Most Recent Links

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.

Featured Article

'Language Gene' Has a Partner

Few genes have made the headlines as much as FOXP2. The first gene associated with language disorders , it was later implicated in the evolution of human speech. Girls make more of the FOXP2 protein, which may help explain their precociousness in learning to talk. Now, neuroscientists have figured out how one of its molecular partners helps Foxp2 exert its effects.

The findings may eventually lead to new therapies for inherited speech disorders, says Richard Huganir, the neurobiologist at Johns Hopkins University School of Medicine in Baltimore, Maryland, who led the work. Foxp2 controls the activity of a gene called Srpx2, he notes, which helps some of the brain's nerve cells beef up their connections to other nerve cells. By establishing what SRPX2 does, researchers can look for defective copies of it in people suffering from problems talking or learning to talk.

Until 2001, scientists were not sure how genes influenced language. Then Simon Fisher, a neurogeneticist now at the Max Planck Institute for Psycholinguistics in Nijmegen, the Netherlands, and his colleagues fingered FOXP2 as the culprit in a family with several members who had trouble with pronunciation, putting words together, and understanding speech. These people cannot move their tongue and lips precisely enough to talk clearly, so even family members often can?t figure out what they are saying. It “opened a molecular window on the neural basis of speech and language,” Fisher says.

Photo credit: Yoichi Araki, Ph.D.

Links 1 - 20 of 22189

Laura Sanders Pain is contagious, at least for mice. After encountering bedding where mice in pain had slept, other mice became more sensitive to pain themselves. The experiment, described online October 19 in Science Advances, shows that pain can move from one animal to another — no injury or illness required. The results “add to a growing body of research showing that animals communicate distress and are affected by the distress of others,” says neuroscientist Inbal Ben-Ami Bartal of the University of California, Berkeley. Neuroscientist Andrey Ryabinin and colleagues didn’t set out to study pain transfer. But the researchers noticed something curious during their experiments on mice who were undergoing alcohol withdrawal. Mice in the throes of withdrawal have a higher sensitivity to pokes on the foot. And surprisingly, so did these mice’s perfectly healthy cagemates. “We realized that there was some transfer of information about pain” from injured mouse to bystander, says Ryabinin, of Oregon Health & Sciences University in Portland. When mice suffered from alcohol withdrawal, morphine withdrawal or an inflaming injection, they become more sensitive to a poke in the paw with a thin fiber — a touchy reaction that signals a decreased pain tolerance. Mice that had been housed in the same cage with the mice in pain also grew more sensitive to the poke, Ryabinin and colleagues found. These bystander mice showed other signs of heightened pain sensitivity, such as quickly pulling their tails out of hot water and licking a paw after an irritating shot. |© Society for Science & the Public 2000 - 20

Keyword: Chemical Senses (Smell & Taste); Pain & Touch
Link ID: 22773 - Posted: 10.20.2016

By Catherine Caruso Imagine you are faced with the classic thought experiment dilemma: You can take a pile of money now or wait and get an even bigger stash of cash later on. Which option do you choose? Your level of self-control, researchers have found, may have to do with a region of the brain that lets us take the perspective of others—including that of our future self. A study, published today in Science Advances, found that when scientists used noninvasive brain stimulation to disrupt a brain region called the temporoparietal junction (TPJ), people appeared less able to see things from the point of view of their future selves or of another person, and consequently were less likely to share money with others and more inclined to opt for immediate cash instead of waiting for a larger bounty at a later date. The TPJ, which is located where the temporal and parietal lobes meet, plays an important role in social functioning, particularly in our ability to understand situations from the perspectives of other people. However, according to Alexander Soutschek, an economist at the University of Zurich and lead author on the study, previous research on self-control and delayed gratification has focused instead on the prefrontal brain regions involved in impulse control. “When you have a closer look at the literature, you sometimes find in the neuroimaging data that the TPJ is also active during delay of gratification,” Soutschek says, “but it's never interpreted.” © 2016 Scientific American

Keyword: Attention
Link ID: 22772 - Posted: 10.20.2016

Hannah Devlin Science correspondent Monkeys have been observed producing sharp stone flakes that closely resemble the earliest known tools made by our ancient relatives, proving that this ability is not uniquely human. Previously, modifying stones to create razor-edged fragments was thought to be an activity confined to hominins, the family including early humans and their more primitive cousins. The latest observations re-write this view, showing that monkeys unintentionally produce almost identical artefacts simply by smashing stones together. The findings put archaeologists on alert that they can no longer assume that stone flakes they discover are linked to the deliberate crafting of tools by early humans as their brains became more sophisticated. Tomos Proffitt, an archaeologist at the University of Oxford and the study’s lead author, said: “At a very fundamental level - if you’re looking at a very simple flake - if you had a capuchin flake and a human flake they would be the same. It raises really important questions about what level of cognitive complexity is required to produce a sophisticated cutting tool.” Unlike early humans, the flakes produced by the capuchins were the unintentional byproduct of hammering stones - an activity that the monkeys pursued decisively, but the purpose of which was not clear. Originally scientists thought the behaviour was a flamboyant display of aggression in response to an intruder, but after more extensive observations the monkeys appeared to be seeking out the quartz dust produced by smashing the rocks, possibly because it has a nutritional benefit. © 2016 Guardian News and Media Limited

Keyword: Evolution
Link ID: 22771 - Posted: 10.20.2016

Tina Hesman Saey VANCOUVER — Zika virus’s tricks for interfering with human brain cell development may also be the virus’s undoing. Zika infection interferes with DNA replication and repair machinery and also prevents production of some proteins needed for proper brain growth, geneticist Feiran Zhang of Emory University in Atlanta reported October 19 at the annual meeting of the American Society of Human Genetics. Levels of a protein called p53, which helps control cell growth and death, shot up by 80 percent in human brain cells infected with the Asian Zika virus strain responsible for the Zika epidemic in the Americas, Zhang said. The lab dish results are also reported in the Oct. 14 Nucleic Acids Research. Increased levels of the protein stop developing brain cells from growing and may cause the cells to commit suicide. A drug that inactivates p53 stopped brain cells from dying, Zhang said. Such p53 inhibitors could help protect developing brains in babies infected with Zika. But researchers would need to be careful giving such drugs because too little p53 can lead to cancer. Zika also makes small RNA molecules that interfere with production of proteins needed for DNA replication, cell growth and brain development, Zhang said. In particular, a small viral RNA called vsRNA-21 reduced the amount of microcephalin 1 protein made in human brain cells in lab dishes. The researchers confirmed the results in mouse experiments. That protein is needed for brain growth; not enough leads to the small heads seen in babies with microcephaly. Inhibitors of the viral RNAs might also be used in therapies, Zhang suggested. |© Society for Science & the Public 2000 - 2016

Keyword: Development of the Brain
Link ID: 22770 - Posted: 10.20.2016

Hannah Devlin Science correspondent Migraine sufferers have a different mix of gut bacteria that could make them more sensitive to certain foods, scientists have found. The study offers a potential explanation for why some people are more susceptible to debilitating headaches and why some foods appear to act as triggers for migraines. The research showed that migraine sufferers had higher levels of bacteria that are known to be involved in processing nitrates, which are typically found in processed meats, leafy vegetables and some wines. The latest findings raise the possibility that migraines could be triggered when nitrates in food are broken down more efficiently, causing vessels in the brain and scalp to dilate. Antonio Gonzalez, a programmer analyst at the University of California San Diego and the study’s first author, said: “There is this idea out there that certain foods trigger migraines - chocolate, wine and especially foods containing nitrates. We thought that perhaps there are connections between what people are eating, their microbiomes and their experiences with migraines.” When nitrates in food are broken down by bacteria in the mouth and gut they are eventually converted into nitric oxide in the blood stream, a chemical that dilates blood vessels and can aid cardiovascular health by boosting circulation. © 2016 Guardian News and Media Limited

Keyword: Pain & Touch; Obesity
Link ID: 22769 - Posted: 10.19.2016

By Meredith Knight In June, international diabetes organizations endorsed provocative new guidelines suggesting physicians should consider gastric bypass surgery for a greatly expanded number of diabetics—those with a body mass index of 30 and above as opposed to just those with a BMI of 40 or more. Research has shown that the surgery helps people lose more weight, maintain the loss longer and achieve better blood glucose levels than those who slim down by changing diet and exercise habits. Now a study in mice suggests the effectiveness of bariatric surgery may stem in part from changes it causes in the brain. According to the study, published in the International Journal of Obesity, gastric bypass surgery causes the hyperactivation of a neural pathway that leads from stomach-sensing neurons in the brain stem to the lateral parabrachial nucleus, an area in the midbrain that receives sensory information from the body, and then to the amygdala, the brain's emotion- and fear-processing center. The obese mice underwent so-called Roux-en-Y bypass surgery, in which surgeons detach most of the stomach, leaving only a tiny pouch connected to the small intestine. Shortly after the surgery, the mice begin to show increased activation in this neural pathway, along with reduced meal size and a preference for less fatty food. They also begin to secrete higher levels of satiety hormones. Similar behavioral and hormonal patterns are found in humans after bypass surgery, suggesting that the brain changes may also be similar—but the authors say looking at this particular circuit in humans with brain imaging is difficult because the resolution is not up to the task. © 2016 Scientific American,

Keyword: Obesity
Link ID: 22768 - Posted: 10.19.2016

Susan Milius For widemouthed, musical midshipman fish, melatonin is not a sleep hormone — it’s a serenade starter. In breeding season, male plainfin midshipman fish (Porichthys notatus) spend their nights singing — if that’s the word for hours of sustained foghorn hums. Males dig trysting nests under rocks along much of North America’s Pacific coast, then await females drawn in by the crooning. New lab tests show that melatonin, familiar to humans as a possible sleep aid, is a serenade “go” signal, says behavioral neurobiologist Ni Feng of Yale University. From fish to folks, nighttime release of melatonin helps coordinate bodily timekeeping and orchestrate after-dark biology. The fish courtship chorus, however, is the first example of the hormone prompting a launch into song, according to Andrew Bass of Cornell University. And what remarkable vocalizing it is. The plainfin midshipman male creates a steady “mmm” by quick-twitching specialized muscles around its air-filled swim bladder up to 100 times per second in chilly water. A fish can extend a single hum for about two hours, Feng and Bass report October 10 in Current Biology. That same kind of super-fast muscle shakes rattle-snake tails and trills vocal structures in songbirds and bats. |© Society for Science & the Public 2000 - 2016

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 22767 - Posted: 10.19.2016

By MARC SANTORA The morning after Christine Grounds gave birth to her son Nicholas, she awoke to find a neurologist examining her baby. It was summer 2006, and Nicholas was her first child. There had been no indication that anything was wrong during her pregnancy, but it was soon clear that there was a problem. “Did you know he has microcephaly?” she remembers the doctor asking matter-of-factly. Confused, she replied, “What is microcephaly?” This was before the Zika virus had spread from Brazil across South and Central America and the Caribbean and reached Florida. It was before doctors had determined that the virus could cause microcephaly, a birth defect in which children have malformed heads and severely stunted brain development. And it was before people had seen the devastating pictures of scores of newborns with the condition in Brazil and elsewhere that shocked the world this year. Ms. Grounds, a 45-year-old psychotherapist, and her husband, Jon Mir, who live in Manhattan, had no idea what microcephaly would mean for them or for their child. “We had a diagnosis but no prognosis,” recalled Mr. Mir, 44, who works in finance. The doctors could offer few answers. “We don’t know if he will walk,” the couple recalled being told. “We don’t know if he will talk. He might be in a vegetative state.” But the truth was, even the doctors did not know. As mosquito season draws to a close in much of the country, taking with it the major risk of new Zika infections, there are still more than 2,600 pregnant women who have tested positive for the virus in the United States and its territories, according to the Centers for Disease Control and Prevention. They, and thousands more around the world, face the prospect of giving birth to a child with microcephaly. © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22766 - Posted: 10.19.2016

By Jessica Hamzelou Is depression caused by an inflamed brain? A review of studies looking at inflammation and depression has found that a class of anti-inflammatory drugs can ease the condition’s symptoms. Golam Khandaker at the University of Cambridge and his colleagues analysed 20 clinical studies assessing the effects of anti-cytokine drugs in people with chronic inflammatory conditions. These drugs block the effects of cytokines – proteins that control the actions of the immune system. Anti-cytokines can dampen down inflammation, and are used to treat rheumatoid arthritis. Together, these trials involved over 5,000 volunteers, and provide significant evidence that anti-cytokine drugs can also improve the symptoms of depression, Khandaker’s team found. These drugs work about as well as commonly used antidepressants, they say. The most commonly used anti-depressant drugs, known as SSRIs, act to increase levels of serotonin in the brain, to improve a person’s mood. But depression might not always be linked to a lack of serotonin, and SSRIs don’t work for everyone. Recent research has found that around a third of people with depression appear to have higher levels of cytokines in their brains, while people with “overactive” immune systems seem more likely to develop depression. Khandaker’s team think that inflammation in the brain might be responsible for the fatigue experienced by people with depression. © Copyright Reed Business Information Ltd.

Keyword: Depression; Neuroimmunology
Link ID: 22765 - Posted: 10.19.2016

By Meredith Wadman The second century C.E. Greek physician and philosopher Galen advised patients suffering from disorders of the spirit to bathe in and drink hot spring water. Modern day brain scientists have posited that Galen’s prescription delivered more than a placebo effect. Lithium has for decades been recognized as an effective mood stabilizer in bipolar disease, and lithium salts may have been present in the springs Galen knew. Yet exactly how lithium soothes the mind has been less than clear. Now, a team led by Ben Cheyette, a neuroscientist at the University of California in San Francisco (UCSF), has linked its success to influence over dendritic spines, tiny projections where excitatory neurons form connections, or synapses, with other nerve cells. Lithium treatment restored healthy numbers of dendritic spines in mice engineered to carry a genetic mutation that is more common in people with autism, schizophrenia, and bipolar disorder than in unaffected people, they report today in Molecular Psychiatry. The lithium also reversed symptoms in these mutant mice—lack of interest in social interactions, decreased motivation, and increased anxiety—that mimic those in the human diseases. “They showed there’s a correlation between the ability of lithium to reverse not only the behavioral abnormalities in the mice, but also the [dendritic] spine abnormalities,” says Scott Soderling, a neuroscientist at Duke University in Durham, North Carolina, who studies how dysfunctions in signaling at brain synapses and lead to psychiatric disorders. Soderling adds that the work also sheds light on the roots of these diseases. “It gives further credence to this idea that these spine abnormalities are functionally linked to the behavioral disorders.” © 2016 American Association for the Advancement of Science.

Keyword: Schizophrenia
Link ID: 22764 - Posted: 10.18.2016

Laura Sanders When the body’s internal sense of time doesn’t match up with outside cues, people can suffer, and not just from a lack of sleep. Such ailments are similar in a way to motion sickness — the queasiness caused when body sensations of movement don’t match the external world. So scientists propose calling time-related troubles, which can afflict time-zone hoppers and people who work at night, “circadian-time sickness.” This malady can be described, these scientists say, with a certain type of math. The idea, to be published in Trends in Neurosciences, is “intriguing and thought-provoking,” says neuroscientist Samer Hattar of Johns Hopkins University. “They really came up with an interesting idea of how to explain the mismatch.” Neuroscientist Raymond van Ee of Radboud University in the Netherlands and colleagues knew that many studies had turned up ill effects from an out-of-whack circadian clock. Depression, metabolic syndromes and memory troubles have been found alongside altered daily rhythms. But despite these results, scientists don’t have a good understanding of how body clocks work, van Ee says. Van Ee and colleagues offer a new perspective by using a type of math called Bayesian inference to describe the circadian trouble. Bayesian inference can be used to describe how the brain makes and refines predictions about the world. This guesswork relies on the combination of previous knowledge and incoming sensory information (SN: 5/28/16, p. 18). In the case of circadian-time sickness, these two cues don’t match up, the researchers propose. |© Society for Science & the Public 2000 - 2016

Keyword: Sleep
Link ID: 22763 - Posted: 10.18.2016

By PERRI KLASS, M.D. It’s a classic which-came-first question: Is the child not getting enough sleep because of problem behaviors, especially at bedtime, or is the child behaving problematically because of not getting enough sleep? The answers are most likely yes and yes, and the back-and-forth currents can drag a child down developmentally. In an editorial in JAMA Pediatrics in 2015, Michelle M. Garrison, a research assistant professor at the University of Washington in the division of child and adolescent psychiatry, described this intersection of sleep and behavior problems in early childhood as a “feedback whirlpool.” Dr. Garrison was commenting on a longitudinal study of more than 32,000 Norwegian mothers and their children who were followed from birth to age 5; the children with sleep problems at 18 months, including short sleep duration (sleeping 10 hours or less) or frequent nocturnal awakenings (three times a night or more) had more emotional and behavioral problems at the age of 5. This held true even when the researchers adjusted for emotional and behavioral problems already present in the 18-month-olds; compared to children at the same behavioral baseline, the kids with sleep problems ran into more difficulties as they developed. “Sleep really does drive behavior problems and behavior problems are driving sleep problems, it really is bidirectional,” Dr. Garrison said. “A child can start having problems with emotional regulation, melting down more, and that makes it more difficult for the family to do all the things they have to do so the child can get good sleep. Sleep gets worse; behavior gets worse. It can really be an awful cycle for the kid and the family both.” Dr. Oskar Jenni, a professor of developmental pediatrics at Zurich University Children’s Hospital, said that there is a great deal of variation in the individual sleep needs of children at any given age. Parents need to understand their children’s sleep needs and rhythms, since behavior problems can also arise when children are compelled to spend more time in bed than they actually need. “My main message is adjusting bedtime to the needs of the children in both directions,” he said. © 2016 The New York Times Company

Keyword: Sleep
Link ID: 22762 - Posted: 10.18.2016

By Michael Price When you’re smiling, it may feel like the whole world is smiling with you, but a new study suggests that some facial expressions may not be so universal. In fact, several expressions commonly understood in the West—including one for fear—have very different meanings to one indigenous, isolated society in Papua New Guinea. The new findings call into question some widely held tenets of emotional theory, and they may undercut emerging technologies, like robots and artificial intelligence programs tasked with reading people’s emotions. For more than a century, scientists have wondered whether all humans experience the same basic range of emotions—and if they do, whether they express them in the same way. In the 1870s, it was the central question Charles Darwin explored in The Expression of the Emotions in Man and Animals. By the 1960s, emeritus psychologist Paul Ekman, then at the University of California (UC) in San Francisco, had come up with an accepted methodology to explore this question. He showed pictures of Westerners with different facial expressions to people living in isolated cultures, including in Papua New Guinea, and then asked them what emotion was being conveyed. Ekman’s early experiments appeared conclusive. From anger to happiness to sadness to surprise, facial expressions seemed to be universally understood around the world, a biologically innate response to emotion. That conclusion went virtually unchallenged for 50 years, and it still features prominently in many psychology and anthropology textbooks, says James Russell, a psychologist at Boston College and corresponding author of the recent study. But over the last few decades, scientists have begun questioning the methodologies and assumptions of the earlier studies. © 2016 American Association for the Advancement of Science.

Keyword: Emotions
Link ID: 22761 - Posted: 10.18.2016

By DONNA DE LA CRUZ Some of the most troubling images of the opioid crisis involve parents buying or using drugs with their children in tow. Now new research offers a glimpse into the addicted brain, finding that the drugs appear to blunt a person’s natural parenting instincts. Researchers at the Perelman School of Medicine at the University of Pennsylvania scanned the brains of 47 men and women before and after they underwent treatment for opioid dependence. While in the scanner, the study subjects looked at various images of babies, and the researchers measured the brain’s response. The brain scans were compared with the responses of 25 healthy people. What the study subjects didn’t know was that the photos had been manipulated to adjust the “baby schema,” the term used to describe the set of facial and other features like round faces and big eyes that make our brains register babies as irresistible, kicking in our instinct to care for them. Sometimes the babies’ features were exaggerated to make them even more adorable; in others, the chubby cheeks and big eyes were reduced, making the faces less appealing. Studies show that a higher baby schema activates the part of the brain called the ventral striatum, a key component of the brain reward pathway. Compared with the brains of healthy people, the brains of people with opioid dependence didn’t produce strong responses to the cute baby pictures. But once the opioid-dependent people received a drug called naltrexone, which blocks the effects of opioids, their brains produced a more normal response. “When the participants were given an opioid blocker, their baby schema became more similar to that of healthy people,” said Dr. Daniel D. Langleben, one of the researchers. “The data also raised in question whether opioid medications may affect social cognition in general.” © 2016 The New York Times Company

Keyword: Drug Abuse; Attention
Link ID: 22760 - Posted: 10.15.2016

Linda Geddes For the first time, a paralysed man has gained a limited sense of touch, thanks to an electric implant that stimulates his brain and allows him to feel pressure-like sensations in the fingers of a robotic arm. The advance raises the possibility of restoring limited sensation to various areas of the body, as well as giving people with spinal-cord injuries better control over prosthetic limbs. But restoring human-like feeling, such as sensations of heat or pain, will prove more challenging, the researchers say. Nathan Copeland had not been able to feel or move his legs and lower arms since a car accident snapped his neck and injured his spinal cord when he was 18. Now, some 12 years later, he can feel when a robotic arm has its fingers touched, because sensors on the fingers are linked to an implant in his brain. Brain implant restores paralysed man's sense of touch Rob Gaunt, a biomedical engineer at the University of Pittsburgh, performs a sensory test on a blindfolded Nathan Copeland. Nathan, who is paralysed, demonstrates his ability to feel by correctly identifying different fingers through a mind-controlled robotic arm. Video credit: UPMC/Pitt Health Sciences. “He says the sensations feel like they’re coming from his own hand,” says Robert Gaunt, a biomedical engineer at the University of Pittsburgh who led the study. © 2016 Macmillan Publishers Limited

Keyword: Robotics; Pain & Touch
Link ID: 22759 - Posted: 10.15.2016

Bruce Bower Scientists, politicians, clinicians, police officers and medical workers agree on one thing: The U.S. mental health system needs a big fix. Too few people get the help they need for mental ailments and emotional turmoil that can destroy livelihoods and lives. A report in the October JAMA Internal Medicine, for instance, concludes that more than 70 percent of U.S. adults who experience depression don’t receive treatment for it. Much attention focuses on developing better psychiatric medications and talk therapies. But those tactics may not be enough. New research suggests that the longstanding but understudied problem of stigma leaves many of those suffering mental ailments feeling alone, often unwilling to seek help and frustrated with treatment when they do. “Stigma about mental illness is widespread,” says sociologist Bernice Pescosolido of Indiana University in Bloomington. And the current emphasis on mental ills as diseases of individuals can unintentionally inflame that sense of shame. An effective mental health care system needs to address stigma’s suffocating social grip, investigators say. “If we want to explain problems such as depression and suicide, we have to see them in a social context, not just as individual issues,” Pescosolido says. |© Society for Science & the Public 2000 - 2016

Keyword: Depression
Link ID: 22758 - Posted: 10.15.2016

By JOHN C. MARKOWITZ The United States government recently announced its new director of the National Institute of Mental Health, Dr. Joshua Gordon. If you think that’s just bureaucracy as usual, think again. Mental health research, under the leadership of the previous director, Dr. Thomas Insel, underwent a quiet crisis, one with worrisome implications for the treatment of mental health. I hope Dr. Gordon will resolve it. For decades, the National Institute of Mental Health provided crucial funding for American clinical research to determine how well psychotherapies worked as treatments (on their own as well as when combined with medications). This research produced empirical evidence supporting the effectiveness of cognitive behavioral therapy, interpersonal psychotherapy and other talking treatments. But over the past 13 years, Dr. Insel increasingly shifted the institute’s focus to neuroscience, strangling its clinical research budget. Dr. Insel wasn’t wrong to be enthusiastic about the possibilities of neuroscientific research. Compared with the psychiatric diagnoses listed in the Diagnostic and Statistical Manual of Mental Disorders (D.S.M.), which can be vague and flawed, brain-based research holds out the promise of a precise and truly scientific understanding of mental illness. Psychiatric diagnoses depend on clusters of signs and symptoms. For major depression, for example, some criteria are low mood; wanting to die; and sleep, appetite and energy changes. These diagnoses lack the specificity of the biological markers that neuroscience seeks to identify. If we could find a genetic, neuroimaging or brain-circuit explanation for a mental illness, it might even yield a cure, rather than just the treatment of what can be recurrent, chronic conditions. But where does that leave patients whom today’s treatments do not help? Can they wait for neuroscience developments that may take decades to appear, or prove illusory? Staking all your money on one bet, as the institute did under Dr. Insel, has consequences. © 2016 The New York Times Company

Keyword: Depression
Link ID: 22757 - Posted: 10.15.2016

Analysis of a trial that used the drug canagliflozin found that as people lost weight, their appetite increased proportionately, leading to consumption of more calories and weight loss plateau (leveling off). The findings provide the first measurement in people of how strongly appetite counters weight loss as part of the body’s feedback control system regulating weight. Results are currently available on BioRxiv (link is external) and will publish in Obesity during Obesity Week 2016. A team led by the NIH’s National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) analyzed data from a year-long, placebo-controlled, double-blind trial in people with type 2 diabetes who could eat and drink without restriction by the study. Of the 242 participants, 153 received canagliflozin, a drug that caused a substantial increase in the amount of glucose excreted in their urine. Those people were not directly aware of that calorie loss, which caused a gradual decrease in weight averaging about eight pounds. The team used a validated math model to calculate the changes in the amount of calories consumed during the study. They found no long-term calorie intake changes in the 89 people who got a placebo. However, for every pound of lost weight, the people treated with canagliflozin consumed about 50 calories per day more than they were eating before the study. This increase in appetite and calorie intake led to slowing of weight loss after about six months. The measurements are consistent with the researchers’ analysis of data from a separate trial on a commercial weight loss program not involving canagliflozin. In the weight loss program trial, despite the dieters’ consistent efforts to reduce calorie intake, their increased appetite resulted in a progressive increase in calorie intake — three times stronger than the changes in caloric expenditure that typically accompany weight loss — and weight loss plateau. Findings from the analyses suggest that persistent effort is required to avoid weight regain.

Keyword: Obesity
Link ID: 22756 - Posted: 10.15.2016

By Jessica Boddy You’d probably never notice a jumping spider across your living room, but it would surely notice you. The arachnids are known for their brilliant eyesight, and a new study shows they have even greater sensory prowess than we thought: Jumping spiders can hear sounds even though they don’t have ears—or even eardrums. To find this out, researchers implanted tiny electrodes in a region of spiders’ brains that would show whether sound was being processed. Then they placed the spiders on a specially designed box to eliminate any vibrations from below—most spiders sense their surroundings through vibrations—and scared the heck out of them with a speaker-produced buzz of one of their predators, the mud dauber wasp. An out-of-earshot, high-frequency buzz and a silent control elicited no response from the spiders. But the 80-hertz wasp buzz made them freeze and look around, startled, just as they would do in the wild. What’s more, data from the electrodes showed a spike in brain activity with each buzz, revealing that spiders actually hear sounds, from a swooping mud dauber wasp to you crunching potato chips on your couch. The researchers, who publish their work today in Current Biology, say further study is needed to see exactly how spiders receive sounds without eardrums, but they believe sensitive hairs on their legs play a part. © 2016 American Association for the Advancement of Science.

Keyword: Hearing
Link ID: 22755 - Posted: 10.15.2016

By Gary Stix The new mantra for researchers fighting Alzheimer’s disease is “go early,” before memory loss or other pathology appears. The rationale for this approach holds that by the time dementia sets in the disease may already be destroying brain cells, placing severe limits on treatment options. Some large clinical trials are now testing drugs intended to clear up the brain’s cellular detritus—the aggregations of amyloid and tau proteins that may ultimately destroy brain cells. So far this approach has had decidedly mixed results. Some researchers are choosing a different direction. They have begun to ask what happens in the brain before the plaques and tangles of amyloid and tau appear—and to look at interventions that might work at this incipient disease stage. The Alzheimer’s Disease Drug Discovery Foundation has focused in recent years on funding new agents that do not target amyloid but are intended to address other manifestations of the disease, such as inflammation and the energy metabolism of neurons. At a meeting last month in Jersey City, N.J., neuroscientist Grace Stutzmann of the Chicago Medical School at Rosalind Franklin University of Medicine and Science presented her work on restoring a basic cellular process—called calcium signaling—that goes off track in Alzheimer’s. Scientific American asked her recently about her work. © 2016 Scientific American,

Keyword: Alzheimers
Link ID: 22754 - Posted: 10.13.2016