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Rae Ellen Bichell Initially, Clint Perry wanted to make a vending machine for bumblebees. He wanted to understand how they solve problems. Perry, a cognitive biologist at Queen Mary University of London, is interested in testing the limits of animal intelligence. "I want to know: How does the brain do stuff? How does it make decisions? How does it keep memory?" says Perry. And how big does a brain need to be in order to do all of those things? He decided to test this on bumblebees by presenting the insects with a puzzle that they'd likely never encounter in the wild. He didn't end up building that vending machine, but he did put bees through a similar scenario. Perry and his colleagues wrote Thursday in the journal Science that, despite bees' miniature brains, they can solve new problems quickly just by observing a demonstration. This suggests that bees, which are important crop pollinators, could in time adapt to new food sources if their environment changed. As we have reported on The Salt before, bee populations around the world have declined in recent years. Scientists think a changing environment is at least partly responsible. Perry and colleagues built a platform with a porous ball sitting at the center of it. If a bee went up to the ball, it would find that it could access a reward, sugar water. One by one, bumblebees walked onto the platform, explored a bit, and then slurped up the sugar water in the middle. "Essentially, the first experiment was: Can bees learn to roll a ball?" says Perry. © 2017 npr
By Claudia Wallis Dinosaurs, Star Wars, train schedules, Disney princesses, maps, LEGO—subjects such as these can become all-consuming passions for children on the autism spectrum. What therapists and educators often call “circumscribed” or “restricted” interests (or, more generously, “special” interests) make up a characteristic symptom of autism spectrum disorder (ASD). The current edition of psychiatry’s Diagnostic and Statistical Manual of Mental Disorders describes them as “highly restricted, fixated interests that are abnormal in intensity or focus.” Roughly 90 percent of high-functioning kids with ASD display at least one such interest during their elementary school years, according to a 2007 survey conducted at the Yale University Child Study Center, one of the few studies to have examined the topic. For a family with an affected child, this kind of narrow preoccupation can be tedious and exhausting. Imagine a kid who will talk about nothing but the exits on the New Jersey Turnpike or the Captain Underpants book series. (Both actual examples.) Therapists and educators have traditionally tried to suppress or modulate a child’s special interest, or use it as a tool for behavior modification: Keep your hands still and stop flapping, and you will get to watch a Star Wars clip; complete your homework or no Harry Potter. But what if these obsessions themselves can be turned into pathways to growth? What if these intellectual cul-de-sacs can open up worlds? That is the idea explored in the film Life, Animated, a contender for the Academy Award for Best Documentary this Sunday night. © 2017 Scientific American
Link ID: 23277 - Posted: 02.24.2017
Jon Brock What if I told you that we can now identify babies who are going to develop autism based on a simple brain scan? This, in essence, is the seductive pitch for a study published last week in the journal Nature, and making headlines around the world. Early identification and diagnosis is one of the major goals of autism research. By definition, people with autism have difficulties with social interaction and communication. But these skills take many years to develop, even in typically developing (i.e., non-autistic) children. Potential early signs of autism are extremely difficult to pick out amidst the natural variation in behaviour and temperament that exists between all babies. A brain scan for autism would be a major step forward. But is the hype justified? Are we really on the brink of a new era in autism diagnostics? Without wishing to detract from the efforts of everyone involved in the study, it’s important to look at the results critically, both in terms of the scientific findings and their potential implications for clinical practice. The study, led by Heather Cody Hazlett at the University of North Carolina, was part of a larger research program investigating the development of babies who have an older sibling with autism. Because autism runs in families, these babies are much more likely to develop autism than babies from the general population.
By KATHRYN SHATTUCK After his short film screened at the Sundance Film Festival in 2008, a euphoric Simon Fitzmaurice was walking the snowy streets of Park City, Utah, when his foot began to hurt. Back home in Ireland that summer, by then dealing with a pronounced limp, he received a shattering diagnosis: motor neuron disease, or M.N.D. (more commonly known in the United States as A.L.S., or Lou Gehrig’s Disease), a neurological disorder that causes increasing muscle weakness and eventual paralysis and is, in most cases, fatal. The doctor gave Mr. Fitzmaurice, then 33, three or four years to live. That might have been the end of any normal existence. But Mr. Fitzmaurice, by his own measure a “bit of a stubborn bastard,” was determined to leave his wife, Ruth, and their two young sons — with a third on the way — a legacy other than self-pity. The result is Mr. Fitzmaurice’s first feature film, and perhaps his salvation — “My Name Is Emily.” The movie, which opened in limited release in the United States on Feb. 17, stars Evanna Lynch, the airy Luna Lovegood of “Harry Potter” fame, as a teenage outlier in both her Dublin foster home and high school who goes on the lam with her only friend (George Webster) to free her father (Michael Smiley) from a mental hospital. The film — with gorgeous scenes of Ms. Lynch plunged, nymphlike, into a cerulean sea or riding shotgun through the emerald countryside in a canary-yellow vintage Renault — won for best cinematography when it debuted at the Galway Film Fleadh in 2015. “I am not trying to prove anything,” Mr. Fitzmaurice wrote in an email, before quickly reconsidering. “Actually, I am trying to prove something. I remember thinking, ‘I must do this to show my children to never give up.’” Mr. Fitzmaurice was writing with his hands when he began the script for “My Name Is Emily.” By the time he was finished, he was writing with his eyes. © 2017 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 23275 - Posted: 02.24.2017
Laurel Hamers Clusters of a toxic bacterial protein have a surprising structure, differing from similar clumps associated with Alzheimer’s and Parkinson’s in humans, scientists report in the Feb. 24 Science. These clusters, called amyloids, are defined in part by their structure: straight regions of protein chains called beta strands, folded accordion-style into flat beta sheets, which then stack up to form a fiber. That definition might now need to be broadened. “All the amyloids that have been structurally looked at so far have certain characteristics,” says Matthew Chapman, a biologist at the University of Michigan in Ann Arbor who wasn’t part of the work. “This is the odd amyloid out right now.” In the human brain, misfolded proteins can form amyloids that trigger neurodegenerative diseases. But amyloids aren’t always a sign of something gone wrong — some bacteria make amyloids to help defend their turf. In Staphylococcus aureus, for example, the PSMα3 protein assembles into amyloids that help the bacteria kill other cells. Previous research suggested that PSMα3 clusters were like any other amyloid. But researchers using X-ray crystallography found that instead of straight beta strands, the PSMα3 fiber was made up of curly structures called alpha helices that resemble an old-fashioned phone cord. The helices still formed a familiar fiber shape just like the beta strands did, but the sheets making up that fiber were rippled instead of flat. |© Society for Science & the Public 2000 - 2017.
Link ID: 23274 - Posted: 02.24.2017
By Diana Kwon Neuroscientists have long debated how itch and pain overlap in the nervous system. Although itch was once thought to arise from the same neurons that generate pain, later observations disputing this theory led many to believe these sensations had distinct neural circuits. In a study published today (February 22) in Neuron, researchers report that a subset of “itch-specific” nerve cells in the murine spinal cord are also involved in sensing pain, bringing the specificity theory into question. “We were surprised that contrary to what the field believes, neurons [in the spinal cord] coded for both pain and itch sensations,” coauthor Shuhao Sun, a neuroscience graduate student at Johns Hopkins University, told The Scientist. “[This] means there can be some crosstalk between these two sensations in the central nervous system.” Historically, the observation that pain could quell itch led many neuroscientists to subscribe to the intensity theory, which suggested that, in the same neurons, weak stimulation generated itch, while strong activation led to pain. However, this theory was largely abandoned around the 1980s when several groups discovered that weak painful stimuli did not lead to itch and that strong itch stimuli did not lead to pain. Instead, many researchers adopted the labeled-line theory, which proposed that there were separate neurons dedicated to each sensation. © 1986-2017 The Scientist
Keyword: Pain & Touch
Link ID: 23273 - Posted: 02.24.2017
Tina Hesman Saey Humans and Neandertals are still in an evolutionary contest, a new study suggests. Geneticist Joshua Akey of the University of Washington in Seattle and colleagues examined gene activity of more than 700 genes in which at least one person carried a human and a Neandertal version of the gene. Human versions of some genes are more active than Neandertal versions, especially in the brain and testes, the researchers report February 23 in Cell. In other tissues, some Neandertal versions of genes were more active than their human counterparts. In the brain, human versions were favored over Neandertal variants in the cerebellum and basal ganglia. That finding may help explain why Neandertals had proportionally smaller cerebellums than humans do. Neandertal versions of genes in the testes, including some needed for sperm function, were also less active than human varieties. That finding is consistent with earlier studies that suggested male human-Neandertal hybrids may have been infertile, Akey says. But Neandertal genes don’t always lose. In particular, the Neandertal version of an immunity gene called TLR1 is more active than the human version, the researchers discovered. Lopsided gene activity may help explain why carrying Neandertal versions of some genes has been linked to human diseases, such as lupus and depression (SN: 3/5/16, p. 18). Usually, both copies contribute equally to a gene’s total activity. Less robust activity of a version inherited from Neandertals might cause total activity to dip to unhealthy levels, for instance. |© Society for Science & the Public 2000 - 2017
By Alice Klein The proof is in the packaging. Making all cigarette packets look the same reduces the positive feelings smokers associate with specific brands and encourages quitting, Australian research shows. The findings come ahead of the UK and Ireland introducing plain tobacco packaging in May. Australia was the first nation to introduce such legislation in December 2012. Since then, all cigarettes have been sold in plain olive packets with standard fonts and graphic health warnings. The primary goal was to make cigarettes less appealing so that people would not take up smoking in the first place. But an added bonus has been the number of existing smokers who have ditched the habit. Between 2010 and 2013, the proportion of daily smokers in Australia dropped from 15.1 to 12.8 per cent – a record decline. The number of calls to quit helplines also increased by 78 per cent after the policy change. Brand betrayal This drop in smoking popularity can be partly explained by a loss of brand affinity, says Hugh Webb at the Australian National University in Canberra. People derive a sense of belonging and identity from brands, he says. For example, you may see yourself as a “Mac person” or a “PC person” and feel connected to other people who choose that brand. “Marketers are extremely savvy about cultivating these brand identities.” © Copyright Reed Business Information Ltd
By RONI CARYN RABIN Older adults who started sleeping more than nine hours a night — but had not previously slept so much — were at more than double the risk of developing dementia a decade later than those who slept nine hours or less, researchers report. The increased risk was not seen in people who had always slept more than nine hours. “We’re not suggesting you go wake up Grandpa. We think this might be a marker for the risk of dementia, not a cause” of the illness, said Dr. Sudha Seshadri, a professor of neurology at Boston University School of Medicine and the senior author of the study, in Neurology. Using data from 2,457 people, average age 72, who were part of a study in Framingham, Mass., the researchers found that those with a new habit of excessive slumber were at a greater risk of all forms of dementia, including Alzheimer’s, which is characterized by a buildup of beta amyloid, a toxic protein fragment that forms plaques in the brain. “My suspicion is that this is a compensatory mechanism: that at a time when amyloid is building up in the brain, people may be sleeping longer as the body is reacting and trying to remove it from the brain,” Dr. Seshadri added. © 2017 The New York Times Company
Link ID: 23270 - Posted: 02.24.2017
Bruce Bower Chimps with little social status influence their comrades’ behavior to a surprising extent, a new study suggests. In groups of captive chimps, a method for snagging food from a box spread among many individuals who saw a low-ranking female peer demonstrate the technique, say primatologist Stuart Watson of the University of St. Andrews in Fife, Scotland, and colleagues. But in other groups where an alpha male introduced the same box-opening technique, relatively few chimps copied the behavior, the researchers report online February 7 in the American Journal of Primatology. “I suspect that even wild chimpanzees are motivated to copy obviously rewarding behaviors of low-ranking individuals, but the limited spread of rewarding behaviors demonstrated by alpha males was quite surprising,” Watson says. Previous research has found that chimps in captivity more often copy rewarding behaviors of dominant versus lower-ranking group mates. The researchers don’t understand why in this case the high-ranking individuals weren’t copied as much. The spread of new behaviors in groups of monkeys and apes depends on a variety of factors — including an innovator’s social status, age and sex — that can interact in unpredictable ways. “That’s why social learning in groups is so interesting to study,” says Elizabeth Lonsdorf, a primatologist at Franklin & Marshall College in Lancaster, Pa., who did not participate in the research. |© Society for Science & the Public 2000 - 2017.
By Kerry Grens Brain scans of 3,242 volunteers aged four to 63 years old revealed that those diagnosed with attention deficit hyperactivity disorder (ADHD)—roughly half of the group—had smaller tissue volumes in five brain regions. Because the differences were largest between children, the researchers concluded that ADHD likely involves a delay in brain maturation. The study, published in The Lancet Psychiatry on February 15, is the largest of its kind to date, and the authors hope it will change public perception of the disorder. “I think most scientists in the field already know that the brains of people with ADHD show differences, but I now hope to have shown convincing evidence … that will reach the general public and show that it has [a basis in the brain] just like other psychiatric disorders,” geneticist and coauthor Martine Hoogman of Radboud University in the Netherlands told The Washington Post. “We know that ADHD deals with stigma, but we also know that increasing knowledge will reduce stigma.” Most pronounced among the brain differences between those with and without ADHD was the amygdala, important for emotional processing. “The amygdala is heavily connected to other brain regions. It is a kind of hub for numerous kinds of signaling around salience and significance of events,” Joel Nigg, a psychiatry professor at Oregon Health & Science University School of Medicine who was not part of the study, told CNN. “The bigger story here is that alterations in amygdala have not been widely accepted as part of ADHD, so seeing that effect emerge here is quite interesting.” © 1986-2017 The Scientist
Patricia Neighmond Many men over 65 with low testosterone levels say their sense of well-being, not to mention sexual function, isn't what it used to be. That's why some doctors prescribe testosterone replacement. But the effectiveness of testosterone has been controversial. Studies of the risks and benefits have been mixed, and the Food and Drug Administration beefed up its warnings about cardiac side effects of testosterone supplementation in 2015. And the findings of five studies released Tuesday aren't likely to clear up the confusion. They appear in JAMA, the journal of the American Medical Association and JAMA Internal Medicine. The studies are collectively called the Testosterone Trials (TTrials) and they compared a testosterone gel, AndroGel, against a placebo. The results are based on 788 men with below normal levels of testosterone studied at 12 sites across the country over a year. Overall, researchers saw improvements in bone density and bone strength in men who used a testosterone gel, which raised their testosterone to levels seen in younger men. In men with unexplained anemia, testosterone also improved iron levels in the blood. (A reviewer of the study raised questions about whether it was done ethically.) But in men using testosterone who had been reporting memory problems at the start of the study, there were no improvements in memory or cognition. And there were worrisome signs of an increase in the risk of cardiovascular problems. © 2017 npr
Daqing Li and Ying Li In 1969 Geoffrey Raisman, who has died aged 77, introduced the term “plasticity” to describe the ability of damaged nerve tissue to form new synaptic connections. He discovered that damaged nerves in the central nervous system (CNS) could be repaired and developed the theory that white matter (nerve fibres and supporting cells) is like a pathway – when it is disrupted by injury, such as spinal cord injury, growth of the regenerating fibres is blocked. In 1985 he described how olfactory ensheathing cells (OECs) “open doors” for newly formed nerve fibres in the nose to enter the CNS. Believing that reconstruction of the damaged pathway is essential to repair of the injured CNS and using the unique door-opening capability of OECs, in 1997, together with colleagues, Geoffrey showed that transplantation of OECs into the damaged spinal cord in experimental models repairs the damaged pathway and results in the regeneration of severed nerve fibres and the restoration of lost functions. The study led to a joint clinical trial with Pawel Tabakow and his team at Wroclaw Medical University, Poland. In 2014 the first patient with a complete severance of the thoracic spinal cord received transplantation of his own OECs. The operation enabled the patient, Darek Fidyka, to gain significant neurological recovery of sensation and voluntary movement. He can now get out of his wheelchair and ride a tricycle. The wider application of OECs has also been investigated. In 2012, with his team at University College London, collaborating with the UCL Institute of Ophthalmology and Southwest hospital, at the Third Military Medical University in Chongqing, China, Geoffrey described the protective effect of OECs in an experimental glaucoma model. The discovery has led to a plan to translate this research to clinical application which, it is hoped, will help many sufferers regain sight.
By Jennifer Couzin-Frankel At least two dozen junior and senior researchers are stuck in scientific limbo after being barred from publishing data collected over a 25-year period at a National Institutes of Health (NIH) lab. The unusual ban follows the firing last summer of veteran neurologist Allen Braun by the National Institute on Deafness and Other Communication Disorders (NIDCD) for what many scientists have told Science are relatively minor, if widespread, violations of his lab’s experimental protocol. Most of the violations, which were unearthed after Braun himself reported a problem, involve the prescreening or vetting of volunteers for brain imaging scans and other experiments on language processing. The fallout from the case was recently chronicled on a blog by one of Braun’s former postdocs, and it highlights a not-uncommon problem across science: the career harm to innocent junior investigators following lab misconduct or accidental violations on the part of senior scientists. But this case, say those familiar with it, is extreme. “We’re truly collateral damage,” says Nan Bernstein Ratner of the University of Maryland in College Park, who researches stuttering. She spent 5 years collaborating with Braun. Now, two of her graduate students have had to shift their master’s theses topics, and an undergraduate she mentored cannot publish a planned paper. “The process has been—you can use this term—surreal.” © 2017 American Association for the Advancement of Science
By Jessica Hamzelou Three people with paralysis have learned to type by thought alone using a brain implant – at the fastest speeds recorded using such a system. Two have motor neurone disease, also known as ALS – a degenerative disorder that destroys neurons associated with movement – while the other has a spinal cord injury. All three have weakness or paralysis in all of their limbs. There is a chance that those with ALS will eventually lose the ability to speak, too, says Jaimie Henderson, a neurosurgeon at Stanford University Medical Center in California. People who have lost the ability to talk may be offered devices that allow them to select letters on a screen using head, cheek or eye movements. This is how Stephen Hawking communicates, for example. But brain-machine interfaces are also being developed in the hope that they may one day be a more intuitive way of communicating. These involve reading brain activity, either externally or via an implant embedded in the brain, and turning it into a signal that can be used to direct something in the environment. At the moment, these devices are a little slow. Henderson and his colleagues wanted to make a device that was quicker and easier to use than those currently in trials. © Copyright Reed Business Information Ltd.
By Michelle Roberts A multiple sclerosis treatment being tested in patients can stop the disease for at least five years, say doctors. The risky therapy involves wiping out the person's immune system with strong cancer drugs and then rebooting it with a stem cell transplant. Doctors say only some patients will be suitable to try it, particularly because it is so high risk. Out of 281 people who had the treatment, nearly half benefited, but eight died shortly afterwards. The work in JAMA Neurology is one of the largest and longest investigations of this aggressive MS treatment. Mark Rye, 41 and from Surrey, had his transplant just before Christmas 2016. Two months on he is doing well. "It was a hard decision, knowing what could go wrong. My wife and I discussed it for many, many hours. We've got small children and I didn't want my MS to get worse and end up in a wheelchair. "I did this to halt the condition and so that I can be there for my children, who are still so young. I want to be able to play rugby and football with them as they grow up." What is not clear is for how long the therapy might ultimately work. Freeze frame MS is not fatal, but it is incurable. The disease causes the immune system to attack the protective coating of nerves in the brain and spinal cord, which can create problems with a person's vision, walking and balance. © 2017 BBC
By Esther Landhuis For much of her life Anne Dalton battled depression. She seldom spoke with people. She stayed home a lot. The days dragged on with a sense of “why bother?” for the 61-year-old from New Jersey who used to work at a Wall Street investment firm. After trying more than a dozen combinations of antidepressant drugs to no avail, things got so bad two years ago that Dalton went in for electroconvulsive therapy—in which “basically they shock your brain,” as she puts it. Like Dalton, most of the estimated 16 million U.S. adults who have reported a major depressive episode in the past year find little relief even after several months on antidepressants—a problem that some researchers say may stem from the way mental illness is diagnosed. Objective lab tests can physically confirm heart disease or cancer, but psychiatric conditions are classified somewhat vaguely as clusters of reported symptoms. Doctors consider people clinically depressed if they say they have low mood and meet at least four additional criteria from an overall list of nine. Yet depression can manifest differently from person to person: One might be putting on pounds and sleeping much of the time whereas another might be losing weight, feeling anxious and finding it difficult to sit still, says Conor Liston, a neuroscientist and psychiatrist at Weill Cornell Medical College. “The fact that we lump people together like this has been a big obstacle in understanding the neurobiology of depression,” Liston explains. © 2017 Scientific American,
By JOANNA KLEIN The good news is, the human brain is flexible and efficient. This helps us make sense of the world. But the bad news is, the human brain is flexible and efficient. This means the brain can sometimes make mistakes. You can watch this tension play out when the brain tries to connect auditory and visual speech. It’s why we may find a poorly dubbed kung fu movie hard to believe, and why we love believing the gibberish in those Bad Lip Reading Videos on YouTube. “By dubbing speech that is reasonably consistent with the available mouth movements, we can utterly change the meaning of what the original talker was saying,” said John Magnotti, a neuroscientist at Baylor College of Medicine in Texas. “Sometimes we can detect that something is a little off, but the illusion is usually quite compelling.” In a study published Thursday in PLOS Computational Biology, Dr. Magnotti and Michael Beauchamp, also a neuroscientist at Baylor College of Medicine, tried to pin down why our brains are susceptible to these kinds of perceptual mistakes by looking at a well-known speech illusion called the McGurk effect. By comparing mathematical models for how the brain integrates senses important in detecting speech, they found that the brain uses vision, hearing and experience when making sense of speech. If the mouth and voice are likely to come from the same person, the brain combines them; otherwise, they are kept separate. “You may think that when you’re talking to someone you’re just listening to their voice,” said Dr. Beauchamp, who led the study. “But it turns out that what their face is doing is actually profoundly influencing what you are perceiving.” © 2017 The New York Times Company
By Sam Wong Can a mouse be mindful? Researchers believe they have created the world’s first mouse model of meditation by using light to trigger brain activity similar to what meditation induces. The mice involved appeared less anxious, too. Human experiments show that meditation reduces anxiety, lowers levels of stress hormones and improves attention and cognition. In one study of the effects of two to four weeks of meditation training, Michael Posner of the University of Oregon and colleagues discovered changes in the white matter in volunteers’ brains, related to the efficiency of communication between different brain regions. The changes, picked up in scans, were particularly noticeable between the anterior cingulate cortex (ACC) and other areas. Since the ACC regulates activity in the amygdala, a region that controls fearful responses, Posner’s team concluded that the changes in white matter could be responsible for meditation’s effects on anxiety. The mystery was how meditation could alter the white matter in this way. Posner’s team figured that it was related to changes in theta brainwaves, measured using electrodes on the scalp. Meditation increases theta wave activity, even when people are no longer meditating. To test the theory, the team used optogenetics – they genetically engineered certain cells to be switched on by light. In this way, they were able to use pulses of light on mice to stimulate theta brainwave-like activity in the ACC. © Copyright Reed Business Information Ltd.
Link ID: 23260 - Posted: 02.21.2017
Hannah Devlin Rambling and long-winded anecdotes could be an early sign of Alzheimer’s disease, according to research that suggests subtle changes in speech style occur years before the more serious mental decline takes hold. The scientists behind the work said it may be possible to detect these changes and predict if someone is at risk more than a decade before meeting the threshold for an Alzheimer’s diagnosis. Janet Cohen Sherman, clinical director of the Psychology Assessment Center at Massachusetts General Hospital, said: “One of the greatest challenges right now in terms of Alzheimer’s disease is to detect changes very early on when they are still very subtle and to distinguish them from changes we know occur with normal ageing.” Speaking at the American Association for the Advancement of Science in Boston, Sherman outlined new findings that revealed distinctive language deficits in people with mild cognitive impairment (MCI), a precursor to dementia. “Many of the studies to date have looked at changes in memory, but we also know changes occur in language,” she said. “I’d hope in the next five years we’d have a new linguistic test.” Sherman cites studies of the vocabulary in Iris Murdoch’s later works, which showed signs of Alzheimer’s years before her diagnosis, and the increasingly repetitive and vague phrasing in Agatha Christie’s final novels – although the crime writer was never diagnosed with dementia. Another study, based on White House press conference transcripts, found striking changes in Ronald Reagan’s speech over the course of his presidency, while George HW Bush, who was a similar age when president, showed no such decline.