By Matt Reynolds Putting on a brave face won’t fool this algorithm. A new system that rates how much pain someone is in just by looking at their face could help doctors decide how to treat patients. By examining tiny facial expressions and calibrating the system to each person, it provides a level of objectivity in an area where that’s normally hard to come by. “These metrics might be useful in determining real pain from faked pain,” says Jeffrey Cohn at the University of Pittsburgh in the US. The system could make the difference between prescribing potentially addictive painkillers and catching out a faker. Objectively measuring pain levels is a tricky task, says Dianbo Liu, who created the system with his colleagues at the Massachusetts Institute of Technology. People experience and express pain differently, so a doctor’s estimate of a patient’s pain can often differ from a self-reported pain score. In an attempt to introduce some objectivity, Liu and his team trained an algorithm on videos of people wincing and grimacing in pain. Each video consisted of a person with shoulder pain, who had been asked to perform a different movement and then rate their pain levels. The result was an algorithm that can use subtle differences in facial expressions to inform a guess about how a given person is feeling. Certain parts of the face are particularly revealing, says Liu. Large amounts of movement around the nose and mouth tended to suggest higher self-reported pain scores. © Copyright New Scientist Ltd.

Keyword: Pain & Touch; Emotions
Link ID: 24026 - Posted: 09.02.2017

By Brian Levine, Carrie Esopenko There are two ways to go about studying a disease. Let’s call them the retrospective and prospective methods. In the retrospective method, scientists identify individuals with the disease and ask about the circumstances that led to the illness. In the prospective method, they start with a representative sample of people and track them over time to see who develops the disease. Both methods have yielded important discoveries, but the retrospective method is much more prone to distortion than the prospective method. Consider the following example. Using the retrospective method, 100 percent of alcoholics drink alcohol. Yet drinking alcohol does not necessarily lead to alcoholism, as can be determined by the prospective method in which it can be seen that the proportion of those who enjoy alcoholic drinks and become alcoholics is less than 100 percent. Boston University’s Chronic Traumatic Encephalopathy (CTE) Center recently reported that 99 percent of NFL alumni who made brain donations at the time of death have CTE (a similar finding was reported in 2013). While researchers acknowledge that those who make brain donations are not representative of retired NFL players (much less those with sports-related concussions in general) it is remarkably easy to make the same mistake as in the alcoholism example—that is, making the assumption that this finding generalizes to the broader population of athletes exposed to concussion. © 2017 Scientific America

Keyword: Brain Injury/Concussion
Link ID: 24025 - Posted: 09.02.2017

By Aggie Mika A drawing based on one of Ramón y Cajal’s “selfies,” with his pyramidal neuron illustrations around him. According to Hunter, Ramón y Cajal obsessively took photos of himself throughout his life. DAWN HUNTER, WITH PERMISSIONIt was in the spring of 2015 when Dawn Hunter saw Santiago Ramón y Cajal’s century-old elaborate drawings of the nervous system in person for the first time, at the late scientist’s exhibit within the National Institutes of Health. She was instantly compelled to recreate his ornate illustrations herself. “I just immediately started drawing [them] because they were so beautiful,” says Hunter, a visual art and design professor at the University of South Carolina. “His drawings in person were even more amazing than I thought they were going to be.” Ramón y Cajal’s drawings first caught Hunter’s eye while doing research for a neuroanatomy textbook she was asked to illustrate in 2012. Ramón y Cajal, hailed by many as the father of modern neuroscience, depicted the inner workings of the brain through thousands of intricate illustrations before his death in 1934. He first posited that unique, inter-connected entities called neurons were the central nervous system’s fundamental unit of function. A recreation of Ramón y Cajal Cajal’s retina depiction. “His retina drawing is particularly interesting because he combines both of his main drawing techniques. . . . Part of the drawing is designed and drawn out preliminarily and part of it is drawn from observation,” says Hunter.DAWN HUNTER, WITH PERMISSIONWhile recreating his work, Hunter was able to shed unprecedented light on how he went about his craft. “Some neuroscientists erroneously think that he traced all of his drawings from a projection, which he did not,” she says. This involves expanding a magnified image of the specimen being viewed under the microscope onto the table using a drawing tube or camera lucida. While he did use this tool in certain instances, she says, he drew some of his drawings, like his famous pyramidal neurons, “through his observation with his eye,” a technique known as perceptual drawing. © 1986-2017 The Scientist

Keyword: Brain imaging
Link ID: 24024 - Posted: 09.02.2017

By Mitch Leslie When people with asthma have trouble breathing, they may reach for an inhaler containing salbutamol, a drug that expands the airways. Salbutamol may have another beneficial effect—protecting against Parkinson’s disease. Individuals who inhaled the highest doses of salbutamol were about half as likely to develop the devastating neurological condition as those who didn’t take the drug, a study reveals. “I’m sure it’s going to be a landmark paper,” says neurologist Joseph Jankovic of Baylor College of Medicine in Houston, Texas, who wasn’t involved in the research. In Parkinson’s disease, gobs of the protein α-synuclein accumulate in certain brain cells and may kill them. Scientists have tried to craft drugs that speed the elimination of the protein or prevent it from clumping. Neurologist and genomicist Clemens Scherzer of Harvard Medical School in Boston and colleagues decided to try a different strategy. “We wanted to find a drug that could turn down the production of α-synuclein,” he says. To identify promising compounds, the team grew human nerve cells in the lab and tested whether more than 1100 medications, vitamins, dietary supplements, and other molecules altered their output of α-synuclein. Three of the drugs that cut the protein’s production, including salbutamol, work by stimulating the b2-adrenoreceptor—a molecule on some body cells that triggers a variety of effects, including relaxing the airways. The researchers found that these drugs appear to alter how tightly the DNA containing the α-synuclein gene coils, and thus whether the gene is active. © 2017 American Association for the Advancement of Science

Keyword: Parkinsons
Link ID: 24023 - Posted: 09.01.2017

You may well be yawning just reading this - it's contagious. Now researchers have looked at what happens in our brains to trigger that response. A University of Nottingham team found it occurs in a part of the brain responsible for motor function. The primary motor cortex also plays a part in conditions such as Tourette's syndrome. So the scientists say understanding contagious yawning could also help understand those disorders too. Contagious yawning is a common form of echophenomena - the automatic imitation of someone else's words or actions. Echophenomena is also seen in Tourette's, as well as in other conditions, including epilepsy and autism. To test what's happening in the brain during the phenomenon, scientists monitored 36 volunteers while they watched others yawning. In the study, published in the journal Current Biology, some were told it was fine to yawn while others were told to stifle the urge. The urge to yawn was down to how each person's primary motor cortex worked - its "excitability". And, using external transcranial magnetic stimulation (TMS), it was also possible to increase "excitability" in the motor cortex and therefore people's propensity for contagious yawns. Georgina Jackson, professor of cognitive neuropsychology who worked on the study, said the finding could have wider uses: "In Tourette's, if we could reduce the excitability we might reduce the ticks, and that's what we are working on." Prof Stephen Jackson, who also worked on the research, added: "If we can understand how alterations in cortical excitability give rise to neural disorders we can potentially reverse them. "We are looking for potential non-drug, personalised treatments, using TMS that might be effective in modulating imbalances in the brain networks." © 2017 BBC

Keyword: Attention
Link ID: 24022 - Posted: 09.01.2017

By Clare Wilson Some people who are blind can echolocate like bats, making clicks with their mouths that help them understand the environment around them. Now researchers are beginning to understand how this works, so non-sighted people may one day be able to learn the technique. While many people who are blind get information from ambient echoes, only a few make noises themselves to echolocate. Some, such as Daniel Kish (pictured), are so proficient they can draw a sketch of a room after clicking their way around it, or even go mountain biking along unfamiliar routes. Daniel Kish: Blind children should be allowed to echolocate like me Previous research revealed that this human echolocation involves some brain areas that are used for vision in sighted people. Kish, who was blind almost from birth, thinks he experiences the sensations as something akin to images. “It’s not computational. There’s a real palpable experience of the image as a spatial representation – here are walls, here are the corners, here is the presence of objects.” In the latest study, Lore Thaler of Durham University, UK, and her team carried out the first in-depth acoustic analysis of the mouth clicks. They worked with Kish and two other blind echolocators from the Netherlands and Austria. © Copyright New Scientist Ltd.

Keyword: Hearing
Link ID: 24021 - Posted: 09.01.2017

Jud Esty-Kendall Josh Hanagarne, 39, and his son Max, 9, recently sat down at StoryCorps to talk about Tourette's syndrome. Josh has dealt with Tourette's since he was Max's age and while Max hasn't been officially diagnosed, he has started to show symptoms, too. Courtesy of StoryCorps Josh Hanagarne is a dad, a librarian and an author, who also has an extreme form of Tourette's syndrome. But he doesn't let it and his tics — his involuntary movements and sounds — stop him from living his life. He says he actually chose to work in a library because it was the quietest place he knew of. Josh first started showing symptoms of Tourette's syndrome when he was in elementary school, about the same age that his son Max is now. Not everyone with Tourette's syndrome has the same tics. Max, 9, describes his dad's as "you hitting yourself and making a lot of noise." "You've seen me hit myself hard enough to almost knock myself out," Josh, 39, says. "I also do all of the blinking and the face things and the little ahem noises." Josh's form of Tourette's is so extreme that his tics have been severe enough that they've put him in the hospital before. "To me, it feels like when you have that urge to sneeze so bad that you just feel like you'll just go insane if you don't let the sneeze out," Josh says. But he says that's not the most difficult part of living with Tourette's. "The hardest thing I do every day is decide to go outside or not, because I know when I walk into a group of strangers, I will yell or I will do something weird and they will all look at me," Josh says. © 2017 npr

Keyword: Tourettes
Link ID: 24020 - Posted: 09.01.2017

Ewen Callaway Japanese researchers report promising results from an experimental therapy for Parkinson’s disease that involves implanting neurons made from ‘reprogrammed’ stem cells into the brain. A trial conducted in monkeys with a version of the disease showed that the treatment improved their symptoms and seemed to be safe, according to a report published on 30 August in Nature1. The study’s key finding — that the implanted cells survived in the brain for at least two years without causing any dangerous effects in the body — provides a major boost to researchers’ hopes of testing stem-cell treatments for Parkinson’s in humans, say scientists. Jun Takahashi, a stem-cell scientist at Kyoto University in Japan who led the study, says that his team plans to begin transplanting neurons made from induced pluripotent stem (iPS) cells into people with Parkinson’s in clinical trials soon. The research is also likely to inform several other groups worldwide that are testing different approaches to treating Parkinson’s using stem cells, with trials also slated to begin soon. Parkinson’s is a neurodegenerative condition caused by the death of cells called dopaminergic neurons, which make a neurotransmitter called dopamine in certain areas of the brain. Because dopamine-producing brain cells are involved in movement, people with the condition experience characteristic tremors and stiff muscles. Current treatments address symptoms of the disease but not the underlying cause. © 2017 Macmillan Publishers Limited,

Keyword: Parkinsons; Stem Cells
Link ID: 24019 - Posted: 08.31.2017

By Ryan Cross Weight loss seems to come easiest to those who want it least. Every year, hundreds of thousands suffer from the loss of appetite that comes with tumor-induced anorexia, which can accompany many late-stage cancers. Now, researchers from three major pharmaceutical companies have independently published papers showing that the culprit behind this condition—a protein called growth differentiation factor-15 (GDF15)—helps mice, rats, and monkeys lose weight without any apparent side effects. “The idea of having another medication to add to our armamentarium is exciting news,” says Katherine Saunders, an obesity medicine physician at Weill Cornell Medicine in New York City who was not involved with the work. There are currently five U.S. Food and Drug Administration–approved obesity medications for long-term weight management, which can help patients lose 5% to 8% of their body weight on average. “That’s very limited,” Saunders says, adding that many drugs used to treat obesity don’t have the same level of specificity as GDF15. GDF15’s potential as a weight-loss agent was first discovered by Samuel Breit, an immunologist and physician at St. Vincent's Hospital in Sydney, Australia. He saw levels of the protein rise 10 to 100 times higher than normal during tumor-induced anorexia in mice with prostate tumors and in humans with advanced prostate cancer. Breit also showed that GDF15 likely exerts its effects through the brain—though he says that until now the protein’s target has befuddled scientists. © 2017 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 24018 - Posted: 08.31.2017

By Colin Hendrie and Alisdair Pickles The current global crisis of depressive illness has a simple root cause: a failure of treatment. This is the result of a broken scientific process that has for nearly 70 years fallen short in delivering the drug therapies it was set up to provide. Given existing antidepressants don’t work for many people, the excitement surrounding the development of a new class of treatments from recreational drugs such as magic mushrooms is understandable. But there are strong reasons to doubt they will have the kind of impact hoped for. Instead, we are more likely to be seeing the latest episode in a long-running saga of repeated disappointment. This saga began when antidepressant use became widespread in the 1950s and 1960s. It was hoped they would have the same transformative effect on mental illness that antibiotics had on non-viral infectious diseases. As it turned out, antidepressants were only of value to some people with depression. Studies involving thousands of people with the condition reveal that the proportion seeing a clinically significant response to antidepressants is often very similar to that seen with a placebo, which is about 40 per cent. In double-blind, placebo-controlled studies, antidepressants don’t fare well. This helps to explain why, by the end of the 20th century, Big Pharma was floundering over the development of new drugs for depression. In 2010, many companies stopped such work. © Copyright New Scientist Ltd.

Keyword: Depression; Drug Abuse
Link ID: 24017 - Posted: 08.31.2017

By Mo Costandi Voluntary movements are one of the brain’s main “outputs,” yet science still knows very little about how networks of neurons plan, initiate and execute them. Now, researchers from Columbia University and the Champalimaud Center for the Unknown in Lisbon, Portugal, say they have discovered an “activity map” that the brain uses to guide animals’ movements. The findings, published Wednesday in Neuron, could advance our understanding of how the brain learns new movements—and of what goes wrong in related disorders such as Parkinson's disease. Movements are controlled and coordinated by multiple brain structures including the primary motor cortex. Located at the back of the frontal lobe, it contains cells whose long fibers extend down through the spinal cord, where they contact “secondary” motor neurons that signal the body muscles. A set of deep brain structures called the basal ganglia are also critical for movement, as evidenced by their degeneration in conditions such as Parkinson’s. One component of the basal ganglia, called the striatum, receives information about possible actions from the motor cortex and is thought to be involved in selecting, preparing and executing the appropriate commands before they are sent to the body. Earlier research had shown that signals leave the striatum along one of two distinct pathways: one that facilitates movement, and another that suppresses it. A number of more recent studies show that both pathways are active during motion, however, suggesting that they do not act by simply sending “stop” and “go” signals. And although it has long been suspected that different groups of neurons in the striatum represent distinct actions, exactly how they might do so has remained unclear. © 2017 Scientific American

Keyword: Parkinsons; Brain imaging
Link ID: 24016 - Posted: 08.31.2017

BY Patrick Skerrett, An international study is casting doubt on the wisdom of eating lots of carbohydrates. Photo by Flickr user Dani Armengol Garreta Fat, once a dirty word when it came to diet, has been edging back toward respectability. New results from a huge international study help continue to reshape its image while at the same time casting doubt on the wisdom of eating lots of carbohydrates and questioning the “more is better” recommendations for eating fruits and vegetables. The latest evidence comes from data released Tuesday by the international Prospective Urban Rural Epidemiology (PURE) study. Its research team recorded the eating habits of 135,000 adults in 18 countries — including high-income, medium-income, and low-income nations — and followed the participants’ health for more than seven years on average. Among the PURE participants, those with the highest intake of dietary fat (35 percent of daily calories) were 23 percent less likely to have died during the study period than those with the lowest fat intake (10 percent of calories). The rates of various cardiovascular diseases were essentially the same across fat intake, while strokes were less common among those with a high fat intake. Upending conventional wisdom, the findings for carbohydrate intake went in the opposite direction. PURE participants with the highest carbohydrate intake (77 percent of daily calories) were 28 percent more likely to have died than those with the lowest carbohydrate intake (46 percent of calories). The results were presented at the European Society of Cardiology meeting in Barcelona, and published in the Lancet. © 1996 - 2017 NewsHour Productions LLC.

Keyword: Obesity
Link ID: 24015 - Posted: 08.31.2017

By The Scientist Staff Researchers demonstrated that the mouse subiculum, a brain region associated with the hippocampus, is important for recalling certain types of memories, but it doesn’t appear to play a role in forming them. When they optogenetically turned off neurons within the subiculum, mice’s abilities to retrieve a memory they had previously formed was disrupted. Some scientists think that brain circuits responsible for forming memories are the same as those necessary for retrieving them, write the authors in their report. These data, however, offer evidence to the contrary. See D.S. Roy et al., “Distinct neural circuits for the formation and retrieval of episodic memories,” Cell, doi:10.1016/j.cell.2017.07.013, 2017. © 1986-2017 The Scientist

Keyword: Learning & Memory; Brain imaging
Link ID: 24014 - Posted: 08.31.2017

By Meredith Wadman Luca Rossi tried to hang himself in a bedroom in Perugia, Italy, in 2012. Suspended by his belt from a wardrobe, he had begun to choke when his fiancée unexpectedly walked in. He struggled to safety, defeated even in this intended last act. The 35-year-old physician had everything to live for: a medical career, plans for a family, and supportive parents. But Rossi* was addicted to crack cocaine. He had begun his habit not long after medical school, confidently assuming that he could control the drug. Now, it owned him. Once ebullient and passionate, he no longer smiled or cried. He knew he might be endangering his patients, but even that didn’t matter. He was indifferent to all except obtaining his next fix. “It pushes you to suicide because it fills you with your own emptiness,” he says. In the first months after his near suicide, Rossi didn’t drop his $3500-a-month habit. Early in 2013, he learned that his fiancée was pregnant. Frightened by impending fatherhood, he smoked even more. He didn’t—couldn’t—stop. Then, in April 2013, Rossi’s father, a chemist, happened upon a local newspaper article describing work just published in Nature. Neuroscientists led by Antonello Bonci and Billy Chen at the National Institute on Drug Abuse (NIDA) in Baltimore, Maryland, had studied rats trained to seek cocaine compulsively—animals so powerfully addicted that they tolerated repeated electric shocks to their feet to get their fixes. The rats had also been genetically engineered so that their neurons could be controlled with light. When the researchers stimulated the animals’ brains in an area that regulates impulse control, the rats essentially kicked their habit. “They would almost instantaneously stop searching for cocaine,” Bonci says. © 2017 American Association for the Advancement of Science

Keyword: Brain imaging; Drug Abuse
Link ID: 24013 - Posted: 08.30.2017

Maria Temming Bacteria living in the human gut have strange influence over mood, depression and more, but it has been unclear exactly how belly-dwelling bacteria exercise remote control of the brain (SN: 4/2/16, p. 23). Now research in rodents suggests that gut microbes may alter the inventory of microRNAs — molecules that help keep cells in working order by managing protein production — in brain regions involved in controlling anxiety. The findings, reported online August 25 in Microbiome, could help scientists develop new treatments for some mental health problems. Mounting evidence indicates “that the way we think and feel might be able to be controlled by our gut microbiota,” says study coauthor Gerard Clarke, a psychiatrist at University College Cork in Ireland. For instance, the presence or absence of gut bacteria can influence whether a mouse exhibits anxiety-like behaviors, such as avoiding bright lights or open spaces. Clarke and colleagues compared normal mice, whose gastrointestinal tracts were teeming with bacteria, with mice bred in sterile environments, whose guts didn’t contain any microbes. The researchers discovered that in brain regions involved in regulating anxiety — the amygdala and prefrontal cortex — microbe-free mice had an overabundance of some types of microRNA and a shortage of others compared with normal mice. After scientists exposed some sterilized mice to microbes, the rodents’ microRNA levels more closely matched those of normal mice. |© Society for Science & the Public 2000 - 2017.

Keyword: Emotions; Stress
Link ID: 24012 - Posted: 08.30.2017

By Michael Nedelman, CNN (CNN)Emily Gavigan was convinced that a nearby truck was following her. Someone was after her. She was a sophomore at the University of Scranton in January 2009 when the "bizarre" behavior began, said her father, Bill. Her parents noticed that she had been rambling, not making any sense. At one point, she called her family and friends to warn them: Something terrible was going to happen to all of them. "Emily was like a different person. We didn't know who she was," Bill Gavigan said. "We had gone from having this daughter who was perfectly normal, happy, vibrant ... with a bright future ahead. "All of a sudden, this all came crashing down." Then, one day, Gavigan disappeared. "We didn't know where she was for more than 24 hours," her father said. She had gotten in her car and driven from Pennsylvania to New Jersey with no money. She went right through toll booths without paying. But she eventually found her way back to her grandparents' house, still convinced that she was being followed. Her grandfather peered out the window, looking for something suspicious. But they soon realized there was no one after her. "I get emotional when I think about it," said Gavigan's grandfather Joseph Chiumento. Her parents showed up and took her to the hospital. Emily Gavigan began exhibiting odd behavior when she was 19, which doctors mistook for a mental illness. Emily Gavigan began exhibiting odd behavior when she was 19, which doctors mistook for a mental illness. Say, 'I love you, dad' Doctors initially thought Gavigan had a mental illness. She spent time in different psychiatric facilities, which made her family uneasy. One in particular reminded her father of the movie "One Flew Over the Cuckoo's Nest." "They just kept trying medication after medication after medication, and none of it worked," Bill Gavigan said. Things kept getting worse. There was some numbness in her face and hands, and she would develop seizures. © 2016 Cable News Network.

Keyword: Schizophrenia; Neuroimmunology
Link ID: 24011 - Posted: 08.30.2017

By Helen Briggs BBC News They migrate thousands of kilometres across the sea without getting lost. The Arctic tern, for instance, spends summer in the UK, then flies to the Antarctic for the winter. Yet, scientists are still unsure exactly how birds perform such extreme feats of migration, arriving in the right place every year. According to new research, smell plays a key role when birds are navigating long distances over the ocean. Researchers from the universities of Oxford, Barcelona and Pisa temporarily removed seabirds' sense of smell before tracking their movements. They found the birds could navigate normally over land, but appeared to lose their bearings over the sea. This suggests that they use a map of smells to find their way when there are no visual cues. Previous experiments had suggested that removing birds' sense of smell impairs homing ability. However, some had questioned whether sensory deprivation might impair some other function, such as the ability to search for food. ''Our new study eliminates these objections, meaning it will be very difficult in future to argue that olfaction is not involved in long-distance oceanic navigation in birds,'' said study researcher Oliver Padget of Oxford University's Department of Zoology. The researchers studied 30 Scopoli's shearwaters living off the coast of Menorca. The birds nest in the Mediterranean, but spend the non-breeding season in the Atlantic, including areas off the west coast of Africa and the east coast of Brazil. Some of the birds were made to temporarily lose their sense of smell through nasal irrigation with zinc sulphate; another group carried small magnets; and a third group acted as a control. © 2017 BBC.

Keyword: Animal Migration; Chemical Senses (Smell & Taste)
Link ID: 24010 - Posted: 08.30.2017

By Jessica Hamzelou For the first time, researchers have shown in a randomised trial that looking at photos of thin women is enough to shape a person’s beauty ideals. It has long been thought that images of slender women in the media influence what people find attractive, and can make a person feel unhappy with their body. But these pictures are now ubiquitous in many places, making testing this idea difficult. To find people who haven’t been exposed to such images, Jean-Luc Jucker at the University of Neuchâtel, Switzerland, and his team travelled to rural villages along the Mosquito Coast of Nicaragua. At first, these villages had no electricity beyond the odd solar panel used to power a bulb. The Nicaraguan government is in the process of adding villages like these to the electricity grid – which is likely to bring TV with it. “When they get electricity, people generally say they want two things – a fridge and a television,” says Jucker. “They go from having no television to 100 channels.” Before two villages were hooked up to the grid, Jucker’s team recruited 80 volunteers from them. These included men and women aged between 16 and 78. The volunteers were first asked to create their “ideal” body shape for a woman, using computer software that enabled them to generate women of different shapes and sizes. © Copyright New Scientist Ltd.

Keyword: Anorexia & Bulimia
Link ID: 24009 - Posted: 08.30.2017

By Diana Kwon Sometimes our brains are on acid—literally. A main source of these temporary surges is the carbon dioxide that is constantly released as the brain breaks down sugar to generate energy, which subsequently turns into acid. Yet the chemistry in a healthy human brain tends to be relatively neutral, because standard processes including respiration—which expels carbon dioxide—help maintain the status quo. Any fleeting acidity spikes usually go unnoticed. But a growing body of work has suggested that for some people, even slight changes in this balance may be linked with certain psychiatric conditions including panic disorders. New findings this month provide additional evidence that such links are real—and suggest they may extend to schizophrenia and bipolar disorder. There were earlier hints that this was the case: Post-mortem studies of dozens of human brains revealed lower pH (higher acidity levels) in patients with schizophrenia and bipolar disorder. Multiple studies in the past few decades have found that when people with panic disorders are exposed to air with a higher-than-normal concentration of carbon dioxide—which can combine with water in the body to form carbonic acid—they are more likely to experience panic attacks than healthy individuals are. Other research has revealed that the brains of people with panic disorders produce elevated levels of lactate—an acidic source of fuel that is constantly produced and consumed in the energy-hungry brain. © 2017 Scientific American

Keyword: Schizophrenia
Link ID: 24008 - Posted: 08.29.2017

By DAVID DeSTENO, CYNTHIA BREAZEAL and PAUL HARRIS Why is educational technology such a disappointment? In recent years, parents and schools have been exposing children to a range of computer-mediated instruction, and adults have been turning to “brain training” apps to sharpen their minds, but the results have not been encouraging. A six-year research project commissioned by the Department of Education examined different cybertechnology programs across thousands of students in hundreds of schools and found little to no evidence that they improved academic performance. Unfortunately, it appears the same goes for cognitive-training programs. Lumos Labs, the company behind Lumosity, one of the leading programs in this area, agreed to pay $2 million to settle charges by the Federal Trade Commission that it misled customers with claims that Lumosity improved people’s performance in school and at work. In our view, the problem stems partly from the fact that the designers of these technologies rely on an erroneous set of assumptions about how the mind learns. Yes, the human brain is an amazing information processor, but it evolved to take in, analyze and store information in a specific way: through social interaction. For millenniums, the environs in which we learned best were social ones. It was through other people’s testimony or through interactive discourse and exploration with them that we learned facts about our world and new ways of solving problems. And it’s precisely because of this history that we can expect the mind to be socially tuned, meaning that it should rely on and incorporate social cues to facilitate learning. © 2017 The New York Times Company

Keyword: Learning & Memory
Link ID: 24007 - Posted: 08.29.2017