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By NICHOLAS BAKALAR There is some evidence that stress prompts people to turn to sweet, high-calorie “comfort foods.” Now scientists have confirmed a link between long-term stress and obesity. The study, published in Obesity, tested 2,527 men and women over 50 years old, quantifying stress by measuring levels of cortisol, the stress hormone, in 2-centimeter hair clippings, or about two months’ growth. After controlling for age, sex, ethnicity, smoking, diabetes and other factors that might be linked to obesity, they found that the higher the level of cortisol, the greater the body weight, B.M.I. and waist circumference. Higher cortisol levels were also associated with persistence of obesity over time. Other studies have relied on measures of cortisol in blood, urine or saliva, which can vary by time of day and be affected by temporary stressors and other factors. But this study was able to measure general stress levels over two months to get a picture of the long-term effect. The researchers acknowledge that they were unable to determine whether chronically high cortisol levels are a cause or a consequence of obesity (feeling “fat,” for example, could raise your stress levels). The lead author, Sarah E. Jackson, an epidemiologist at University College London, said that while it may not be possible to eliminate stress, “you may be able to find ways to control it. Even just being aware that stress might make you eat more may help.” © 2017 The New York Times Company
Amanda Montañez A couple of weeks ago I listened to an excellent podcast series on poverty in America. One message that stuck with me is just how many factors the poor have working against them—factors that, if you’re not poor, are all too easy to deny, disregard, or simply fail to notice. In the March issue of Scientific American, neuroscientist Kimberly Noble highlights one such invisible, yet very real, element of poverty: its effect on brain development in children. When considering such a complex topic, any sort of data-driven approach can feel mired in confounding factors and variables. After all, it’s not as if money itself has any impact on the structure or function of one’s brain; rather, it is likely to be an amalgamation of environmental and/or genetic influences accompanying poverty, which results in an overall trend of relatively low achievement among poor children. By definition, this is a multifaceted problem in which correlation and causation seem virtually impossible to untangle. Nonetheless, Noble’s lab is tackling this challenge using the best scientific tools and methods available. First, it is essential to define the problem: in what specific ways does poverty impact brain function? To address this question, Noble recruited some 150 children from various socioeconomic backgrounds and used standard psychological testing methods to evaluate their abilities in several cognitive areas associated with particular parts of the brain. As outlined in the graphs below, the relationships are clear, especially in terms of language skills. © 2017 Scientific American,
By Daniel Engber It took scientists six months to train Alexandra the red-footed tortoise, but by midsummer 2009 she’d finally learned to fake a yawn. A formal experiment came right after. Once per day for several weeks, the research team placed Alexandra on one side of a small tank and another tortoise—either Moses, Aldous, Wilhemina, Quinn, Esme, or Molly—just across from her. They then signaled her to tilt back her head and drop her jaw, just as she’d been taught, while they watched the other tortoise. Would Moses drop his jaw? Would Aldous or Wilhemina? Was there any sign at all that Alexandra’s tortoise yawn could be contagious? There was not. The research team tried again, this time having Alexandra fake her yawn not just once but twice or three times over; still, the observer tortoises did not respond. Next the scientists made Moses and the others watch a video of Alexandra in the middle of a natural yawn, not the fake one that she’d been practicing for months. Again, the yawn was not contagious. “It is possible that a real yawn is necessary to stimulate the observer tortoise,” the authors concluded in their 2011 paper, published in Current Zoology. But “our findings are more consistent with the suggestion that tortoises do not yawn in a contagious manner.” This finding, or lack thereof, may on its surface seem banal. But given what we know about the replication crisis in science, the tortoise paper might be a sign of things to come. Is it possible that the entire body of research on contagious yawning—a small but lively field that dates back 30 years—is resting on a shaky premise?
Link ID: 23308 - Posted: 03.03.2017
By Veronique Greenwood A number of studies have used functional MRI to see what our brain looks like as we recall pleasant memories, watch scary movies or listen to sad music. Scientists have even had some success telling which of these stimuli a subject is experiencing by looking at his or her scans. But does this mean it is possible to tell what emotions we are experiencing in the absence of prompts, as we let our mind wander naturally? That is a difficult question to answer, in part because psychologists disagree about how emotions should be defined. Nevertheless, some scientists are trying to tackle it. In a study reported in the June 2016 issue of Cerebral Cortex, Heini Saarimäki of Aalto University in Finland and her colleagues observed volunteers in a brain scanner who were being prompted to recall memories they associated with words drawn from six emotional categories or to reflect on a movie clip selected to provoke certain emotions. The participants also completed a questionnaire about how closely linked different emotions were—rating, for instance, whether “anxiety” is closer to “fear” than to “happiness.” The researchers found that pattern-recognition software could detect which category of emotion a person had been prompted with. In addition, the more closely he or she linked words in the questionnaire, the more his or her brain scans for those emotions resembled one another. Another study, published in September 2016 in PLOS Biology by Kevin LaBar of Duke University and his colleagues, attempted to match brain scans of people lying idle in a scanner to seven predefined patterns associated with specific emotions provoked in an earlier study. The researchers found they could predict the subjects' self-reported emotions from the scans about 75 percent of the time. © 2017 Scientific American,
Sam Nastase was taking a break from his lab work to peruse Twitter when he saw a tweet about his manuscript. A PhD in cognitive neuroscience at Dartmouth College, Nastase had sent his research out for review at a journal, and hadn’t yet heard back from the scientists who would read the paper and—normally—provide anonymous comments. But here, in this tweet, was a link to a review of his paper. “I was like, ‘Oh that’s my paper, OK.’ So that was a little bit nerve-wracking,” says Nastase. A few weeks later, he received the same review as part of a response from the journal, “copied and pasted, basically.” So much for secret, anonymous peer review. The tweet linked to the blog of a neuroscientist named Niko Kriegeskorte, a cognitive neuroscientist at the Medical Research Council in the UK who, since December 2015, has performed all of his peer review openly. That means he publishes his reviews as he finishes them on his personal blog—sharing on Twitter and Facebook, too—before a paper is even accepted. Scientists traditionally keep reviews of their papers to themselves. The reviewers are anonymous, and publishers protect their reviewers’ identities fastidiously, all in the name of honest, uncensored appraisal of scientific work. But for many, the negatives of this system have started to outweigh the positives. So scientists like Kriegeskorte, and even the journals themselves, are starting to experiment. Kriegeskorte’s posting policy has made a lot of people uncomfortable. He’s faced resistance from journal staff, scientific editors, and even one scientist who anonymously reviewed a paper that he reviewed openly. “People in the publishing business, my feeling is that they feel that this is deeply illicit,” Kriegeskorte says, “but they don’t know exactly which rule it breaks.” Still, after more than a year of this experiment with exclusively writing reviews on his blog—he’s done 12 now—Kriegeskorte says he’ll never write a secret review again.
Link ID: 23306 - Posted: 03.03.2017
By Jessica Wright, Spectrum The prevalence of autism in the United States has risen steadily since researchers first began tracking it in 2000. The rise in the rate has sparked fears of an autism ‘epidemic.’ But experts say the bulk of the increase stems from a growing awareness of autism and changes to the condition’s diagnostic criteria. Here’s how researchers track autism’s prevalence and explain its apparent rise. How do clinicians diagnose autism? There is no blood test, brain scan or any other objective test that can diagnose autism—although researchers are actively trying to develop such tests. Clinicians rely on observations of a person’s behavior to diagnose the condition. In the U.S., the criteria for diagnosing autism are laid out in the “Diagnostic and Statistical Manual of Mental Disorders” (DSM). The criteria are problems with social communication and interactions, and restricted interests or repetitive behaviors. Both of these ‘core’ features must be present in early development. What is the prevalence of autism in the U.S.? The Centers for Disease Control and Prevention (CDC) estimates that 1 in 68children in the U.S. have autism. The prevalence is 1 in 42 for boys and 1 in 189 for girls. These rates yield a gender ratio of about five boys for every girl. © 2017 Scientific American,
Link ID: 23305 - Posted: 03.03.2017
Susan Milius Fitbit-style tracking of two wild African elephants suggests their species could break sleep records for mammals. The elephants get by just fine on about two hours of sleep a day. Much of that shut-eye comes while standing up — the animals sleep lying down only once every three or four days, new data show. Most of what scientists previously knew about sleeping elephants came from captive animals, says neuroethologist Paul Manger of the University of the Witwatersrand, Johannesburg. In zoos and enclosures, elephants have been recorded snoozing about three hours to almost seven over a 24-hour period. Monitoring African elephants in the wild, however, so far reveals more extreme behavior. Data are hard to collect, but two females wearing activity recorders for about a month averaged less sleep than other recorded mammals. Especially intriguing is the elephants’ ability to skip a night’s sleep without needing extra naps later, Manger and colleagues report March 1 in PLOS ONE. “The remarkably short amount of sleep in wild elephants is a real elephant in the room for several theories for the function of sleep,” says Niels Rattenborg of the Max Planck Institute for Ornithology in Seewiesen, Germany. Ideas that sleep restores or resets aspects of the brain for peak performance can’t explain animals that sleep only a little and don’t need catch-up rest, says Rattenborg, who wasn’t involved in the elephant study. The results also don’t fit well with the thought that animals need sleep to consolidate memories. “Elephants are usually not considered to be forgetful animals,” he says. |© Society for Science & the Public 2000 - 2017.
Sleeping too much or too little can increase the likelihood of becoming obese, researchers have discovered. The study found abnormal sleeping patterns increased the risk of being overweight for those genetically predisposed to obesity. The effect was seen regardless of diet, health or socio-demographic group. The University of Glasgow study also found no clear link between sleep duration and body weight in those with a low genetic risk of obesity. Researchers looked at the effects of a short sleep of less than seven hours a night and a long sleep - more than nine hours - along with daytime napping and shift work. Negative effect They found that in people with a high genetic risk of obesity, both short-sleep and long-sleep durations further increased risk of carrying excess weight, compared with people who slept for normal durations of between seven and nine hours a night. Long sleepers with a risk of obesity were about 4kg heavier and short sleepers were about 2kg heavier than those with a similarly high genetic obesity risk with normal sleep durations. The negative affect happened irrespective of what subjects ate, their health concerns or socio-demographic factors, the research team said. The findings, based on data from almost 120,000 UK Biobank participants, showed no obvious link between sleep duration and body weight in those considered to be at a low genetic risk of obesity. Dr Jason Gill, from the Institute of Cardiovascular and Medical Sciences, said: "These data show that in people with high genetic risk for obesity, sleeping for too short or too long a time, napping during the day and shift work appears to have a fairly substantial adverse influence on body weight. © 2017 BBC.
Link ID: 23303 - Posted: 03.02.2017
By Matt Reynolds If you’re happy and you know it, clap someone else’s hands. A muscle stimulation system aims to evoke empathy by triggering involuntary hand gestures in one person in response to mood changes in another. “If you’re moving in the same way as another person you might understand that person better,” says Max Pfeiffer at the University of Hannover in Germany. Pfeiffer and his team wired up four people to an EEG machine that measured changes in the electrical activity in their brain as they watched film clips intended to provoke three emotional responses: amusement, anger and sadness. These people were the “emotion senders”. Each sender was paired with an “emotion recipient” who wore electrodes on their arms that stimulated their muscles and caused their arms and hands to move when the mood of their partner changed. The gestures they made were based on American Sign Language for amusement, anger and sadness. To express amusement, volunteers had their muscles stimulated to raise one arm, to express anger they raised an arm and made a claw gesture, and to express sadness they slowly slid an arm down their chest. These resemble natural movements associated with the feelings, so the team hypothesised that they would evoke the relevant emotion. Asked to rate how well the gestures corresponded to the emotions, the volunteers largely matched the gestures to the correct mood. © Copyright Reed Business Information Ltd.
Keyword: Brain imaging
Link ID: 23302 - Posted: 03.02.2017
Recently, an international team of researchers reported that the cerebellum may play a previously unforeseen role in brain alterations associated with the addictive consumption of drugs. Until now, the cerebellum—which has historically been viewed by most neuroscientists as primarily the seat of fine-tuned motor control and coordination—has gone under the radar of drug addiction specialists. The latest reports linking the cerebellum and drug addiction were based on a broad range of groundbreaking research published over the past two years. These findings were recently compiled and featured in two different journals: Neuroscience & Biobehavioral Reviews and the Journal of Neuroscience. Bringing all of this research together was the brainchild of Marta Miquel, professor in the research group Addiction and Neuroplasticity at the Universitat Jaume I (UJI) in Spain. Miguel spearheaded her own original research as well as the initiative to collect multidisciplinary research from a broad spectrum of international institutions and to present these cerebellar findings cohesively under one umbrella. (Cerebellar is the sister word to cerebral and means “relating to or located in the cerebellum.”) In addition to the UJI team, contributing research for this compilation of studies on the cerebellum and addiction came from the University of Cambridge and University of Leeds (United Kingdom); University of Turin (Italy); Universidad Veracruzana (Mexico); the University of Kentucky, Washington State University, and McLean Hospital Translational Neuroscience Laboratory and Mailman Research Center (USA). Psychology Today © 1991-2017 Sussex Publishers, LLC
Keyword: Drug Abuse
Link ID: 23301 - Posted: 03.02.2017
By Andy Coghlan People who have autoimmune disorders may be 20 per cent more likely to develop dementia. That’s according to an analysis of 1.8 million hospital cases in England. Based on data collected between 1999 and 2012, the study’s findings add to mounting evidence that chronic inflammation – a common feature of many autoimmune disorders – may be a trigger of dementia and Alzheimer’s disease. Previous studies have found that if infections or chronic inflammatory diseases – including diabetes – have pushed a person’s immune system into overdrive, this can lead to immune cells attacking healthy brain tissue. Varying effect According to the analysis, people with multiple sclerosis are among those with autoimmune disorders who are most likely to develop dementia. This finding isn’t very surprising, as the disorder is caused by the immune system attacking the central nervous system. The study, led by Michael Goldacre at the University of Oxford, found that people with the condition have double the risk of developing dementia. But other autoimmune disorders were also associated with rises in dementia risk. The skin condition psoriasis was linked to a 29 per cent increase, while the risk of developing dementia was 46 per cent higher in people who have lupus erythematosus, a disorder that involves rashes and fatigue. © Copyright Reed Business Information Ltd.
By NICHOLAS BAKALAR Acupuncture can relieve wrist pain, and researchers have tracked the brain and nervous system changes that may help explain why. Scientists randomized 80 people with mild or moderate carpal tunnel syndrome — pain caused by nerve compression at the wrist — to one of three groups. The first received acupuncture at the wrist and ankle. The second got acupuncture at the wrist alone. And the third received sham acupuncture, using “fake” needles near the affected wrist, as a placebo. Using functional M.R.I. and nerve conduction tests before and after the procedures, they measured the effect on brain and nerves. All three groups found relief from pain, but both of the true acupuncture groups showed measurable physiological improvements in pain centers in the brain and nerves, while sham acupuncture did not produce such changes. Improvement in brain measures predicted greater pain relief three months after the tests, a long-term effect that placebo did not provide. The study is in Brain. “What’s really interesting here is that we’re evaluating acupuncture using objective outcomes,” said the senior author, Vitaly Napadow, a researcher at Harvard. Sham acupuncture was good at relieving pain temporarily, he said, but true acupuncture had objective physiological — and enduring — effects. “Acupuncture is a safe, low-risk, low side-effect intervention,” he continued. “It’s perfect for a first-line approach, and it’s something patients should consider before trying more invasive procedures like surgery.” © 2017 The New York Times Company
Keyword: Pain & Touch
Link ID: 23299 - Posted: 03.02.2017
By Hanoch Ben-Yami Human intelligence, even in its most basic forms, is expressed in our language, and is also partly dependent on our linguistic capacity. Homer, Darwin and Einstein could obviously not have achieved what they did without language—but neither could a child in kindergarten. And this raises an important question about animal intelligence. Although we don’t expect a chimpanzee to write an epic or a dolphin to develop a scientific theory, it has frequently been asked whether these or other animals are close in intelligence to children in young children. If so, we must wonder whether animals can acquire a language. In the last half century, much effort has been put trying answer that question by teaching animals, primarily apes, a basic language. There have been some limited successes, with animals using signs to obtain things in which they were interested, for instance. But no animal has yet acquired the linguistic capability that children have already in their third year of life. “Why?” This is a question children start asking during by the age of three at the latest. No animal has yet asked anything. “Why?” is a very important question: it shows that those asking it are aware they don’t know something they wish to know. Understanding the why-question is also necessary for the ability to justify our actions and thoughts. The fact that animals don’t ask “why?” shows they don’t aspire to knowledge and are incapable of justification. “No!” © 2017 Scientific American,
by Laura Sanders Amid a flurry of cabinet appointments and immigration policies, the Trump administration has announced one thing it will not do: pursue policies that protect transgender children in public schools. The Feb. 22 announcement rescinds Obama administration guidelines that, among other protections, allow transgender kids to use bathrooms and participate in sports that correspond with their genders, and to be called by their preferred names and pronouns. In a Feb. 23 news briefing, White House press secretary Sean Spicer said that this is a states’ rights issue. “States should enact laws that reflect the values, principles, and will of the people in their particular state,” he said. “That's it, plain and simple.” But this “plain and simple” move could be quite dangerous, even deadly, science suggests. Transgender children, who are born one biological sex but identify as the other, already face enormous challenges as they move through a society that often doesn’t understand or accept them. Consider this: Nearly half (46.5 percent) of young transgender adults have attempted suicide at some point in their lives, a recent survey of over 2,000 people found. Nearly half. For comparison, the attempted suicide rate among the general U.S. population is estimated to be about 4.6 percent. What’s more, a 2015 study in the Journal of Adolescent Health found that transgender youth are two to three times as likely as their peers to suffer from depression and anxiety disorders, or to attempt suicide or harm themselves. These troublesome stats, based on a sample of 180 transgender children and young adults in Boston ages 12 to 29, applied equally to those who underwent male-to-female transitions and those who underwent female-to-male transitions. © Society for Science & the Public 2000 - 2017.
By Drake Baer If you’re going to get any sort of science done, an experiment needs a control group: the unaffected, possibly placebo-ed population that didn’t take part in whatever intervention it is you’re trying to study. Back in the earlier days of cognitive neuroscience, the control condition was intuitive enough: Just let the person in the brain scanner lie in repose, awake yet quiet, contemplating the tube they’re inside of. But in 1997, 2001, and beyond, studies kept coming out saying that it wasn’t much of a control at all. When the brain is “at rest,” it’s doing anything but resting. When you don’t give its human anything to do, brain areas related to processing emotions, recalling memory, and thinking about what’s to come become quietly active. These self-referential streams of thought are so pervasive that in a formative paper Marcus Raichle, a Washington University neurologist who helped found the field, declared it to be the “the default mode of brain function,” and the constellation of brain areas that carry it out are the default mode network, or DMN. Because when given nothing else to do, the brain defaults to thinking about the person it’s embedded in. Since then, the DMN has been implicated in everything from depression to creativity. People who daydream more tend to have a more active DMN; relatedly, dreaming itself appears to be an amplified version of mind-wandering. In Buddhist traditions, this chattering described by neuroscientists as the default mode is a dragon to be tamed, if not slain. Chögyam Trungpa, who was instrumental in bringing Tibetan Buddhism to the U.S., said the meditation practice is “necessary generally because our thinking pattern, our conceptualized way of conducting our life in the world, is either too manipulative, imposing itself upon the world, or else runs completely wild and uncontrolled,” he wrote in Cutting Through Spiritual Materialism. “Therefore, our meditation practice must begin with ego’s outermost layer, the discursive thoughts which continually run through our minds, our mental gossip.” © 2017, New York Media LLC.
By Edward G. Barrett It’s no secret that fewer than 10 percent of investigational drugs achieve regulatory approval and reach the marketplace. But the chances of success for drugs developed to treat Alzheimer’s disease are even more grim. Despite researchers’ valiant efforts to stall, slow, or even beat this devastating neurodegenerative condition, there are still no effective drugs available to the estimated 5.4 million Americans with the disease. The scientific community has watched in dismay, time and again, as potential Alzheimer’s drugs that produced promising data in rodent models failed to work as expected in humans. For the most part, these drugs have pursued the promising “amyloid hypothesis,” which states that the disease may be caused by accumulation of beta-amyloid peptide in brain tissue resulting in neuron-killing plaques. But so far, no drug candidates targeting the beta-amyloid pathway have prevailed through late-stage clinical trials. Earlier this year, for example, Merck halted a Phase 2/3 trial of verubecestat, a small molecule inhibitor of a protein implicated in the buildup of beta-amyloid, called beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), due to a lack of efficacy. Another high-profile example occurred late last year, when Eli Lilly’s solanezumab, a monoclonal antibody active against the beta-amyloid peptide, failed to prevent cognitive decline in a Phase 3 trial. These accumulating failures call into question the promise of targeting the formation and occurrence of amyloid plaques as a viable approach for treating Alzheimer’s. So how do we break the chain? Are there other approaches we could be taking that could give us valuable insight before investing in human studies? © 1986-2017 The Scientist
Link ID: 23295 - Posted: 03.01.2017
By GRETCHEN REYNOLDS For some people with early-stage Alzheimer’s disease, frequent, brisk walks may help to bolster physical abilities and slow memory loss, according to one of the first studies of physical activity as an experimental treatment for dementia. But the study’s results, while encouraging, showed that improvements were modest and not universal, raising questions about just how and why exercise helps some people with dementia and not others. Alzheimer’s disease affects more than five million people in the United States and more than 35 million worldwide, a number that is expected to double within 20 years. There are currently no reliable treatments for the disease. But past studies of healthy elderly people have found relationships between regular exercise and improved memories. Physically active older people are, for instance, significantly less likely than those who are sedentary to develop mild cognitive impairment, a frequent precursor to Alzheimer’s disease. Physically fit older people also tend to have more volume in their brain’s hippocampus than do sedentary people of the same age, brain scans show. The hippocampus is the portion of the brain most intimately linked with memory function. But most of this research has examined whether exercise might prevent Alzheimer’s disease. Little has been known about whether it might change the trajectory of the disease in people who already have the condition. So for the new study, published in February in PLoS One, researchers at the University of Kansas decided to work directly with people who had previously been given a diagnosis of Alzheimer’s disease. Because the disease can affect coordination as it progresses, the researchers focused on men and women in its early stages, who were still living at home and could safely walk by themselves or perform other types of light exercise. © 2017 The New York Times Company
Link ID: 23294 - Posted: 03.01.2017
By Victoria Sayo Turner When you want to learn something new, you practice. Once you get the hang of it, you can hopefully do what you learned—whether it’s parallel parking or standing backflips—on the next day, and the next. If not, you fall back to stage one and practice some more. But your brain may have a shortcut that helps you lock in learning. Instead of practicing until you’re decent at something and then taking a siesta, practicing just a little longer could be the fast track to solidifying a skill. “Overlearning” is the process of rehearsing a skill even after you no longer improve. Even though you seem to have already learned the skill, you continue to practice at that same level of difficulty. A recent study suggests that this extra practice could be a handy way to lock in your hard-earned skills. In the experiment, participants were asked to look at a screen and say when they saw a stripe pattern. Then two images were flashed one after the other. The images were noisy, like static on an old TV, and only one contained a hard-to-see stripe pattern. It took about twenty minutes of practice for people to usually recognize the image with stripes in it. The participants then continued to practice for another twenty minutes for the overlearning portion. Next, the participants took a break before spending another twenty minutes learning a similar “competitor” task where the stripes were oriented at a new angle. Under normal circumstances, this second task would compete with the first and actually overwrite that skill, meaning people should now be able to detect the second pattern but no longer see the first. The researchers wanted to see if overlearning could prevent the first skill from disappearing. © 2017 Scientific American
Keyword: Learning & Memory
Link ID: 23293 - Posted: 03.01.2017
Ed Yong It’s a good time to be interested in the brain. Neuroscientists can now turn neurons on or off with just a flash of light, allowing them to manipulate the behavior of animals with exceptional precision. They can turn brains transparent and seed them with glowing molecules to divine their structure. They can record the activity of huge numbers of neurons at once. And those are just the tools that currently exist. In 2013, Barack Obama launched the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative—a $115 million plan to develop even better technologies for understanding the enigmatic gray blobs that sit inside our skulls. John Krakaeur, a neuroscientist at Johns Hopkins Hospital, has been asked to BRAIN Initiative meetings before, and describes it like “Maleficent being invited to Sleeping Beauty’s birthday.” That’s because he and four like-minded friends have become increasingly disenchanted by their colleagues’ obsession with their toys. And in a new paper that’s part philosophical treatise and part shot across the bow, they argue that this technological fetish is leading the field astray. “People think technology + big data + machine learning = science,” says Krakauer. “And it’s not.” He and his fellow curmudgeons argue that brains are special because of the behavior they create—everything from a predator’s pounce to a baby’s cry. But the study of such behavior is being de-prioritized, or studied “almost as an afterthought.” Instead, neuroscientists have been focusing on using their new tools to study individual neurons, or networks of neurons. According to Krakauer, the unspoken assumption is that if we collect enough data about the parts, the workings of the whole will become clear. If we fully understand the molecules that dance across a synapse, or the electrical pulses that zoom along a neuron, or the web of connections formed by many neurons, we will eventually solve the mysteries of learning, memory, emotion, and more. “The fallacy is that more of the same kind of work in the infinitely postponed future will transform into knowing why that mother’s crying or why I’m feeling this way,” says Krakauer. And, as he and his colleagues argue, it will not. © 2017 by The Atlantic Monthly Group
Keyword: Brain imaging
Link ID: 23292 - Posted: 02.28.2017
By Robert F. Service Scientists are chasing a new lead on a class of drugs that may one day fight both pain and opioid addiction. It’s still early days, but researchers report that they’ve discovered a new small molecule that binds selectively to a long-targeted enzyme, halting its role in pain and addiction while not interfering with enzymes critical to healthy cell function. The newly discovered compound isn’t likely to become a medicine any time soon. But it could jumpstart the search for other binders that could do the job. Pain and addiction have many biochemical roots, which makes it difficult to treat them without affecting other critical functions in cells. Today, the most potent painkillers are opioids, including heroin, oxycodone, and hydrocodone. In addition to interrupting pain, they inhibit enzymes known as adenylyl cyclases (ACs) that convert cells’ energy currency, ATP, into a molecule involved in intracellular chemical communication known as cyclic AMP (cAMP). Chronic opioid use can make cells increase the activity of ACs to compensate, causing cAMP levels to skyrocket. When opioid users try to stop using, their cAMP levels remain high, and drugs that reduce those levels—like buprenorphine—have unwanted side effects. A promising candidate for selectively reducing cAMP is one particular AC enzyme, known as AC1. Humans have 10 ACs, all of which convert ATP to cAMP. But they are expressed at different levels in different tissues, suggesting they serve disparate purposes. Over the last 15 years, experiments on mice without the gene for AC1 have shown they have reduced sensitivity to pain and fewer signs of opioid dependence. But the enzyme, along with its close relative AC8, also appears to be heavily involved in memory formation in a brain region known as the hippocampus. © 2017 American Association for the Advancement of Science.
Keyword: Pain & Touch
Link ID: 23291 - Posted: 02.28.2017