam, 35, had electrical pulses beamed into their spines to stimulate their leg muscles as they practised walking in a supportive harness on a treadmill. Doctors believe the timing of the pulses – to coincide with natural movement signals that were still being sent from the patients’ brains – was crucial. It appeared to encourage nerves that bypassed the injuries to form new connections and improve the men’s muscle control. In many spinal cord injuries a small portion of nerves remain intact but the signals they carry are too feeble to move limbs or support a person’s body weight. “They have both recovered control of their paralysed muscles and I don’t think anyone with a chronic injury, one they’ve had for six or seven years, has been able to do that before,” said Grégoire Courtine, a neuroscientist at the Swiss Federal Institute of Technology in Lausanne. “When you stimulate the nerves like this it triggers plasticity in the cells. The brain is trying to stimulate, and we stimulate at same time, and we think that triggers the growth of new nerve connections.” Mzee was paralysed in a gymnastics accident in 2010. He recovered the use of his upper body and some control of his right leg after intensive rehabilitation at a paraplegic centre in Zurich. Doctors there told him further improvement was unlikely, but after five months of training with electrical stimulation, he regained control of the muscles in his right leg and can now take a few steps without assistance. © 2018 Guardian News and Media Limited

Keyword: Regeneration; Robotics
Link ID: 25633 - Posted: 11.01.2018

Aimee Cunningham The appendix, a once-dismissed organ now known to play a role in the immune system, may contribute to a person’s chances of developing Parkinson’s disease. An analysis of data from nearly 1.7 million Swedes found that those who’d had their appendix removed had a lower overall risk of Parkinson’s disease. Also, samples of appendix tissue from healthy individuals revealed protein clumps similar to those found in the brains of Parkinson’s patients, researchers report online October 31 in Science Translational Medicine. Together, the findings suggest that the appendix may play a role in the early events of Parkinson’s disease, Viviane Labrie, a neuroscientist at the Van Andel Research Institute in Grand Rapids, Mich., said at a news conference on October 30. Parkinson’s, which affects more than 10 million people worldwide, is a neurodegenerative disease that leads to difficulty with movement, coordination and balance. It’s unknown what causes Parkinson’s, but one hallmark of the disease is the death of nerve cells, or neurons, in a brain region called the substantia nigra that helps control movement. Lewy bodies, which are mostly made of clumped bits of the protein alpha-synuclein (SN: 1/12/2013, p. 13), also build up in those neurons but the connection between the cells’ death and the Lewy bodies isn’t clear yet. Symptoms related to Parkinson’s can show up in the gut earlier than they do in the brain (SN: 12/10/2016, p. 12). So Labrie and her colleagues turned their attention to the appendix, a thin tube around 10 centimeters long that protrudes from the large intestine on the lower right side of the abdomen. Often considered a “useless organ,” Labrie said, “the appendix is actually an immune tissue that’s responsible for sampling and monitoring pathogens.” |© Society for Science & the Public 2000 - 2018.

Keyword: Parkinsons
Link ID: 25632 - Posted: 11.01.2018

Jeffrey M. Perkel Randal Burns recalls that the brain-science community was “abuzz” in 2011. Burns, a computer scientist at Johns Hopkins University in Baltimore, Maryland, was focusing on astrophysics and fluid dynamics data management at the time. But he was intrigued when Joshua Vogelstein, a neuroscientist and colleague at Johns Hopkins, told him that the first large-scale neural-connectivity data sets had just been collected and asked for his help to present them online. “It was the first time that you had data of that quality, at that resolution and scale, where you had the sense that you could build a neural map of an interesting portion of the brain,” says Burns. Vogelstein worked with Burns to build a system that would make those data — 20 trillion voxels’ worth — available to the larger neuroscience community. The team has now generalized the software to support different classes of imaging data and describes the system this week (J. T. Vogelstein et al. Nature Meth. 15, 846-847; 2018). NeuroData is a free, cloud-based collection of web services that supports large-scale neuroimaging data, from electron microscopy to magnetic resonance imaging and fluorescence photomicrographs. Key to its functionality, Vogelstein says, is the spatial database bossDB, which allows researchers to retrieve images of any section of the brain, at any resolution, and in several standard formats. Users can then explore those data using a tool known as Neuroglancer. As they navigate the images, the URL changes to reflect their specific view, allowing them to share particular visualizations with their colleagues. “These links become a core part of the way in which we communicate and pass data back and forth to one another,” says Forrest Collman, a neuroscientist at the Allen Institute for Brain Science in Seattle, Washington, and a co-author of the paper. © 2018 Springer Nature Limited.

Keyword: Brain imaging
Link ID: 25631 - Posted: 11.01.2018

A new study puts a fresh spin on what it means to “go with your gut.” The findings, published in Nature, suggest that gut bacteria may control movement in fruit flies and identify the neurons involved in this response. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “This study provides additional evidence for a connection between the gut and the brain, and in particular outlines how gut bacteria may influence behavior, including movement,” said Margaret Sutherland, Ph.D., program director at NINDS. Researchers led by Sarkis K. Mazmanian, Ph.D., professor of microbiology at the California Institute of Technology in Pasadena, and graduate student Catherine E. Schretter, observed that germ-free flies, which did not carry bacteria, were hyperactive. For instance, they walked faster, over greater distances, and took shorter rests than flies that had normal levels of microbes. Dr. Mazmanian and his team investigated ways in which gut bacteria may affect behavior in fruit flies. “Locomotion is important for a number of activities such as mating and searching for food. It turns out that gut bacteria may be critical for fundamental behaviors in animals,” said Dr. Mazmanian. Fruit flies carry between five and 20 different species of bacteria and Dr. Mazmanian’s team treated the germ-free animals with individual strains of those microbes. When the flies received Lactobacillus brevis, their movements slowed down to normal speed. L. brevis was one of only two species of bacteria that restored normal behavior in the germ-free flies.

Keyword: Movement Disorders
Link ID: 25630 - Posted: 11.01.2018

Serge Rivest The signals transmitted between neurons through synaptic connections are responsible for most, if not all, brain functions, from learning to decision-making. During brain development, synapses that are stimulated less often than others are eliminated through a process called pruning, whereas those that are highly stimulated are retained. This refines the brain’s ability to respond to stimuli and environmental cues. Microglia, the brain’s innate immune cells, have a key role in pruning — they engulf and digest synapses through a process called phagocytosis. But the mechanism that determines which synapses they avoid has been unclear. Writing in Neuron, Lehrman et al.1 describe a ‘don’t eat me’ signal, involving a protein called cluster of differentiation 47 (CD47), that prevents inappropriate synaptic pruning by microglia. About a decade ago, it was shown that synapses requiring elimination send an ‘eat me’ signal to microglia2 (Fig. 1a). This signal involves the proteins C1q and CR3, which are part of the complement cascade — a complex series of interactions that is best known for activating cells of the innate immune system to eliminate disease-causing organisms and damaged cells. ‘Don’t eat me’ signals act to limit the effects of ‘eat me’ signals in the immune system, but it was not known whether the same process occurs during synaptic pruning in the developing brain. CD47 is a cell-surface protein that has many immune functions, including acting as a ‘don’t eat me’ signal for macrophages3, microglia’s sister cells, which exist outside the brain. Lehrman et al. analysed whether CD47 is expressed in the dorsal lateral geniculate nucleus (dLGN), a region of the brain involved in vision. This region receives inputs from neurons called retinal ganglion cells (RGCs) that originate in the retina. The authors demonstrated in mice that, at five days after birth, synapses from RGCs to other neurons in the dLGN are being pruned at high levels. © 2018 Springer Nature Limited

Keyword: Development of the Brain; Neuroimmunology
Link ID: 25629 - Posted: 10.31.2018

Laura Sanders Taking a monthlong break from pot helps clear away young people’s memory fog, a small study suggests. The results show that not only does marijuana impair teenagers’ and young adults’ abilities to take in information, but that this memory muddling may be reversible. Scientists have struggled to find clear answers about how marijuana affects the developing brain, in part because it’s unethical to ask children to begin using a drug for a study. But “you can do the opposite,” says neuropsychologist Randi Schuster. “You can get kids who are currently using, and pay them to stop.” For a study published October 30 in the Journal of Clinical Psychiatry, Schuster and her colleagues did just that. The team recruited 88 Boston-area youngsters ages 16 to 25 years old who reported using marijuana at least once a week, and offered 62 of them money to quit for a month. Participants were paid more money as the experiment went along, with top earners banking $535 for their month without pot. The money “worked exceptionally well,” says Schuster, of Massachusetts General Hospital in Boston and Harvard Medical School. Urine tests showed that 55 of the 62 participants stopped using marijuana for the 30 days of the experiment. Along with regular drug tests, participants underwent attention and memory tests. Tricky tasks that required close monitoring of number sequences and the directions and locations of arrows revealed that, over the month, young people’s ability to pay attention didn’t seem to be affected by their newfound abstinence. |© Society for Science & the Public 2000 - 2018

Keyword: Drug Abuse; Learning & Memory
Link ID: 25628 - Posted: 10.31.2018

The transmission speed of neurons fluctuates in the brain to achieve an optimal flow of information required for day-to-day activities, according to a National Institutes of Health study. The results, appearing in PNAS, suggest that brain cells called astrocytes alter the transmission speed of neurons by changing the thickness of myelin, an insulation material, and the width of gaps in myelin called nodes of Ranvier, which amplify signals. “Scientists used to think that myelin could not be thinned except when destroyed in demyelinating diseases, such as multiple sclerosis,” said R. Douglas Fields, Ph.D., senior author and chief of the Section on Nervous System Development and Plasticity at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “Our study suggests that under normal conditions, the myelin sheath and structure of the nodes of Ranvier are dynamic, even in adults.” The brain is composed of neurons, which have extensions called axons that can stretch for long distances. Axons are wrapped by layers of myelin, which serve as insulation to increase the speed of signals relayed by neurons. Gaps between segments of myelin are called nodes of Ranvier, and the number and width of these gaps can also regulate transmission speed. “Myelin can be located far from the neuron’s synapse, where signals originate,” said NICHD’s Dipankar Dutta, Ph.D., the lead author of the study. “We wanted to understand how myelin, and the cells that regulate it, help synchronize signals that come from different areas of the brain.”

Keyword: Learning & Memory; Glia
Link ID: 25627 - Posted: 10.31.2018

By Sam Rose One of neuroscience’s foundational experiments wasn’t performed in a Nobel laureate’s lab, but occurred in a railyard in 1848 when an accidental explosion sent a tamping iron through 25 year-old Phineas Gage’s forehead. Gage survived, but those studying his history detailed distinct personality changes resulting from the accident. He went from even-tempered to impulsive and profane. The case is likely the earliest—and most famous—of using a “lesion” to link a damaged brain region to its function. In the ensuing decades, to study the brain was to study lesions. Lesion cases fed most of the era’s knowledge of the brain. One might think that modern neuroscience, with its immense toolkit of experimental techniques, no longer needs lesions like Gage’s to parse the brain’s inner workings. Lesion studies, though, seem to be having a revival. A new method called lesion network mapping is clearing the cobwebs off the lesion study and uniting it with modern brain connectivity data. The results are revealing surprising associations between brain regions and disorders. Thankfully, most lesions aren’t a tamping iron through the forehead. Strokes, hemorrhages, or tumors make up most lesion cases. 19th century neurologists like Paul Broca made foundational discoveries by studying patients with peculiar symptoms resulting from these common neurological insults. Broca and his contemporaries synthesized a theory of the brain from lesions: that the brain is segmented. Different regions control different functions. Lesion studies lend a lawyerly logic to the brain: if region X is destroyed and function Y no longer occurs, then region X must control function Y. Advertisement © 2018 Scientific American,

Keyword: Stroke
Link ID: 25626 - Posted: 10.31.2018

Anna Nowogrodzki On a cold morning in Minneapolis last December, a man walked into a research centre to venture where only pigs had gone before: into the strongest magnetic resonance imaging (MRI) machine built to scan the human body. First, he changed into a hospital gown, and researchers made sure he had no metal on his body: no piercings, rings, metal implants or pacemakers. Any metal could be ripped out by the immensely powerful, 10.5-tesla magnet — weighing almost 3 times more than a Boeing 737 aeroplane and a full 50% more powerful than the strongest magnets approved for clinical use. Days earlier, he had passed a check-up that included a baseline test of his sense of balance to make sure that any dizziness from exposure to the magnets could be assessed properly. In the MRI room at the University of Minnesota’s Center for Magnetic Resonance Research, he lay down inside a 4-metre-long tube, surrounded by 110 tonnes of magnet and 600 tonnes of iron shielding, for an hour’s worth of imaging of his hips, whose thin cartilage would test the limits of the machine’s resolution. The centre’s director, Kamil Ugurbil, had been waiting for years for this day. The magnet faced long delays because the liquid helium needed to fill it was in short supply. After the machine was finally delivered, on a below-freezing day in 2013, it took four years of animal testing and ramping up the field strength before Ugurbil and his colleagues were comfortable sending in the first human. Even then, they didn’t quite know what they’d see. But it was worth the wait: when the scan materialized on screen, the fine resolution revealed intricate details of the wafer-thin cartilage that protects the hip socket. “It was extremely exciting and very rewarding,” Ugurbil says. © 2018 Springer Nature Limited

Keyword: Brain imaging
Link ID: 25625 - Posted: 10.31.2018

Jon Hamilton An ancient part of the brain long ignored by the scientific world appears to play a critical role in everything from language and emotions to daily planning. It's the cerebellum, which is found in fish and lizards as well as people. But in the human brain, this structure is wired to areas involved in higher-order thinking, a team led by researchers from Washington University in St. Louis reports Thursday in the journal Neuron. "We think that the cerebellum is acting as the brain's ultimate quality control unit," says Scott Marek, a postdoctoral research scholar and the study's first author. The finding adds to the growing evidence that the cerebellum "isn't only involved in sensory-motor function, it's involved in everything we do," says Dr. Jeremy Schmahmann, a neurology professor at Harvard and director of the ataxia unit at Massachusetts General Hospital. Schmahmann, who wasn't involved in the new study, has been arguing for decades that the cerebellum plays a key role in many aspects of human behavior, as well as mental disorders such as schizophrenia. But only a handful of scientists have explored functions of the cerebellum beyond motor control. "It's been woefully understudied," says Dr. Nico Dosenbach, a professor of neurology at Washington University whose lab conducted the study. Even now, many scientists think of the cerebellum as the part of the brain that lets you pass a roadside sobriety test. It helps you do things like walk in a straight line or stand on one leg or track a moving object — if you're not drunk. © 2018 npr

Keyword: Attention; Language
Link ID: 25624 - Posted: 10.27.2018