By Julia Shaw Every memory you have ever had is chock-full of errors. I would even go as far as saying that memory is largely an illusion. This is because our perception of the world is deeply imperfect, our brains only bother to remember a tiny piece of what we actually experience, and every time we remember something we have the potential to change the memory we are accessing. I often write about the ways in which our memory leads us astray, with a particular focus on ‘false memories.’ False memories are recollections that feel real but are not based on actual experience. For this particular article I invited a few top memory researchers to comment on what they wish everyone knew about their field. First up, we have Elizabeth Loftus from the University of California, Irvine, who is one of the founders of the area of false memory research, and is considered one of the most ‘eminent psychologists of the 20th century.’ Elizabeth Loftus says you need independent evidence to corroborate your memories. According to Loftus: “The one take home message that I have tried to convey in my writings, and classes, and in my TED talk is this: Just because someone tells you something with a lot of confidence and detail and emotion, it doesn't mean it actually happened. You need independent corroboration to know whether you're dealing with an authentic memory, or something that is a product of some other process.” Next up, we have memory scientist Annelies Vredeveldt from the Vrije Universiteit Amsterdam, who has done fascinating work on how well we remember when we recall things with other people. © 2016 Scientific American,

Keyword: Learning & Memory
Link ID: 22530 - Posted: 08.09.2016

By TATIANA SCHLOSSBERG Need a laugh? Get online and take a look at videos of baby Japanese macaques smiling as they sleep. Their faces twitch, usually just on one side and for less than a second. A lip curls, a nose wrinkles — as if they were hairy, wry elves. Newborn Japanese macaques -- like humans and chimpanzees -- were found to make facial expressions called "spontaneous smiles." Watch the full video. Credit Kyoto University Primate Research Institute Maybe you don’t laugh, maybe you just smile back — O.K., fine. But you may owe that smile to the human version of this infant’s facial spasm. Some scientists suspect spontaneous smiles in these monkeys echo the development of our own expressions. Scientists from the Primate Research Institute at Kyoto University in Japan have observed these spontaneous smiles in Japanese macaques for the first time, according to a new study published in the journal Primates. Spontaneous smiles have previously been observed in infant humans and chimpanzees, but this is the first time they have been seen in another primate species. The scientists watched seven macaque monkeys for an average of 44 minutes, during which the monkeys happened to fall asleep. During REM sleep, each of the monkeys spontaneously smiled at least once, for a little less than a second on average. All told, the seven monkeys smiled 58 times, mostly on the left side of their faces. Human and macaque infants alike primarily smile on one side of their faces. But after two months, human babies begin to smile bilaterally. Around the same time, they also begin to offer up “social smiles,” indicating to others a feeling of happiness. According to the study, scientists think that the earliest spontaneous smiles are key to the development of the zygomaticus major muscle, which is responsible for moving your lips up or to the side, allowing you to smile, among other things. Spontaneous smiles in these monkeys echo the development of our own expressions. Watch the full video.

Keyword: Emotions; Evolution
Link ID: 22529 - Posted: 08.09.2016

Seth Stephens-Davidowitz Feeling worried? These days, much of America is. Over the past eight years, Google search rates for anxiety have more than doubled. They are higher this year than they have been in any year since Google searches were first tracked in 2004. So far, 2016 has been tops for searches for driving anxiety, travel anxiety, separation anxiety, anxiety at work, anxiety at school and anxiety at home. Americans have also become increasingly terrified of the morning. Searches for “anxiety in the morning” have risen threefold over the past decade. But this is nothing compared with the fear of night. Searches for “anxiety at night” have risen ninefold. For years, I have confidently pontificated on topics that I think are important but that I have little experience of — child abuse, racism, sexism, sex. Now I am ready to tackle a topic I actually know something about. Over the past few weeks, I’ve taken a break from worrying about my own anxiety to studying our country’s. While I am not sure I totally nailed down why anxiety seems to have risen so much during the Obama era, I did learn a lot. The places where anxiety is highest are not where I would have expected. When I was growing up, if you had asked me which people were the most anxious, I would have said New York Jews. And a decade of interacting with our country’s urban intelligentsia, Jewish and otherwise, has confirmed that pretty much all of us are a neurotic mess. © 2016 The New York Times Company

Keyword: Stress
Link ID: 22528 - Posted: 08.08.2016

By PHYLLIS KORKKI Ever experienced a bout of anxiety at work? I just did. One day last week I had several assignments to finish in quick succession. I could feel thoughts pinging around in my brain as I tried and failed to decide what to focus on first. Once I was able to get the pandemonium under control, my brain felt like mush. So what did I do? I breathed deeply from the middle of my body. I imagined the top of my head, and pictured arrows coming out the sides of my shoulders. I stood up for a while and then walked around the newsroom. And went back to work. These simple solutions to anxiety are not so easy to practice in an era of multitasking, multiple screens and mindless distractions. I learned them only after signing a contract to write a book — and becoming so anxious about it that I developed back and stomach pains. Unable to score a prescription for Klonopin (it’s addictive, my doctor said), I was reduced to seeking out natural methods to relieve my anxiety. The methods I learned helped me write the book. But they also made me realize that workers of all stripes could use them to reduce stress, and to think more clearly and creatively. My first stop was Belisa Vranich, a clinical psychologist who teaches — or rather reteaches — people how to breathe. Dimly I sensed that the way I was inhaling and exhaling was out of whack, and she confirmed it by giving me some tests. First off, like most people, I was a “vertical” breather, meaning my shoulders moved upward when I inhaled. Second, I was breathing from my upper chest, where the lungs don’t have much presence. © 2016 The New York Times Company

Keyword: Stress
Link ID: 22527 - Posted: 08.08.2016

Pete Etchells Mind gamers: How good do you reckon your memory is? We might forget things from time to time, but the stuff we do remember is pretty accurate, right? The trouble is, our memory isn’t as infallible as we might want to believe, and you can test this for yourself using the simple experiment below. All done? Great. Now we’re going to do a simple recognition test – below is another list of words for you to look at. Without looking back, note down which of them appeared in the three lists you just scanned. No cheating! If you said that top, seat and yawn were in the lists, you’re spot on. Likewise, if you think that slow, sweet and strong didn’t appear anywhere, you’re also right. What about chair, mountain and sleep though? They sound like they should have been in the lists, but they never made an appearance. Some of you may have spotted this, but a lot of people tend to say, with a fair amount of certainty, that the words were present. This experiment comes from a classic 1995 study by Henry L. Roediger and Kathleen McDermott at Rice University in Texas. Based on earlier work by James Deese (hence the name Deese-Roediger-McDermott, or DRM, paradigm), participants heard a series of word lists, which they then had to recall from memory. After a brief conversation with the researcher, the participants were then given a new list of words. Critically, this new list contained some words that were associated with every single item on each of the initial lists – for example, while sleep doesn’t appear on list 3 above, it’s related to each word that does appear (bed, rest, tired, and so on). © 2016 Guardian News and Media Limited

Keyword: Learning & Memory
Link ID: 22526 - Posted: 08.08.2016

By EUGENE M. CARUSO, ZACHARY C. BURNS and BENJAMIN A. CONVERSE Watching slow-motion footage of an event can certainly improve our judgment of what happened. But can it also impair judgment? This question arose in the 2009 murder trial of a man named John Lewis, who killed a police officer during an armed robbery of a Dunkin’ Donuts in Philadelphia. Mr. Lewis pleaded guilty; the only question for the jury was whether the murder resulted from a “willful, deliberate and premeditated” intent to kill or — as Mr. Lewis argued — from a spontaneous, panicked reaction to seeing the officer enter the store unexpectedly. The key piece of evidence was a surveillance video of the shooting, which the jury saw both in real time and in slow motion. The jury found that Mr. Lewis had acted with premeditation, and he was sentenced to death. Mr. Lewis appealed the decision, arguing that the slow-motion video was prejudicial. Specifically, he claimed that watching the video in slow motion artificially stretched the relevant time period and created a “false impression of premeditation.” Did it? We recently conducted a series of experiments whose results are strikingly consistent with that claim. Our studies, published this week in the Proceedings of the National Academy of Sciences, show that seeing replays of an action in slow motion leads viewers to believe that the actor had more time to think before acting than he actually did. The result is that slow motion makes actions seem more intentional, more premeditated. In one of our studies, participants watched surveillance video of a fatal shooting that occurred outside a convenience store during an armed robbery. We gave them a set of instructions similar to those given to the jurors in Mr. Lewis’s case, asking them to decide whether the crime was premeditated or not. We assigned half our participants to watch the video in slow motion and the other half to watch it at regular speed. © 2016 The New York Times Company

Keyword: Attention
Link ID: 22525 - Posted: 08.08.2016

By MARTHA C. WHITE A graphic 30-year-old drug education campaign from Partnership for a Drug-Free America is being updated. For a generation of commercial-watching adolescents, it was an indelible image: an egg, sizzling in a frying pan, representing “your brain on drugs.” It was a straightforward message, and the ad’s final line — “Any questions?” — asked as the egg white clouded and cooked, was strictly rhetorical. Three decades later, the Partnership for Drug-Free Kids (the group formerly known as the Partnership for a Drug-Free America) is bringing the frying pan out of retirement and firing up the stove again. But this time questions are the point. The group hopes it can tap into the nostalgia parents may have for the old frying egg ad while also letting them know their children do indeed want answers about drugs. “‘Any questions’ was the end. Now it’s the beginning,” said Scott Seymour, chief creative officer at BFG Communications, which created print and digital banner ads for the new campaign. “The landscape of drugs has really gotten a lot more complex, so we took this idea of having a succession of questions delivered by kids,” he said. The group drew on real inquiries from parents to develop the questions featured in the ads, which cover topics like prescription drugs and marijuana legalization. Children today feel empowered and entitled to ask questions about drugs, and parents are more willing to entertain those questions, observers say. “Because of parenting styles today, parents are engaged with their kids in a different way,” said Kristi Rowe, chief marketing officer at the Partnership for Drug-Free Kids. “They’re really stumped by the questions. They don’t know how to answer them.” © 2016 The New York Times Company

Keyword: Drug Abuse
Link ID: 22524 - Posted: 08.08.2016

Helen Thompson A roughly 27-million-year-old fossilized skull echoes growing evidence that ancient whales could navigate using high-frequency sound. Discovered over a decade ago in a drainage ditch by an amateur fossil hunter on the South Carolina coast, the skull belongs to an early toothed whale. The fossil is so well-preserved that it includes rare inner ear bones similar to those found in modern whales and dolphins. Inspired by the Latin for “echo hunter,” scientists have now named the ancient whale Echovenator sandersi. “It suggests that the earliest toothed whales could hear high-frequency sounds,” which is essential for echolocation, says Morgan Churchill, an anatomist at the New York Institute of Technology in Old Westbury. Churchill and his colleagues describe the specimen online August 4 in Current Biology. Modern whales are divided on the sound spectrum. Toothed whales, such as orcas and porpoises, use high-frequency clicking sounds to sense predators and prey. Filter-feeding baleen whales, on the other hand, use low-frequency sound for long-distance communication. Around 35 million years ago, the two groups split, and E. sandersi emerged soon after. CT scans show that E. sandersi had a few features indicative of ultrasonic hearing in modern whales and dolphins. Most importantly, it had a spiraling inner ear bone with wide curves and a long bony support structure, both of which allow a greater sensitivity to higher-frequency sound. A small nerve canal probably transmitted sound signals to the brain. © Society for Science & the Public 2000 - 2016. All rights reserved.

Keyword: Hearing; Evolution
Link ID: 22523 - Posted: 08.06.2016

By Roxanne Khamsi, What if controlling the appetite were as easy as flipping a switch? It sounds like the stuff of science fiction, but Jeffrey Friedman of Rockefeller University and his colleagues did exactly this in genetically engineered mice to try to shed light on how the brain influences appetite. Friedman and his colleagues used magnetic stimulation to switch on neurons in a region of the brain called the ventromedial hypothalamus and found that doing so increased the rodents' blood sugar levels and decreased levels of the hormone insulin. Turning on the neurons also caused the mice to eat more than their control counterparts. The ultimate confirmation came when they inhibited these neurons and saw the opposite effects: it drove blood sugar down, elevated insulin levels and suppressed the animals' urge to consume their chow. That the brain influences hunger is not an unexpected finding, but scientists have recently narrowed in on how it has sway on what ends up in the gut—and how the gut talks to the mind. This two-way communication, defined as the 'gut–brain axis', happens not only through nerve connections between the organs, but also through biochemical signals, such as hormones, that circulate in the body. “The idea that there is bidirectional communication between the gastrointestinal tract and brain that affects metabolism traces back more than a century,” Friedman says, referring to the work of the nineteenth-century French scientist Claude Bernard, who made seminal discoveries into how the body maintains physiological equilibrium. “Our new findings that insulin-producing cells in the pancreas can be controlled by certain neurons in the brain that sense blood sugar provides further experimental evidence supporting this notion.” © 2016 Scientific American,

Keyword: Obesity
Link ID: 22522 - Posted: 08.06.2016

Tina Hesman Saey Alcoholism may stem from using genes incorrectly, a study of hard-drinking rats suggests. Rats bred either to drink heavily or to shun alcohol have revealed 930 genes linked to a preference for drinking alcohol, researchers in Indiana report August 4 in PLOS Genetics. Human genetic studies have not found most of the genetic variants that put people at risk for alcoholism, says Michael Miles, a neurogenomicist at Virginia Commonwealth University in Richmond. The new study takes a “significant and somewhat novel approach” to find the genetic differences that separate those who will become addicted to alcohol from those who drink in moderation. It took decades to craft the experiment, says study coauthor William Muir, a population geneticist at Purdue University in West Lafayette, Ind. Starting in the 1980s, rats bred at Indiana University School of Medicine in Indianapolis were given a choice to drink pure water or water mixed with 10 percent ethanol, about the same amount of alcohol as in a weak wine. For more than 40 generations, researchers selected rats from each generation that voluntarily drank the most alcohol and bred them to create a line of rats that consume the rat equivalent of 25 cans of beer a day. Simultaneously, the researchers also selected rats that drank the least alcohol and bred them to make a line of low-drinking rats. A concurrent breeding program produced another line of high-drinking and teetotaling rats. For the new study, Muir and colleagues collected DNA from 10 rats from each of the high- and low-drinking lines. Comparing complete sets of genetic instructions from all the rats identified 930 genes that differ between the two lines. |© Society for Science & the Public 2000 - 2016.

Keyword: Drug Abuse; Genes & Behavior
Link ID: 22521 - Posted: 08.06.2016

By Nicholas Bakalar A drug used to treat rheumatoid arthritis may have benefits against Alzheimer’s disease, researchers report. Rheumatoid arthritis is an autoimmune disease believed to be driven in part by tumor necrosis factor, or T.N.F., a protein that promotes inflammation. Drugs that block T.N.F., including an injectable drug called etanercept, have been used to treat rheumatoid arthritis for many years. T.N.F. is also elevated in the cerebrospinal fluid of Alzheimer’s patients. Researchers identified 41,109 men and women with a diagnosis of rheumatoid arthritis and 325 with both rheumatoid arthritis and Alzheimer’s disease. In people over 65, the prevalence of Alzheimer’s disease was more than twice as high in people with rheumatoid arthritis as in those without it. The study is in CNS Drugs. But unlike patients treated with five other rheumatoid arthritis drugs, those who had been treated with etanercept showed a significantly reduced risk for Alzheimer’s disease. Still, the lead author, Dr. Richard C. Chou, an assistant professor of medicine at Dartmouth, said that it is too early to think of using etanercept as a treatment for Alzheimer’s. “We’ve identified a process in the brain, and if you can control this process with etanercept, you may be able to control Alzheimer’s,” he said. “But we need clinical trials to prove and confirm it.” © 2016 The New York Times Company

Keyword: Alzheimers
Link ID: 22520 - Posted: 08.06.2016

By LUKE DITTRICH ‘Can you tell me who the president of the United States is at the moment?” A man and a woman sat in an office in the Clinical Research Center at the Massachusetts Institute of Technology. It was 1986, and the man, Henry Molaison, was about to turn 60. He was wearing sweatpants and a checkered shirt and had thick glasses and thick hair. He pondered the question for a moment. “No,” he said. “I can’t.” The woman, Jenni Ogden, was a visiting postdoctoral research fellow from the University of Auckland, in New Zealand. One of the greatest thrills of her time at M.I.T. was the chance to have sit-down sessions with Henry. In her field — neuropsychology — he was a legendary figure, something between a rock star and a saint. “Who’s the last president you remember?” “I don’t. ... ” He paused for a second, mulling over the question. He had a soft, tentative voice, a warm New England accent. “Ike,” he said finally. Dwight D. Eisenhower’s inauguration took place in 1953. Our world had spun around the sun more than 30 times since, though Henry’s world had stayed still, frozen in orbit. This is because 1953 was the year he received an experimental operation, one that destroyed most of several deep-­seated structures in his brain, including his hippocampus, his amygdala and his entorhinal cortex. The operation, performed on both sides of his brain and intended to treat Henry’s epilepsy, rendered him profoundly amnesiac, unable to hold on to the present moment for more than 30 seconds or so. That outcome, devastating to Henry, was a boon to science: By 1986, Patient H.M. — as he was called in countless journal articles and textbooks — had become arguably the most important human research subject of all time, revolutionizing our understanding of how memory works. © 2016 The New York Times Company

Keyword: Learning & Memory
Link ID: 22519 - Posted: 08.04.2016

By Jonathan Webb Science reporter, BBC News Scientists have glimpsed activity deep in the mouse brain which can explain why we get thirsty when we eat, and why cold water is more thirst-quenching. A specific "thirst circuit" was rapidly activated by food and quietened by cooling down the animals' mouths. The same brain cells were already known to stimulate drinking, for example when dehydration concentrates the blood. But the new findings describe a much faster response, which predicts the body's future demand for water. The researchers went looking for this type of system because they were puzzled by the fact that drinking behaviour, in humans as well as animals, seems to be regulated very quickly. "There's this textbook model for homeostatic regulation of thirst, that's been around for almost 100 years, that's based on the blood," said the study's senior author Zachary Knight, from the University of California, San Francisco. "There are these neurons in the brain that… generate thirst when the blood becomes too salty or the blood volume falls too low. But lots of aspects of everyday drinking can't possibly be explained by that homeostatic model because they occur much too quickly." Take the "prandial thirst" that comes while we consume a big, salty meal - or the fact that we feel quenched almost as soon as we take a drink. © 2016 BBC.

Keyword: Miscellaneous
Link ID: 22518 - Posted: 08.04.2016

By Alice Klein Rise and shine! Neuronal switches have been discovered that can suddenly rouse flies from slumber – or send them into a doze. There are several parallels between sleep in flies and mammals, making fruit flies a good choice for investigating how we sleep. One way to do this is to use optogenetics to activate specific neurons to see what they do. This works by using light to turn on cells genetically modified to respond to certain wavelengths. Gero Miesenböck at the University of Oxford and his team have discovered how to wake flies up. Using light as the trigger the team stimulated neurons that release a molecule called dopamine. The dopamine then switched off sleep-promoting neurons in what’s called the dorsal fan-shaped body, waking the flies. Meanwhile, Fang Guo at Brandeis University in Waltham, Massachusetts, and his team have found that activating neurons that form part of a fly’s internal clock will send it to sleep. When stimulated, these neurons released glutamate, which turned off activity-promoting neurons in the master pacemaker area of the brain. While human and fly brains are obviously very different in structure, being asleep or awake are similar states regardless of the kind of brain an animal has, says Bruno van Swinderen at the University of Queensland, Australia. © Copyright Reed Business Information Ltd.

Keyword: Sleep; Genes & Behavior
Link ID: 22517 - Posted: 08.04.2016

By Sarah Kaplan Sleep just doesn't make sense. "Think about it," said Gero Miesenböck, a neuroscientist at the University of Oxford. "We do it. Every animal with a brain does it. But obviously it has considerable risks." Sleeping animals are incredibly vulnerable to attacks, with no obvious benefit to make up for it — at best, they waste precious hours that could be used finding food or seducing a mate; at worst, they could get eaten. "If evolution had managed to invent an animal that doesn’t need to sleep ... the selective advantage for it would be immense," Miesenböck said. "The fact that no such animal exists indicates that sleep is really vital, but we don't know why." But Miesenböck is part of team of sleep researchers who believe they are inching closer to to an answer. In a paper published in the journal Nature on Wednesday, they describe a cluster of two dozen brain cells in fruit flies that operate as a homeostatic sleep switch, turning on when the body needs rest and off again when it's time to wake up. "It's like a thermostat," Miesenböck said of the switch, "But instead of responding to temperature it responds to something else." If he and his colleagues could find out what that "something" is, "we might have the answer to the mystery of sleep."

Keyword: Sleep; Genes & Behavior
Link ID: 22516 - Posted: 08.04.2016

By Megan Scudellari In late 2013, psychologist Raphael Bernier welcomed a 12-year-old girl and her parents into his office at the University of Washington (UW) in Seattle. The girl had been diagnosed with autism spectrum disorder, and Bernier had invited the family in to discuss the results of a genetic analysis his collaborator, geneticist Evan Eichler, had performed in search of the cause. As they chatted, Bernier noticed the girl’s wide-set eyes, which had a slight downward slant. Her head was unusually large, featuring a prominent forehead. The mother described how her daughter had gastrointestinal issues and sometimes wouldn’t sleep for two to three days at a time. The girl’s presentation was interesting, Bernier recalls, but he didn’t think too much of it—until a week later, when he met an eight-year-old boy with similarly wide-set eyes and a large head. Bernier did a double take. The “kiddos,” as he calls children who come to see him, could have been siblings. According to the boy’s parents, he also suffered from gastrointestinal and sleep problems. The similarities between the unrelated children were remarkable, especially for a disorder so notoriously complex that it has been said, “If you’ve met one child with autism, you’ve met one child with autism.” But Bernier knew that the patients shared another similarity that might explain the apparent coincidence: both harbored a mutation in a gene known as chromodomain helicase DNA binding protein 8 (CHD8). © 1986-2016 The Scientist

Keyword: Autism; Genes & Behavior
Link ID: 22515 - Posted: 08.04.2016

By JoAnna Klein I expected a bumpy ride on a whitewater trip, so when I fell off my raft and coughed up the water I’d inhaled, I wasn’t afraid. But at the time I didn’t know I was swimming with a deadly parasite. I’d been at a bachelorette party at the U.S. National Whitewater Center in Charlotte, N.C., but after returning home I learned that I had shared the churning rapids with Naegleria fowleri, a single-celled amoeba found mostly in soil and warm freshwater lakes, rivers and hot springs. An Ohio teenager had contracted the amoeba infection after visiting the center around the same time I did, and some of the waters and sediment at and around the center had tested positive for the bug. News that my friends and I had all been at risk of exposure triggered a few days of worry. The illness is rare and, if infected, symptoms show up between one and 10 days after exposure. Chances were that we were fine (we were), but the experience prompted me to learn more about the parasite. Naegleria fowleri lives in fresh water, but not in salt water. If forced up the nose, it can enter the brain and feed on its tissue, resulting in an infection known as primary amebic meningoencephalitis. Death occurs in nearly all of those infected with the parasite, usually within five days after infection. The 18-year-old Ohio woman who died most likely contracted the parasite when she sucked water through her nose after falling from a raft during a church trip. Samples from a channel at the rafting center, collected by the Centers for Disease Control and Prevention, tested positive for the bug. The center’s channels are man-made, and it gets its water from the Charlotte-Mecklenburg Utilities Department and two wells on its property. The center has announced that it disinfects all water with ultraviolet radiation and chlorine, and it added more after the water tests. © 2016 The New York Times Company

Keyword: Miscellaneous
Link ID: 22514 - Posted: 08.04.2016

By Anna Vlasits A small corner of the neuroscience world was in a frenzy. It was mid-June and a scientific paper had just been published claiming that years worth of results were riddled with errors. The study had dug into the software used to analyze one kind of brain scan, called functional MRI. The software’s approach was wrong, the researchers wrote, calling into doubt “the validity of some 40,000 fMRI studies”—in other words, all of them. The reaction was swift. Twitter lit up with panicked neuroscientists. Bloggers and reporters rained down headlines citing “seriously flawed” “glitches” and “bugs.” Other scientists thundered out essays defending their studies. Finally, one of the authors of the paper, published in Proceedings of the National Academy of Sciences, stepped into the fray. In a blog post, Thomas Nichols wrote, “There is one number I regret: 40,000.” Their finding, Nichols went on to write, only affects a portion of all fMRI papers—or, some scientists think, possibly none at all. It wasn’t nearly as bad as the hype suggested. The brief kerfuffle could just be dismissed as a tempest in a teapot, science’s self-correcting mechanisms in action. But the study, and its response, heralds a new level of self-scrutiny for fMRI studies, which have been plagued for decades by accusations of shoddy science and pop-culture pandering. fMRI, in other words, is growing up, but not without some pains along the way. A bumpy start for brain scanning © 2016 Scientific American,

Keyword: Brain imaging
Link ID: 22513 - Posted: 08.04.2016

The brains of overweight middle-aged people resemble brains that are a decade older in healthier people. A study of 473 adults has found that people who are overweight have less white matter, which connects different brain areas and enables signaling between them. The volume of white matter in the brains of overweight people at 50 were similar to that seen in the brains of lean people at 60. Human brains naturally shrink with age, but previous research has shown that this seems to happen more quickly in obese people. “As our brains age, they naturally shrink in size, but it isn’t clear why people who are overweight have a greater reduction in the amount of white matter,” says Lisa Ronan, at the University of Cambridge, a member of the research team. “We can only speculate on whether obesity might in some way cause these changes or whether obesity is a consequence of brain changes.” Intriguingly, the difference between lean and overweight people’s brains was only apparent from middle age onwards. It’s possible that this is because we are particularly vulnerable in some way at this time, says team-member Paul Fletcher, also at the University of Cambridge. However, despite this reduction in white matter, cognitive tests did not find any evidence that being overweight was linked to reduced brain function. “We don’t yet know the implications of these changes in brain structure,” says Sadaf Farooqi, at the University of Cambridge, who was also involved in the research. © Copyright Reed Business Information Ltd.

Keyword: Obesity
Link ID: 22512 - Posted: 08.04.2016

by Helen Thompson Pinky and The Brain's smarts might not be so far-fetched. Some mice are quicker on the uptake than others. While it might not lead to world domination, wits have their upside: a better shot at staying alive. Biologists Audrey Maille and Carsten Schradin of the University of Strasbourg in France tested reaction time and spatial memory in 90 African striped mice (Rhabdomys pumilio) over the course of a summer. For this particular wild rodent, surviving harsh summer droughts means making it to mating season in the early fall. The team saw some overall trends: Females were more likely to survive if they had quick reflexes, and males were more likely to survive if they had good spatial memory. Cognitive traits like reacting quickly and remembering the best places to hide are key to eluding predators during these tough times but may come with trade-offs for males and females. The results show that an individual mouse’s cognitive strengths are linked to its survival odds, suggesting that the pressure to survive can shape basic cognition, Maille and Schradin write August 3 in Biology Letters. |© Society for Science & the Public 2000 - 2016

Keyword: Intelligence; Evolution
Link ID: 22511 - Posted: 08.04.2016