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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.
By Ann Gibbons Depressed? Your inner Neandertal may be to blame. Modern humans met and mated with these archaic people in Europe or Asia about 50,000 years ago, and researchers have long suspected that genes picked up in these trysts might be shaping health and well-being today. Now, a study in the current issue of Science details their impact. It uses a powerful new method for scanning the electronic health records of 28,000 Americans to show that some Neandertal gene variants today can raise the risk of depression, skin lesions, blood clots, and other disorders. Neandertal genes aren’t all bad. “These variants sometimes protect against a disease, sometimes make people more susceptible to disease,” says paleogeneticist Svante Pääbo of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. Two other new studies identified three archaic genes that boost immune response. And most archaic genes that persist in humans were likely beneficial in prehistoric times. But some now cause disease because modern lifestyles and environments are so different. Living people carry only trace amounts of Neandertal DNA, which makes its impact on health more striking. “The Neandertal genetic contribution to present-day people seems to have larger physiological effects than I would have naïvely thought,” says Pääbo, who helped launch this avenue of research by sequencing the first ancient genomes but was not involved in these studies. On average, Europeans and Asians have inherited about 1.5% of their genomes from Neandertals. Island Melanesians carry an additional 2% to 3% of DNA inherited from another extinct group, the Denisovans. Most Africans lack this archaic DNA because the interbreeding happened after modern humans left Africa. © 2016 American Association for the Advancement of Science
Mo Costandi Tell me where dwell the thoughts, forgotten till thou call them forth? Tell me where dwell the joys of old, and where the ancient loves, And when will they renew again, and the night of oblivion past, That I might traverse times and spaces far remote, and bring Comforts into a present sorrow and a night of pain? Where goest thou, O thought? To what remote land is thy flight? If thou returnest to the present moment of affliction, Wilt thou bring comforts on thy wings, and dews and honey and balm, Or poison from the desert wilds, from the eyes of the envier? In his epic poem, Visions of the Daughters of Albion, William Blake wonders about the nature of memory, its ability to mentally transport us to distant times and places, and the powerful emotions, both positive and negative, that our recollections can evoke. The poem contains questions that remain highly pertinent today, such as what happens to our long-lost memories, and how do we retrieve them? More than two centuries later, the mechanisms of memory storage and retrieval are the most intensively studied phenomena in the brain sciences. It’s widely believed that memory formation involves the strengthening of connections between sparsely distributed networks of neurons in a brain structure called the hippocampus, and that subsequent retrieval involves reactivation of the same neuronal ensembles. And yet, neuroscientists still struggle to answer Blake’s questions definitely. Now, a team of researchers at the University of Geneva have made another important advance in our understanding of the neural mechanisms underlying memory formation. Using a state-of-the-art method called optogenetics, they show how the neuronal ensembles that encode memories emerge, revealing that ensembles containing too many neurons – or too few – impair memory retrieval. © 2016 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 21893 - Posted: 02.13.2016
Sara Reardon Mice are sensitive to minor changes in food, bedding and light exposure. It’s no secret that therapies that look promising in mice rarely work in people. But too often, experimental treatments that succeed in one mouse population do not even work in other mice, suggesting that many rodent studies may be flawed from the start. “We say mice are simpler, but I think the problem is deeper than that,” says Caroline Zeiss, a veterinary neuropathologist at Yale University in New Haven, Connecticut. Researchers rarely report on subtle environmental factors such as their mice’s food, bedding or exposure to light; as a result, conditions vary widely across labs despite an enormous body of research showing that these factors can significantly affect the animals’ biology. “It’s sort of surprising how many people are surprised by the extent of the variation” between mice that receive different care, says Cory Brayton, a pathologist at Johns Hopkins University in Baltimore, Maryland. At a meeting on mouse models at the Wellcome Genome Campus in Hinxton, UK, on 9–11 February, she and others explored the many biological factors that prevent mouse studies from being reproduced. Christopher Colwell, a neuroscientist at the University of California, Los Angeles, has first-hand experience with these issues. He and a colleague studied autism in the same genetically modified mouse line, but obtained different results on the same behaviour tests. Eventually they worked out why: Colwell, who studies circadian rhythms, keeps his mice dark in the daytime to trick their body clocks into thinking day is night, so that the nocturnal animals are more alert when tested during the day. His colleague does not. © 2016 Nature Publishing Group
By Uri Bram Early-life exposure to pathogenic bacteria can induce a lifelong imprinted olfactory memory in C. elegans through two distinct neural circuits, according to a study published today (February 11) in Cell. Researchers from Rockefeller University in New York City have shown that early-life pathogen exposure leads the nematode to have a lifelong aversion to the specific associated bacterial odors, whereas later-in-life exposure spurs only transient aversion. “This study is very exciting,” said Yun Zhang of Harvard who studies learning in C. elegans but was not involved in the present work. “Imprinting is a form of learning widely observed in many animals [but] finding this in C. elegans is very meaningful because this nematode is genetically tractable, and its small nervous system is well described.” A classic example of imprinting is how geese form attachments to the first moving object they see after birth; Nobel laureate Konrad Lorenz famously showed that the “moving object” could be himself instead of a mother goose. During the critical period at the start of life, animals often have unusual abilities to create and maintain long-term memories. For the present study, Rockefeller’s Xin Jin and colleagues described a form of aversive imprinting in their C. elegans: newly hatched nematodes exposed to Pseudomonas aeruginosa PA14 or toxin-emitting Escherichia coli BL21 established a long-term olfactory aversion to it. Animals that experienced the pathogen immediately after hatching were able to synthesize and maintain the aversive memory for the whole of their four-day lifespans, while animals trained in adulthood only retained the aversive memory for up to 24 hours. © 1986-2016 The Scientist
Alan Yuhas in Washington DC Scientists working on genetically modified worms have made what they hope are the first steps towards developing a preventative treatment for Alzheimer’s disease. The study, published in the journal Science Advances and presented at the American Association for the Advancement of Science conference, describes how researchers modified nematode worms to develop Alzheimer’s-like symptoms, and then applied the existing anti-cancer drug, bexarotene, at various stages of the disease. “We showed that these worms that were doomed to develop Alzheimer’s disease could be rescued,” said study author Michele Vendruscolo, of the University of Cambridge. “It is a powerful first step,” he said. “It is very exciting, but at the same time we are very aware it the first step and many things can go wrong.” Researchers believe that Alzheimer’s destroys brain function through a catastrophic cascade of events: natural proteins start folding and glomming onto each other in dysfunctional ways, a process that in turn creates the toxic molecules thought to kill brain cells. When the proteins started malfunctioning in the worms, the drug could do nothing to save them. But if administered before symptoms developed, it prevented the first stage of the process. © 2016 Guardian News and Media Limited
Janet Raloff WASHINGTON ― Many people have turned to electronic cigarettes in hopes of avoiding the heart and cancer risks associated with smoking conventional tobacco products. But vaping appears far from benign, a trio of toxicologists reported February 11 and 12 at the American Association for the Advancement of Science annual meeting. If used as a means to totally wean people off of tobacco products, then e-cigarettes might have value, concedes Ilona Jaspers of the University of North Carolina at Chapel Hill. But she’s not sure. Unpublished data that she and the others presented at the meeting link e-cig products to a host of new risks. So vaping may not eliminate risks associated with conventional smoking, Jaspers maintains ― “and may actually be introducing new ones.” Her group examined scraped cells from the noses of otherwise healthy people who had a history of smoking, vaping or doing neither. The researchers then measured the activity levels in these cells of 594 genes associated with the body’s ability to fight infections. Among smokers, the activity of 53 genes was substantially diminished, compared with people who neither smoked nor vaped. Among vapers, those same 53 genes showed significantly diminished activity, Jaspers reported, as did 305 more. The normal role of these genes would suggest that the lung tissue as well as nasal tissue of smokers ― and especially vapers ―“may be more susceptible to any kind of infection.” © Society for Science & the Public 2000 - 2016.
Keyword: Drug Abuse
Link ID: 21889 - Posted: 02.13.2016
By Julia Shaw The approach to Valentine's Day is a reminder that we humans are so intrigued by the idea of love that we have made it into something to celebrate in it’s own right. Love is something amazing. Love is something special. But what are the implications of love for our memories? Remember those “your brain on drugs” awareness posters? You can essentially substitute “love” for “drugs” and the same warnings apply. Scientists have found that being in love actually makes you activate some of the same brain regions as when you take addictive drugs, like ecstasy or cocaine. Neuroscientist Kayo Takahashi and his team have described passionate love as an “all-encompassing experience” which has “disorienting effects” and is generally considered “highly pleasurable”. While you probably don’t need a bunch of scientists to tell you that, you probably do need them to explain what that actually means in the brain. In 2015 Kayo and his team were keen on exploring the role of one particular culprit of the feel-good effects of love, the neurotransmitter dopamine. Among many other effects, dopamine generally makes us feel pleasure. Kayo and his team looked into the brains of people who were in the early stages of romantic relationships, and they found that when shown pictures of their romantic partners, participants experienced a flood of dopamine to parts of their brains. As it turns out, brains need to release dopamine in order to store long-term memories. © 2016 Scientific American
By PAM BELLUCK The risk of developing dementia is decreasing for people with at least a high school education, according to an important new study that suggests that changes in lifestyle and improvements in physical health can help prevent or delay cognitive decline. The study, published Wednesday in The New England Journal of Medicine, provides the strongest evidence to date that a more educated population and better cardiovascular health are contributing to a decline in new dementia cases over time, or at least helping more people stave off dementia for longer. The findings have implications for health policy and research funding, and they suggest that the long-term cost of dementia care may not be as devastatingly expensive as policy makers had predicted, because more people will be able to live independently longer. There are wild cards that could dampen some of the optimism. The study participants were largely white and suburban, so results may not apply to all races and ethnicities. Still, a recent study showed a similar trend among African-Americans in Indianapolis, finding that new cases of dementia declined from 1992 to 2001. The 2001 participants had more education, and although they had more cardiovascular problems than the 1992 participants, those problems were receiving more medical treatment. Another question mark is whether obesity and diabetes, which increase dementia risk, will cause a surge in dementia cases when the large number of overweight or diabetic 40- and 50-year-olds become old enough to develop dementia. © 2016 The New York Times Company
By Sheena Goodyear, A brain implant the size of a paper-clip might one day help paralyzed people regain the ability to use their arms and legs via a wireless connection that will transmit their thoughts to an exoskeleton. It's not the first technology to allow paralyzed people to operate mechanical limbs with signals from their brain, but it has the potential to revolutionize the field because it's minimally invasive and totally wireless. It's made possible because of a matchstick-sized implant called a stentrode, crafted from nitinol, an alloy that is commonly used in brassiere underwires and eyeglass frames, according to a study published in the journal Nature Biotechnology. "It's really a new method for getting brain data out of the brain without performing brain surgery," Thomas Oxley, a neurologist at the University of Melbourne who designed the device, told CBC News. "Part of the reason that brain-machine interfaces have not been successful to this point is because they get rejected by the body, and the reason they get rejected is because they all require direct implantation into the brain. And to do that you have to take off the skull — you have to perform a craniotomy." ©2016 CBC/Radio-Canada.
Link ID: 21886 - Posted: 02.11.2016
Rae Ellen Bichell There's been a male tilt to biomedical research for a long time. The National Institutes of Health is trying to change that and is looking to bring gender balance all the way down to the earliest stages of research. As a condition of NIH funding, researchers will now have to include female and male animals in their biomedical studies. As late as the 1990s, researchers worried that testing drugs in women who could be pregnant or become pregnant might lead to birth defects, so experimental drugs were mainly tested in men. Research in animals followed the same pattern. "There was not the understanding that it really isn't scientifically appropriate to study men and apply your findings to women. We just didn't know that back then," says Dr. Janine Clayton, director of the Office of Research on Women's Health at the NIH. When the drugs this way finally went to market and women took them, sometimes things went wrong. To try to fix the problem, the NIH and Congress required that women and men be included in research involving human subjects. Now, there are more women than men participating in clinical trials, at least in studies funded by the NIH. But there's still a mystery: Why do women still report many more bad reactions to medications than men do? "Men and women respond to medications differently. In fact, one study looked at the drugs that have been taken off the market and 8 of the 10 drugs taken off the market in that particular time period had more severe effects in women," says Clayton. © 2016 npr
Keyword: Sexual Behavior
Link ID: 21885 - Posted: 02.11.2016
Jo Marchant The brain cells of people with Parkinson’s disease can be trained to reliably respond to placebo drugs, Italian neuroscientists report. The training wears off after 24 hours but the effect shows it may be possible to reduce the medication needed to treat Parkinson’s by interspersing real drugs with inert injections or pills, says placebo researcher Fabrizio Benedetti at the University of Turin, Italy, who led the work. A few people with Parkinson’s disease do respond dramatically to placebos, but most do not1. People with the condition suffer characteristic tremors and stiff muscles because their dopamine-producing brain cells are gradually dying off. They alleviate their symptoms by taking drugs such as apomorphine, which activate receptors for dopamine. For some conditions — such as pain and immune disorders — trials have shown2 that it is possible to train people to respond to placebos, although this practice hasn’t made its way into clinical care. Benedetti and his colleagues wondered whether the same effect might be possible for neurological disorders. They studied 42 people with advanced Parkinson’s disease who were having electrodes implanted into their brains for a therapy called deep brain stimulation, which eases symptoms by stimulating affected brain areas directly. That surgery gave Benedetti’s team a rare opportunity to measure the activity of individual neurons in the thalamus, a brain region known to be inhibited by lack of dopamine in people with Parkinson's. © 2016 Nature Publishing Grou
Link ID: 21884 - Posted: 02.10.2016
By CARL ZIMMER The Zika virus has quickly gained Ebola-level notoriety as it has spread through the Western Hemisphere in recent months. Researchers in Brazil, where it was first detected in May, have linked infections in pregnant women to a condition known as microcephaly: infants born with undersize heads. Where birth defects are concerned, however, the Zika virus is far from unique. A number of other viruses, such as rubella and cytomegalovirus, pose a serious risk during pregnancy. Researchers have uncovered some important clues about how those pathogens injure fetuses — findings that are now helping to guide research into the potential link between Zika and microcephaly. “I think we’ll discover a lot of parallels,” said Dr. Mark R. Schleiss, the director of pediatric infectious diseases and immunology at the University of Minnesota Medical School. The risk that viruses pose during pregnancy came to light in the mid-1900s, when outbreaks of rubella, or German measles, led to waves of birth defects, including microcephaly, cataracts and deformed hearts and livers. The number of infants affected was staggering. In an epidemic in Philadelphia in 1965, 1 percent of all babies were born with congenital rubella syndrome, which can also cause deafness, developmental disability, low birth weight and seizures. Because of vaccinations, such devastation is now rare in the United States and a number of other countries. “I’m 52, and I’ve seen one case of congenital rubella syndrome,” said Dr. David W. Kimberlin, a professor of pediatrics at the University of Alabama at Birmingham. But the virus is still a grave threat in developing countries. Worldwide, more than 100,000 children are born each year with congenital rubella syndrome. © 2016 The New York Times Company
Keyword: Development of the Brain
Link ID: 21883 - Posted: 02.10.2016
By Jordana Cepelewicz Seasonal variations play a major role in the animal kingdom—in reproduction, food availability, hibernation, even fur color. Whether this seasonality has such a significant influence on humans, however, is an open question. Its best-known association is with mood—that is, feeling down during the colder months and up in the summer—and, in extreme cases, seasonal depression, a phenomenon known as seasonal affective disorder (SAD). A new study published in this week’s Proceedings of the National Academy of Sciences seeks to delve deeper into how human biology has adapted not only to day/night cycles (circadian rhythms) but to yearly seasonal patterns as well. Scientists have previously found seasonal variation in the levels and concentrations of certain compounds associated with mood (including dopamine and serotonin), conception and even mortality. Now for the first time, using functional MRI, “it’s [been] conclusively shown that cognition and the brain’s means of cognition are seasonal,” says neuroscientist Gilles Vandewalle of the University of Liège in Belgium, the study’s lead researcher. These findings come at a time when some scientists are disputing the links between seasonality and mental health. Originally aiming to investigate the impact of sleep and sleep deprivation on brain function, Vandewalle and his fellow researchers placed 28 participants on a controlled sleep/wake schedule for three weeks before bringing them into the laboratory, where they stayed for 4.5 days. During this time they underwent a cycle of sleep deprivation and recovery in the absence of seasonal cues such as natural light, time information and social interaction. Vandewalle’s team repeated the entire procedure with the same subjects several times throughout the course of nearly a year and a half. © 2016 Scientific American
By Michelle Roberts Health editor, Exposure to short flashes of light at night could help sleeping travellers adjust to new time zones and avoid jet lag, according to US scientists. The light beams travel through the eyelids and this tells the brain to re-set the body's inner biological clock, the Stanford researchers believe. They tested the method in 39 volunteers and found it shifted a person's body clock by about two hours. An hour of the flashlight therapy was enough to achieve this effect. People's bodies synchronise to the 24-hour pattern of daytime and night they are used to. And when they travel across time zones to a new light-dark schedule, they need to realign. While most people can easily manage a long-haul flight across one or two time zones, crossing several time zones messes with the body clock. Jet lag can leave travellers tired, irritable and disorientated for days. As a remedy, some people take melatonin tablets, which mimic a hormone released in the evening. Some try phototherapy - light boxes that simulate daylight. But Dr Jamie Zeitzer and colleagues at Stanford University School of Medicine believe sleeping in front of a strobe light could work better. They asked volunteers to go to bed and wake up at the same times every day for about two weeks. Next, they were asked to sleep in the lab, where some were exposed to continuous light and others a strobe light (two-millisecond flashes of light, similar to a camera flash, 10 seconds apart) for an hour. The flashing-light group reported a nearly two-hour delay in the onset of sleepiness the following night. In comparison, the delay in sleepiness was 36 minutes for the continuous-light group. Dr Zeitzer calls his therapy "biological hacking". Cells in the back of the eye that detect the light send messages to a part of the brain that sets the body clock. The light fools the brain into thinking the day is longer than it really is, which shifts the inner clock. © 2016 BBC.
Keyword: Biological Rhythms
Link ID: 21881 - Posted: 02.10.2016
Ice cream lovers, look away now. Studies on a simulated human gut have added further evidence that emulsifiers, found in most processed foods, might be linked to obesity, diabetes and inflammatory bowel disorders. Emulsifiers are used to improve a food’s texture and to prevent mixtures from separating, particularly in ice cream. Last year, Benoit Chassaing of Georgia State University showed that mice that drank water containing one of two emulsifiers underwent changes in gut bacteria and inflammation of the gut – changes that led to obesity and diabetes in these animals. However, mice that didn’t have any gut bacteria because they had been raised in a sterile environment didn’t become ill when given the same additives, suggesting that it is the emulsifiers’ effect on the microbiome that is to blame. When the ill mice stopped consuming emulsifiers, their gut bacteria gradually returned to normal. The question is whether the same might be true for humans. The growing use of emulsifiers has coincided with a rise in obesity and diabetes, says Chassaing, while these conditions aren’t as common in countries where less processed food is consumed. Now Chassaing has supported his findings in mice using a simulation of the human gut. Working with a team in Belgium, he looked at two emulsifiers: carboxymethylcellulose (E566 on EU labels) and polysorbate-80 (E433). When added to a series of flasks that mimic the conditions of the human digestive tract, each caused an increase in the levels of a bacterial protein called flagellin, known to cause inflammation at high concentrations. Chassaing presented the results at a recent meeting at the Royal Society in London. © Copyright Reed Business Information Ltd.
Link ID: 21880 - Posted: 02.10.2016
By Nicholas Bakalar Eating seafood is linked to a reduced risk of dementia-associated brain changes in people who carry the ApoE4 gene variation, which increases the risk for Alzheimer’s disease. Eating seafood was not linked to similar changes in those who carried other forms of the ApoE gene. The study, published in JAMA, looked at 286 autopsied brains and also found that eating seafood was linked to increased mercury in the brain, but that mercury levels were not linked to brain abnormalities. After controlling for age, sex, education and other factors, the researchers found that compared with those who ate less seafood, ApoE4 carriers who had one seafood meal or more a week had lower densities of the amyloid plaques and neurofibrillary tangles typical of Alzheimer’s disease. Over all, they had a 47 percent lower likelihood of having a post-mortem diagnosis of Alzheimer’s. Consumption of fish oil supplements was not correlated with pathological brain changes. The lead author, Martha Clare Morris, a professor of epidemiology at Rush University, said that mercury from fish appears to pose little risk for aging people. But, she said, there are studies that show that mercury consumption in pregnancy can cause cognitive problems in babies. “Most studies in dementia have found that one seafood meal a week is beneficial,” she said, though “they haven’t found that the more you eat, the lower the risk.” © 2016 The New York Times Company
Link ID: 21879 - Posted: 02.10.2016
By Virginia Morell Like fearful humans, horses raise the inner brow of their eyes when threatened or surprised. Altogether their faces can convey 17 emotions (ours express 27), and they readily recognize the expressions on their fellow equines. But can they read our facial cues? To find out, researchers tested 28 horses, including 21 geldings and seven mares, from stables in the United Kingdom. Each horse was led by his/her halter rope to a position in the stable, and then presented with a life-size color photograph of the face of a man. The man was either smiling or frowning angrily. The scientists recorded the animals’ reactions, and measured their heart rates. Other studies have shown that stressed horses’ heart rates fluctuate, and when the horses looked at the angry man, their hearts reached a maximum heart rate more quickly than when they viewed the smiling image. When shown the angry face, 20 of the horses also turned their heads so that they could look at it with their left eye—a response that suggests they understood the expression, the scientists report online today in Biology Letters, because the right hemisphere of the brain is specialized for processing negative emotions. Dogs, too, have this “left-gaze bias” when confronting angry faces. Also, like dogs, the horses showed no such bias, such as moving their heads to look with the right eye, when viewing the happy faces—perhaps because the animals don’t need to respond to nonthreatening cues. But an angry expression carries a warning—the person may be about to strike. The discovery that horses as well as dogs—the only two animals this has been tested in—can read our facial expressions spontaneously and without training suggests one of two things: Either these domesticated species devote a lot of time to learning our facial cues, or the ability is innate and more widespread in the animal kingdom than previously thought. © 2016 American Association for the Advancement of Scienc
By John Bohannon Didn't get your 40 winks last night? Better not get yourself arrested, or you may admit to a crime you didn't commit. False confessions are surprisingly easy to extract from people simply by keeping them awake, according to a new study of sleep deprivation. It puts hard numbers to a problem that criminal law reformers have worried about for decades. The “crime” in question took place in a sleep lab run by Kimberly Fenn at Michigan State University in East Lansing. Together, she and Elizabeth Loftus, a psychologist at the University of California (UC), Irvine, and two of their former Ph.D. students recruited 88 Michigan State students to take part in an experiment. During two separate visits, the students worked at computers solving problems and filling out questionnaires. They were all given a stern warning: Do not press the escape key, because it will erase important study data. After their second session, the subjects were split into two groups. Half of them were forced to stay awake all night under the watch of the researchers. Scrabble, TV shows, and a card game called euchre seemed to do the trick. The rest were allowed to get a full night's sleep. But that also required policing. "We actually had a student leave the study because he wanted to stay awake all night to study for an exam the next day," Fenn says, adding that "I certainly do not advocate this!" The next morning, everyone received a typed statement describing their performance. The statement accused them of hitting the escape key on the first day, even though none of them actually did so—the computers recorded all keystrokes. © 2016 American Association for the Advancement of Science
Bruce Bower Winter doesn’t deserve its dour reputation as the season of depression, scientists say. Rates of major depression, a psychiatric condition marked by intense sadness, hopelessness, insomnia and a general loss of interest or pleasure, don’t markedly change from one season to another among U.S. adults, says a team led by psychologist Steven LoBello of Auburn University at Montgomery in Alabama. Neither do symptoms intensify or become more numerous during winter among those already suffering from depression, the researchers report online January 19 in Clinical Psychological Science. A small number of people with regular fall or winter depression may have gone undetected in the new study, which surveyed more than 30,000 U.S. adults. Still, it’s becoming harder to justify the current psychiatric diagnosis of major depression “with seasonal pattern,” LoBello and Auburn colleagues Megan Traffanstedt and Sheila Mehta conclude. Because it’s a recurring disorder, depression can strike in two consecutive winters by chance, the researchers say. Depression in three or more consecutive winters could be due to personal and social factors unrelated to shorter days, they add. “Being depressed during winter is not evidence that one is depressed because of winter,” LoBello says. © Society for Science & the Public 2000 - 2016
By Jordana Cepelewicz As the Panthers and Broncos faced off in the third quarter of last night’s Super Bowl, wide receiver Philly Brown suffered a possible concussion—and to the disappointment of Panthers fans, he never returned to the game. But for good reason: concussions are now known to be much more serious injuries than once thought. And the danger may not be limited to the immediate repercussions. Researchers have already linked more severe traumatic brain injury to later suicide—particularly in military veterans and professional athletes—and have more recently explored the connection between concussion and depression. Now, new research published in the Canadian Medical Association Journal shows that even mild concussions sustained in ordinary community settings might be more detrimental than anyone anticipated; the long-term risk of suicide increases threefold in adults if they have experienced even one concussion. That risk increases by a third if the concussion is sustained on a weekend instead of a weekday—suggesting recreational concussions are riskier long-term than those sustained on the job. “The typical patient I see is a middle-aged adult, not an elite athlete,” says Donald Redelmeier, a senior scientist at the University of Toronto and one of the study’s lead authors. “And the usual circumstances for acquiring a concussion are not while playing football; it is when driving in traffic and getting into a crash, when missing a step and falling down a staircase, when getting overly ambitious about home repairs—the everyday activities of life.” Redelmeier and his team wanted to examine the risks of the concussions acquired under those circumstances. © 2016 Scientific American