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By John Horgan In 1990 The New York Times published a front-page article by Lawrence Altman, a reporter with a medical degree, announcing that scientists had discovered “a link between alcoholism and a specific gene.” The evidence for the "feel-good gene," which supposedly reduces anxiety, is flimsy, just like the evidence linking specific genes to high intelligence, violent aggression, homosexuality, bipolar disorder and countless other complex human traits and ailments. That was merely one in a string of reports in which the Times and other major media hyped what turned out to be erroneous claims linking complex traits and disorders—from homosexuality and high intelligence to schizophrenia and bipolar disorder—to specific genes. I thought those days were over, and that scientists and the media have learned to doubt extremely reductionist genetic accounts of complex traits and behaviors. I was wrong. Last Sunday, the “Opinion” section of the Times published an essay, “The Feel-Good Gene,” which states: “For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide–the so-called bliss molecule and our natural marijuana–in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character.” This article, like the one touting the alcoholism gene 25 years ago, was written by a physician, Richard Friedman, professor of psychiatry at Weill Cornell Medical College. I emphasize this fact because scientific hype is often blamed on supposedly ignorant journalists like me rather than on physicians and other so-called experts. © 2015 Scientific American
By Matthew J.X. Malady One hour and seven minutes into the decidedly hit-or-miss 1996 comedy Black Sheep, the wiseass sidekick character played by David Spade finds himself at an unusually pronounced loss for words. While riding in a car driven by Chris Farley’s character, he glances at a fold-up map and realizes he somehow has become unfamiliar with the name for paved driving surfaces. “Robes? Rouges? Rudes?” Nothing seems right. Even when informed by Farley that the word he’s looking for is roads, Spade’s character continues to struggle: “Rowds. Row-ads.” By this point, he’s become transfixed. “That’s a total weird word,” he says, “isn’t it?” Now, it’s perhaps necessary to mention that, in the context of the film, Spade’s character is high off nitrous oxide that has leaked from the car’s engine boosters. But never mind that. Row-ad-type word wig outs similar to the one portrayed in that movie are things that actually happen, in real life, to people with full and total control over their mental capacities. These wordnesias sneak up on us at odd times when we’re writing or reading text. I was in a full-on wordnesiac state. On one of my spelling attempts, I think I even threw a K into the mix. It was bad. Here’s how they work: Every now and again, for no good or apparent reason, you peer at a standard, uncomplicated word in a section of text and, well, go all row-ads on it. If you’re typing, that means inexplicably blanking on how to spell something easy like cake or design. The reading version of wordnesia occurs when a common, correctly spelled word either seems as though it can’t possibly be spelled correctly, or like it’s some bizarre combination of letters you’ve never before seen—a grouping that, in some cases, you can’t even imagine being the proper way to compose the relevant term. © 2014 The Slate Group LLC.
Link ID: 20688 - Posted: 03.14.2015
By Maggie Fox Teenagers who use marijuana heavily grow up to have poor memories and also have brain abnormalities, a new study shows. The study cannot say which came first — the brain structure differences or the pot use. But it suggests there could be long-term effects of heavy marijuana use. A team at Northwestern University looked at 97 volunteers with and without mental illness. The dope smokers said they'd used marijuana daily starting at age 16 or 17, and said they had not used other drugs. The daily marijuana users had an abnormally shaped hippocampus and performed about 18 percent more poorly on long-term memory tasks, the researchers reported in the journal Hippocampus. The hippocampus is a part of the brain used in storing long-term memory. "The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said Dr. John Csernansky, who worked on the study. Previous research by the same Northwestern team showed heavy pot smokers had poor short-term and working memory and abnormally shaped brain structures including the striatum, globus pallidus and thalamus. "It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Matthew Smith, who led the study, said in a statement.
When it comes to fight or flight for brawling crickets, a chemical in the brain is in charge. Being roughed up in a skirmish can trigger nerve cells in Mediterranean field crickets (Gryllus bimaculatus) to release nitric oxide, making the losing cricket run away, scientists report online March 13 in Science Advances. Watch in this video as two crickets face off. When the loser hits its limit, it flees the fight. In a second bout, the loser then tries to avoid the winner. Nitric oxide prompts this continued submissive behavior, which lasts several hours before a cricket’s will to fight returns. “If you block nitric oxide they recover quickly, and if you give them nitric oxide they don’t,” says Paul Stevenson, a coauthor of the new research and behavioral neurobiologist at Leipzig University in Germany. “It’s a very simple algorithm for controlling a very complicated social situation.” P. Stevenson and J. Rillich. Adding up the odds—Nitric oxide signaling underlies the decision to flee and post-conflict depression of aggression. Science Advances. Published online March 13, 2015.doi: 10.1126/sciadv.1500060. © Society for Science & the Public 2000 - 2015.
Link ID: 20686 - Posted: 03.14.2015
By Emily Underwood From imaging babies to blasting apart kidney stones, ultrasound has proved to be a versatile tool for physicians. Now, several research teams aim to unleash the technology on some of the most feared brain diseases. The blood-brain barrier, a tightly packed layer of cells that lines the brain's blood vessels, protects it from infections, toxins, and other threats but makes the organ frustratingly hard to treat. A strategy that combines ultrasound with microscopic blood-borne bubbles can briefly open the barrier, in theory giving drugs or the immune system access to the brain. In the clinic and the lab, that promise is being evaluated. This month, in one of the first clinical tests, Todd Mainprize, a neurosurgeon at the University of Toronto in Canada, hopes to use ultrasound to deliver a dose of chemotherapy to a malignant brain tumor. And in some of the most dramatic evidence of the technique's potential, a research team reports this week in Science Translational Medicine that they used it to rid mice of abnormal brain clumps similar to those in Alzheimer's disease, restoring lost memory and cognitive functions. If such findings can be translated from mice to humans, “it will revolutionize the way we treat brain disease,” says biophysicist Kullervo Hynynen of the Sunnybrook Research Institute in Toronto, who originated the ultrasound method. Some scientists stress that rodent findings can be hard to translate to humans and caution that there are safety concerns about zapping the brain with even the low-intensity ultrasound used in the new study, which is similar to that used in diagnostic scans. © 2015 American Association for the Advancement of Science.
Link ID: 20685 - Posted: 03.12.2015
|By Daisy Yuhas The brain is a hotbed of electrical activity. Scientists have long known that brain cells communicate via electrical missives, created by charged atoms and molecules called ions as they travel across the membranes of those cells. But a new study suggests that in the days and weeks that lead up to a brain forming in an embryo or fetus, altering the electrical properties of these cells can dramatically change how the ensuing brain develops. Researchers at Tufts University and the University of Minnesota have investigated how the difference in charge on either side of a resting cell’s membrane—its electrical potential—helps build the brain. In previous work Tufts University developmental biologist Michael Levin found that patterns of electrical potentials in the earliest stages of an embryo’s development can direct how an animal’s body grows, and that manipulating those potentials can cause a creature to sprout extra limbs, tails or functioning eyes. Now, Levin’s group has investigated how these potentials shape the brain. Working with frog embryos the researchers first used dyes to see the patterns of electrical potentials that precede brain development. They noticed that before the development of a normal brain the cells lining the neural tube, a structure that eventually becomes the brain and spinal cord, have extreme differences in ionic charge within and outside the membrane that houses the cells. In other words, these cells are extremely polarized. © 2015 Scientific American
Keyword: Development of the Brain
Link ID: 20684 - Posted: 03.12.2015
Older people could improve or maintain their mental function through heart healthy lifestyle changes, a large randomized trial for dementia prevention shows. Researchers in Finland and Sweden designed a trial to tackle risk factors for Alzheimer's disease. The 1,260 Finns aged 60 to 77 participating in the study were all considered at risk of dementia based on standard test scores. Half were randomly assigned to receive advice from health professionals on maintaining a healthy diet, aerobic and muscle training exercises, brain training exercises and regular checks of blood pressure, height and weight for body mass index and physical exams for two years or regular health advice. Participants in the Finnish Geriatric Intervention Study to Prevent Cognitive Impairment and Disability or FINGER study had their cognitive function measured in a battery of mental tests. "The main hypothesis was that simultaneous changes in several risk factors (even of smaller magnitude) would lead to a protective effect on cognition," Miia Kivipelto from the Karolinska Institute in Stockholm and her co-authors said in Wednesday's issue of The Lancet. Overall, test scores were 25 per cent in the diet and training group than the control group. There was no effect on memory. ©2015 CBC/Radio-Canada.
Link ID: 20683 - Posted: 03.12.2015
Mutations in the presenilin-1 gene are the most common cause of inherited, early-onset forms of Alzheimer’s disease. In a new study, published in Neuron, scientists replaced the normal mouse presenilin-1 gene with Alzheimer’s-causing forms of the human gene to discover how these genetic changes may lead to the disorder. Their surprising results may transform the way scientists design drugs that target these mutations to treat inherited or familial Alzheimer’s, a rare form of the disease that affects approximately 1 percent of people with the disorder. The study was partially funded by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. For decades, it has been unclear exactly how the presenilin mutations cause Alzheimer’s disease. Presenilin is a component of an important enzyme, gamma secretase, which cuts up amyloid precursor protein into two protein fragments, Abeta40 and Abeta42. Abeta42 is found in plaques, the abnormal accumulations of protein in the brain which are a hallmark of Alzheimer’s. Numerous studies suggested that presenilin-1 mutations increased activity of gamma-secretase. Investigators have developed drugs that block gamma-secretase, but they have so far failed in clinical trials to halt the disease. The study led by Raymond Kelleher, M.D., Ph.D. and Jie Shen, Ph.D., professors of neurology at Harvard Medical School, Boston, provides a plot twist in the association of presenilin-1 mutations and inherited Alzheimer’s disease. Using mice with altered forms of the presenilin gene, Drs. Kelleher and Shen discovered that the mutations may cause the disease by decreasing, rather than increasing, the activity of gamma-secretase.
|By Esther Landhuis As we age, we seem to get worse at ignoring irrelevant stimuli. It's what makes restaurant conversations challenging—having to converse while also shutting out surrounding chatter. New research bears out the aging brain's distractibility but also suggests that training may help us tune out interference. Scientists at Brown University recruited seniors and twentysomethings for a visual experiment. Presented with a sequence of letters and numbers, participants were asked to report back only the numbers—all the while disregarding a series of meaningless dots. Sometimes the dots moved randomly, but other times they traveled in a clear direction, making them harder to ignore. Older participants ended up accidentally learning the dots' patterns, based on the accuracy of their answers when asked which way the dots were moving, whereas young adults seemed able to suppress that information and focus on the numbers, the researchers reported last November in Current Biology. In a separate study published in Neuron, scientists at the University of California, San Francisco, showed they could train aging brains to become less distractible. Their regimen helped aging rats as well as older people. The researchers played three different sounds and rewarded trainees for identifying a target tone while ignoring distracter frequencies. As the subjects improved, the task grew more challenging—the distracting tone became harder to discriminate from the target. © 2015 Scientific American,
By Gretchen Reynolds An easy, two-minute vision test administered on the sidelines after a young athlete has hit his or her head can help to reliably determine whether the athlete has sustained a concussion, according to a new study of student athletes, some as young as 5. The test is so simple and inexpensive that any coach or parent potentially could administer it, the study’s authors believe, and any league afford to provide it as a way to help evaluate and safeguard players. Those of us who coach or care for young athletes know by now that an athlete who falls or collides with something during play or seems dazed, dizzy, loses consciousness or complains of head pain should be tested for a concussion, which occurs when the brain is physically jostled within the skull. But most of us are clueless about how to test young athletes. The most commonly recommended sideline test is the Standardized Assessment of Concussion, a multipart examination during which athletes are asked to name the date, describe how they feel, memorize and recall lists of words, and do jumping jacks and other tests of coordination. Ideally, this assessment should be administered and evaluated by a medical professional. But while the sidelines of college and professional games are crowded with doctors and certified athletic trainers, few high schools and youth leagues have those resources. Most of the time, concussion testing in youth sports falls to volunteer coaches or parents with little if any medical experience. That situation prompted researchers at New York University’s Langone Concussion Center to begin wondering recently whether there might be other, easier diagnostic tools to check young players for concussions. Their thoughts soon turned to vision. “About 50 percent of the brain’s pathways are tied in some to way to vision and visual processing,” said Dr. Steven Galetta, chairman of neurology at N.Y.U. Langone Medical Center and senior author of the study, which was published in The Journal of Neuro-Ophthalmology. © 2015 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 20680 - Posted: 03.12.2015
By Douglas Starr In 1906, Hugo Münsterberg, the chair of the psychology laboratory at Harvard University and the president of the American Psychological Association, wrote in the Times Magazine about a case of false confession. A woman had been found dead in Chicago, garroted with a copper wire and left in a barnyard, and the simpleminded farmer’s son who had discovered her body stood accused. The young man had an alibi, but after questioning by police he admitted to the murder. He did not simply confess, Münsterberg wrote; “he was quite willing to repeat his confession again and again. Each time it became richer in detail.” The young man’s account, he continued, was “absurd and contradictory,” a clear instance of “the involuntary elaboration of a suggestion” from his interrogators. Münsterberg cited the Salem witch trials, in which similarly vulnerable people were coerced into self-incrimination. He shared his opinion in a letter to a Chicago nerve specialist, which made the local press. A week later, the farmer’s son was hanged. Münsterberg was ahead of his time. It would be decades before the legal and psychological communities began to understand how powerfully suggestion can shape memory and, in turn, the course of justice. In the early nineteen-nineties, American society was recuperating from another panic over occult influence; Satanists had replaced witches. One case, the McMartin Preschool trial, hinged on nine young victims’ memories of molestation and ritual abuse—memories that they had supposedly forgotten and then, after being interviewed, recovered. The case fell apart, in 1990, because the prosecution could produce no persuasive evidence of the victims’ claims. A cognitive psychologist named Elizabeth Loftus, who had consulted on the case, wondered whether the children’s memories might have been fabricated—in Münsterberg’s formulation, involuntarily elaborated—rather than actually recovered.
Keyword: Learning & Memory
Link ID: 20679 - Posted: 03.12.2015
|By Anne Skomorowsky On a Saturday night last month, 12 students at Wesleyan University in Connecticut were poisoned by “Molly,” a hallucinogenic drug they had taken to enhance a campus party. Ambulances and helicopters transported the stricken to nearby hospitals, some in critical condition. Molly—the street name for the amphetamine MDMA—can cause extremely high fevers, liver failure, muscle breakdown, and cardiac arrest. Given the risks associated with Molly, why would anybody take it? The obvious answer—to get high—is only partly true. Like many drugs of abuse, Molly causes euphoria. But Molly is remarkable for its “prosocial” effects. Molly makes users feel friendly, loving, and strongly connected to one another. Molly is most commonly used in settings where communion with others is highly valued, such as raves, music festivals, and college parties. Recently, psychiatrists have taken an interest in its potential to enhance psychotherapy; this has led to new research into the mechanisms by which MDMA makes people feel closer. It appears that MDMA works by shifting the user’s attention towards positive experiences while minimizing the impact of negative feelings. To investigate this, a 2012 study by Cedric Hysek and colleagues used the Reading the Mind in the Eyes Test (RMET), which was developed to evaluate people with autism. In the RMET, participants are shown 36 pictures of the eye region of faces. Their task is to describe what the person in the picture is feeling. Volunteers taking MDMA, under carefully controlled conditions, improved in their recognition of positive emotions; but their performance in recognizing negative emotions declined. In other words, they incorrectly attributed positive or neutral feelings to images that were actually negative in emotional tone. They mistook negative and threat-related images for friendly ones. © 2015 Scientific American
Keyword: Drug Abuse
Link ID: 20678 - Posted: 03.12.2015
Mo Costandi Neuroscientists in France have implanted false memories into the brains of sleeping mice. Using electrodes to directly stimulate and record the activity of nerve cells, they created artificial associative memories that persisted while the animals snoozed and then influenced their behaviour when they awoke. Manipulating memories by tinkering with brain cells is becoming routine in neuroscience labs. Last year, one team of researchers used a technique called optogenetics to label the cells encoding fearful memories in the mouse brain and to switch the memories on and off, and another used it to identify the cells encoding positive and negative emotional memories, so that they could convert positive memories into negative ones, and vice versa. The new work, published today in the journal Nature Neuroscience, shows for the first time that artificial memories can be implanted into the brains of sleeping animals. It also provides more details about how populations of nerve cells encode spatial memories, and about the important role that sleep plays in making such memories stronger. Karim Benchenane of the French National Centre for Scientific Research (CNRS) in Paris and his colleagues implanted electrodes into the brains of 40 mice, targeting the medial forebrain bundle (MFB), a component of the reward circuitry, and the CA1 region of the hippocampus, which contains at least three different cell types that encode the memories needed for spatial navigation. © 2015 Guardian News and Media Limited
By Nicholas Bakalar People sometimes take Valium or Ativan to relieve anxiety before surgery, but a new study suggests that these benzodiazepine drugs have little beneficial effect and may even delay recovery. Researchers studied 1,062 patients admitted to French hospitals for surgery requiring general anesthesia. A third took 2.5 milligrams of lorazepam (brand name Ativan), a third received a placebo, and a third were given no premedication. Patients completed questionnaires assessing anxiety, pain levels and quality of sleep before and a day after their operations, while researchers recorded their time to having ventilation tubes removed and to recovering full wakefulness. The study was published in JAMA. Lorazepam was associated with more postsurgery amnesia and a longer time to recover cognitive abilities. Quality of sleep was impaired in the lorazepam group, but not in the others. And ventilation tubes were kept in significantly longer in the lorazepam group. Pain scores did not differ between the lorazepam and the no-medication groups, but there was more pain in the group given the placebo. The lead author, Dr. Axel Maurice-Szamburski, an anesthesiologist at Timone Hospital in Marseille, cited recent surveys showing that benzodiazepines are widely prescribed before surgery. “But until now,” he added, “sedatives have not been evaluated from the patient’s point of view. It’s the patient who should be happy, not the doctor.” © 2015 The New York Times Company
Link ID: 20676 - Posted: 03.10.2015
Jon Hamilton Alzheimer's, Parkinson's and amyotrophic lateral sclerosis ravage the brain in very different ways. But they have at least one thing in common, says Corinne Lasmezas, a neuroscientist and professor at Scripps Research Institute, in Jupiter, Fla. Each spreads from brain cell to brain cell like an infection. "So if we could block this [process], that might prevent the diseases," Lasmezas says. It's an idea that's being embraced by a growing number of researchers these days, including Nobel laureate Dr. Stanley Prusiner, who first recognized in the 1980s the infectious nature of brain proteins that came to be called prions. But the idea that mad cow prions could cause disease in people has its origins in an epidemic of mad cow disease that occurred in Europe and the U.K. some 15 years ago. Back then, Lasmezas was a young researcher in France studying how mad cow, formally known as bovine spongiform encephalopathy, was transmitted. "At that time, nobody knew if this new disease in cows was actually transmissible to humans," she says. In 1996, Lasmezas published a study strongly suggesting that it was. "So that was my first great research discovery," she says. Prions, it turns out, become toxic to brain cells when folded into an abnormal shape. "This misfolded protein basically kills the neurons," Lasmezas says. © 2015 NPR
By CELIA WATSON SEUPEL Every year, nearly 40,000 Americans kill themselves. The majority are men, and most of them use guns. In fact, more than half of all gun deaths in the United States are suicides. Experts and laymen have long assumed that people who died by suicide will ultimately do it even if temporarily deterred. “People think if you’re really intent on dying, you’ll find a way,” said Cathy Barber, the director of the Means Matters campaign at Harvard Injury Control Research Center. Prevention, it follows, depends largely on identifying those likely to harm themselves and getting them into treatment. But a growing body of evidence challenges this view. Suicide can be a very impulsive act, especially among the young, and therefore difficult to predict. Its deadliness depends more upon the means than the determination of the suicide victim. Now many experts are calling for a reconsideration of suicide-prevention strategies. While mental health and substance abuse treatment must always be important components in treating suicidality, researchers like Ms. Barber are stressing another avenue: “means restriction.” Instead of treating individual risk, means restriction entails modifying the environment by removing the means by which people usually die by suicide. The world cannot be made suicide-proof, of course. But, these researchers argue, if the walkway over a bridge is fenced off, a struggling college freshman cannot throw herself over the side. If parents leave guns in a locked safe, a teenage son cannot shoot himself if he suddenly decides life is hopeless. With the focus on who dies by suicide, these experts say, not enough attention has been paid to restricting the means to do it — particularly access to guns. © 2015 The New York Times Company
Link ID: 20674 - Posted: 03.10.2015
If you missed the great dress debate of 2015 you were probably living under a rock. Staffrooms across the globe threatened to come to a standstill as teachers addressed the all-important question – was the dress white and gold or blue and black? This is just one example of how our brains interpret things differently. So, with the 20th anniversary of Brain Awareness Week from 16 to 22 March, this week we bring you a collection of ideas and resources to get students’ synapses firing. The brain is one of our most interesting organs, and advances in technology and medicine mean we now know more about it than ever before. Brain Awareness Week is a global campaign to raise awareness of the progress and benefits of brain research. The organisers, the Dana Foundation, have put together an assortment of teaching materials for primary and secondary students. For children aged five to nine, the Mindboggling Workbook is a good place to start. It includes information on how the brain works, what it does and how to take care of it. There’s also a section on the nervous system, which you could turn into a fun group activity. Ask one student to lie down on a large sheet of paper while others trace around them. Add a drawing of the brain and the spinal cord. Use different coloured crayons to illustrate how neurons send messages around your body when you a) touch something hot, b) get stung on the leg by a wasp, and c) wriggle your toes after stepping in sand. Can students explain why the brain is described as being more powerful than a computer? © 2015 Guardian News and Media Limited
Link ID: 20673 - Posted: 03.10.2015
Robin Tricoles The first time it happened, I was 8. I was tucked in bed reading my favorite book when my tongue swelled up to the size of a cow’s, like the giant tongues I had seen in the glass display case at the neighborhood deli. At the same time, the far wall of my bedroom began to recede, becoming a tiny white rectangle floating somewhere in the distance. In the book I was holding, the typeface grew vast on the page. I was intrigued, I remember, but not afraid. Over the next six years, the same thing happened to me dozens of times. Forty years later, while working as a science writer, I stumbled on a scientific paper describing almost exactly what I had experienced. The paper attributed those otherworldly sensations to something called Alice in Wonderland syndrome, or its close cousin, Alice in Wonderland-like syndrome. People with Alice in Wonderland syndrome (AWS) perceive parts of their body to be changing size. For example, their feet may suddenly appear smaller and more distant, or their hands larger than they had been moments before. Those with the closely related Alice in Wonderland-like syndrome (AWLS) misperceive the size and distance of objects, seeing them as startlingly larger, smaller, fatter, or thinner than their natural state. People who experience both sensations, like I did, are classified as having AWLS. The syndrome’s name is commonly attributed to English psychiatrist John Todd, who in 1955 described his adult patients’ illusions of corporal and objective distortions in a paper in the Canadian Medical Association Journal. © 2015 by The Atlantic Monthly Group.
Link ID: 20672 - Posted: 03.10.2015
By Rachel Rabkin Peachman Many women with a history of depression who take antidepressants assume that once they get pregnant, they should try to wean themselves off their meds to avoid negative side effects for the baby. A new large study published in the journal Pediatrics challenges one reason behind that assumption. The research found that taking selective serotonin reuptake inhibitors (the antidepressants also known as S.S.R.I.s) while pregnant does not increase the risk of asthma in the resulting babies. What is associated with an increased risk of asthma? According to this study and other research, untreated prenatal depression. “The mechanisms underlying the association of prenatal depression and asthma are unknown,” said Dr. Xiaoqin Liu, the lead author of the Pediatrics study and an epidemiologist at Aarhus University in Denmark. An association between prenatal depression and asthma does not mean that prenatal depression causes asthma. There could be other reasons for the correlation, genetic or environmental, or both. For example, people who live in dense, polluted urban areas could be at an increased risk of both asthma and depression. The researchers used Denmark’s national registries to evaluate all singleton babies born from 1996 to 2007, and identify the mothers who had a diagnosis of depression or had used antidepressants, or both, during pregnancy or one year beforehand. Using a statistical model, the study authors found that prenatal depression — with or without the use of antidepressants — was associated with a 25 percent increased risk of asthma in children as compared with children whose mothers did not have a record of depression. © 2015 The New York Times Company
Alison Abbott Mediators appointed to analyse the rifts within Europe’s ambitious €1-billion (US$1.1-billion) Human Brain Project (HBP) have called for far-reaching changes both in its governance and its scientific programmes. Most significantly, the report recommends that systems neuroscience and cognitive neuroscience should be reinstated into the HBP. The mediation committee, led by engineer Wolfgang Marquardt, director of Germany’s national Jülich Research Centre, sent its final report to the HBP board of directors on 9 March, and issued a press release summarizing its findings. (The full report will not be published until after the board, a 22-strong team of scientists, discusses its contents at a meeting on 17–18 March). The European Commission flagship project, which launched in October 2013, is intended to boost supercomputing through neuroscience, with the aim of simulating the brain in a computer. But the project has been racked by dissent from the outset. In early 2014, a three-person committee of scientists who ran the HBP’s scientific direction revealed that they planned to eliminate cognitive neuroscience from the initiative, which precipitated a mass protest. More than 150 of Europe’s leading neuroscientists signed a letter to the European Commission, complaining about the project’s management and charging that the HBP plan to simulate the brain using only ‘bottom-up’ data on the behaviour of neurons was doomed to failure if it did not include the top-down constraints provided by systems and cognitive neuroscience. © 2015 Nature Publishing Group
Keyword: Brain imaging
Link ID: 20670 - Posted: 03.10.2015