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|By Gary Stix Implantation of electrodes deep within the brain is now commonly performed for treatment of the neurological disorders Parkinson’s disease and essential tremor. But the use of deep-brain stimulation, as it is known, is expanding. It is now being assessed in as many as 200 patients for major depression—and is being considered for other disorders such as anorexia. Helen Mayberg, a neurologist from Emory University, has pioneered the use of imaging techniques to understand the functioning of different brain circuits to determine how to tailor various treatments for depression, including deep-brain stimulation, to a patient’s needs. Learn about her work below in “Deep-Brain Stimulation: A Decade of Progress with Helen Mayberg,” a Webinar put on by the Brain & Behavior Research Foundation. © 2015 Scientific American
Link ID: 20584 - Posted: 02.16.2015
By Rachel Ehrenberg SAN JOSE, Calif. — New moms suffering from postpartum depression change their activity on Facebook, suggesting that the social media site could help detect the onset of the baby blues. Many new parents share pictures and videos of their babies on Facebook and use the site to interact with friends they might be too busy to see in person. But compared with most typical new moms, those suffering from postpartum depression are less active on the social media site, Munmun De Choudhury of Georgia Tech reported February 14 at the annual meeting of the American Association for the Advancement of Science. She and her colleagues at Microsoft Research in Redmond, Wash., conducted an elaborate study that included a depression screening questionnaire, interviews and an analysis of Facebook activity and interactions of 165 mothers both before and after they had their babies. These women also tend to keep a stiff upper lip on the site, refraining from reporting on their emotional well-being and instead posting objective content geared toward getting feedback or advice on a specific matter, De Choudhury and her colleagues discovered. The scientists also found they could train a computer program to identify which moms had the blues. Such research might help with designing interventions, whereby moms could be warned that they might be sinking into depression and encouraged to reach out for social support or medical attention. M. De Choudhury. Online Social Dynamics and Emotional Wellbeing. American Association for the Advancement of Science Annual Meeting, San Jose, Calif., February 14, 2015. © Society for Science & the Public 2000 - 2015
By Lizzie Wade SAN JOSE, CALIFORNIA—Humans have been using cannabis for more than 5000 years. So why don’t scientists know more about it? Three experts gathered here at the annual meeting of AAAS (which publishes Science) to discuss what scientists and doctors know about the drug and what they still need to learn. “By the end of this session, you’ll know more about cannabis than your physician does,” said Mark Ware, a family physician at the McGill University Health Center in Montreal, Canada, who organized the talk. How does marijuana work? Our brains are primed to respond to marijuana, because “there are chemicals in our own bodies that act like THC [the psychoactive ingredient in pot]” and other compounds in cannabis called cannabinoids, explained Roger Pertwee, a neuropharmacologist at the University of Aberdeen in the United Kingdom who has studied cannabinoids since the 1960s. Cannabinoids produced by our bodies or ingested through marijuana use react with a series of receptors in our brains called the endocannabinoid system, which is involved in appetite, mood, memory, and pain sensation. Scientists have discovered 104 cannabinoids so far, but “the pharmacology of most of them has yet to be investigated,” Pertwee said. What are the known medical uses of marijuana? Marijuana has been used for decades to stimulate appetite and treat nausea and vomiting, especially in patients undergoing chemotherapy. Its success in easing the symptoms of multiple sclerosis patients led to the development of Sativex, a drug manufactured by GW Pharmaceuticals that includes THC and cannabidiol (CBD), a cannabinoid that isn’t psychoactive. © 2015 American Association for the Advancement of Science
Smoking potent cannabis was linked to 24% of new psychosis cases analysed in a study by King's College London. The research suggests the risk of psychosis is three times higher for users of potent "skunk-like" cannabis than for non-users. The study of 780 people was carried out by KCL's Institute of Psychiatry, Psychology and Neuroscience. A Home Office spokesman said the report underlines the reasons why cannabis is illegal. Scientists found the risk of psychosis was five times higher for those who use it every day compared with non-users. They also concluded the use of hash, a milder form of the drug, was not associated with increased risk of psychosis. Psychosis refers to delusions or hallucinations that can be present in certain psychiatric conditions such as schizophrenia and bipolar disorder. "Compared with those who had never tried cannabis, users of high potency skunk-like cannabis had a threefold increase in risk of psychosis,' said Dr Marta Di Forti, lead author on the research. She added: "The results show that psychosis risk in cannabis users depends on both the frequency of use and cannabis potency." Dr Di Forti told BBC Radio 4's Today programme that the availability of skunk-like cannabis was becoming more widespread. "In London, it's very difficult to find anything else," she said. "There were lots of reports from police across the UK saying we have become a great producer of skunk. And not only do we use it locally but we export, so this is a Made in England product." Someone suffering from psychosis would often be "extremely paranoid and become very suspicious" about the people around them, she added. She has called for "a clear public message" to cannabis users, comparable to medical advice on alcohol and tobacco. © 2015 BBC
By Jane E. Brody Bereavement — how one responds and adjusts to the death of a loved one — is a very individual matter. It is natural to experience a host of negative reactions in the weeks and months following the loss of a loved one: among them, sadness, difficulty sleeping, painful reminders of the person, difficulty enjoying activities once shared, even anger. Grief is a normal human reaction, not a disease, and there is no one right way to get through it. Most often, within six months of a death, survivors adjust and are more or less able to resume usual activities, experience joy, and remember their loved ones without intense pain. But sometimes, even when the loss is neither sudden nor unexpected, as is true in the majority of deaths in the United States, survivors close to the deceased can experience extremely disruptive grief reactions that persist far longer. In a report last month in The New England Journal of Medicine, Dr. M. Katherine Shear presents a composite portrait of what is known as complicated grief, an extreme, unrelenting reaction to loss that persists for more than six months and can result in a serious risk to health. She describes a 68-year-old widow who continued to be seriously impaired by grief four years after her husband died. The woman slept on the couch because she could not bear to sleep in the bed she had shared with him. She found it too painful to engage in activities they used to do together. She no longer ate regular meals because preparing them was a too-distressing reminder of her loss. And she remained alternately angry with the medical staff who cared for him and with herself for not recognizing his illness earlier. Symptoms of complicated grief commonly include intense yearning, longing or emotional pain; frequent preoccupying, intrusive thoughts and memories of the person lost; a feeling of disbelief or inability to accept the loss; and difficulty imagining a meaningful life without that person. © 2015 The New York Times Company
By Tia Ghose A woman who had persistent headaches found there was a strange culprit for her pain: a Pilates class that caused her brain fluid to leak, according to a new case report. The brain fluid leak led to a persistent, worsening headache that was only alleviated when the 42-year-old British woman laid down, according to the report that was published in December in the Journal of Medical Case Reports. Though doctors never identified the exact location of the leak, the patient improved after a few weeks of bed rest and pain relievers. [The 16 Oddest Medical Cases] Cerebrospinal fluid is a clear liquid that flows between the brain and its outer covering, and between the spinal cord and its outer covering. Both of these structures' outer coverings are called the dura. This fluid cushions the brain and spinal cord and helps clear metabolic waste from the brain. However, sometimes holes can emerge in the dura, said Dr. Amber Luong, an otolaryngologist at the University of Texas Health Sciences Center in Houston. "The most common cause [of such leaks is] trauma, like a car accident," Luong told Live Science. Often, cerebrospinal fluid leaks out of a person's nose because there is a crack in the base of the skull and a tear in the dura lining the brain. One telltale sign of a cerebrospinal leak is that there is clear, metallic-tasting fluid coming out of just one nostril, Luong said. (The woman in this case did not experience this symptom because her tear was around the spinal cord, not the brain.)
Keyword: Brain Injury/Concussion
Link ID: 20579 - Posted: 02.16.2015
By PAULA SPAN The word “benzodiazepines” and the phrase “widely prescribed for anxiety and insomnia” appear together so frequently that they may remind you of the apparently unbreakable connection between “powerful” and “House Ways and Means Committee.” But now we have a better sense of just how widely prescribed these medications are. A study in this month’s JAMA Psychiatry reports that among 65- to 80-year-old Americans, close to 9 percent use one of these sedative-hypnotics, drugs like Valium, Xanax, Ativan and Klonopin. Among older women, nearly 11 percent take them. “That’s an extraordinarily high rate of use for any class of medications,” said Michael Schoenbaum, a senior adviser at the National Institutes of Mental Health and a co-author of the new report. “It seemed particularly striking given the identified clinical concerns associated with benzodiazepine use in anybody, but especially in older adults.” He was referring to decades of warnings about the potentially unhappy consequences of benzodiazepines for older users. The drugs still are recommended for a handful of specific disorders, including acute alcohol withdrawal and, sometimes, seizures and panic attacks. But concerns about the overuse of benzodiazepines have been aired again and again: in the landmark nursing home reform law of 1987, in the American Geriatrics Society’s Choosing Wisely list of questionable practices in 2013, in last year’s study in the journal BMJ suggesting an association with Alzheimer’s disease. Benzodiazepine users face increased risks of falls and fractures, of auto accidents, of reduced cognition. “Even after one or two doses, you have impaired cognitive performance on memory and other neuropsychological tests, compared to a placebo,” said Dr. D.P. Devanand, director of geriatric psychiatry at Columbia University Medical Center. © 2015 The New York Times Company
Carl Zimmer In 2010, a graduate student named Tamar Gefen got to know a remarkable group of older people. They had volunteered for a study of memory at the Feinberg School of Medicine at Northwestern University. Although they were all over age 80, Ms. Gefen and her colleagues found that they scored as well on memory tests as people in their 50s. Some complained that they remembered too much. She and her colleagues referred to them as SuperAgers. Many were also friends. “A couple tried to set me up with their grandsons,” Ms. Gefen said. She was impressed by their resilience and humor: “It takes wisdom to a whole new level.” Recently, Ms. Gefen’s research has taken a sharp turn. At the outset of the study, the volunteers agreed to donate their brains for medical research. Some of them have died, and it has been Ms. Gefen’s job to look for anatomical clues to their extraordinary minds. “I had this enormous privilege I can’t even begin to describe,” she said. “I knew them and tested them in life and in death. At the end, I was the one looking at them through a microscope.” Ms. Gefen and her colleagues are now starting to publish the results of these post-mortem studies. Last month in The Journal of Neuroscience, the scientists reported that one of the biggest differences involves peculiar, oversize brain cells known as von Economo neurons. SuperAgers have almost five times as many of them as other people. Learning what makes these brains special could help point researchers to treatments for Alzheimer’s disease and other kinds of mental decline. But it is hard to say how an abundance of von Economo neurons actually helps the brain. © 2015 The New York Times Company
|By Esther Landhuis Whereas cholesterol levels measured in a routine blood test can serve as a red flag for heart disease, there’s no simple screen for impending Alzheimer’s. A new Silicon Valley health start-up hopes to change that. A half million Americans die of Alzheimer’s disease each year. Most are diagnosed after a detailed medical workup and extensive neurological and psychological tests that gauge mental function and rule out other causes of dementia. Yet things begin going awry some 10 to 15 years before symptoms show. Spinal fluid analyses and positron emission tomography (PET) scans can detect a key warning sign—buildup of amyloid-beta protein in the brain. Studies suggest that adults with high brain amyloid have elevated risk for Alzheimer’s and stand the best chance of benefiting from treatments should they become available. Getting Alzheimer’s drugs to market requires long and costly clinical studies, which some experts say have failed thus far because experimental drugs were tested too late in the disease process. By the time people show signs of dementia, their brains have lost neurons and no current therapy can revive dead cells. That is why drug trials are looking to recruit seniors with preclinical Alzheimer’s who are on the verge of decline but otherwise look healthy. This poses a tall order. Spinal taps are cumbersome and PET costs $3,000 per scan. “There’s no cheap, fast, noninvasive test that can accurately identify people at risk of Alzheimer’s,” says Brad Dolin, chief technology officer of Neurotrack. The company is developing a computerized visual test that might fit the bill. © 2015 Scientific American
Dr. Lisa Sanders. On Wednesday, we challenged Well readers to take on the case of a 21-year-old college student with chronic headaches who suddenly became too dizzy to walk. She had a medical history that was complicated by back surgery and a subsequent infection, and chronic headaches after a car accident. More than 300 of you wrote in with suggested diagnoses, but only a handful of you noticed the clue that led the medical student who saw the patient to the right answer. The cause of the young woman’s dizziness was… Postural tachycardia syndrome, or POTS. The first reader to make this diagnosis was Theresa Baker, a retired bookkeeper and mother from Philomath, Ore. She said she immediately recognized the disorder because her young niece has suffered from it for over a decade. Her episodes of dizziness and fainting had started when she was just 13. Well done, Ms. Baker! The Diagnosis Postural tachycardia syndrome — also called postural orthostatic tachycardia syndrome — is an unusual condition in which simply being upright causes symptoms of lightheadedness, sometimes to the point of fainting, along with an increase in heart rate faster than 130 beats per minute, all of which improves when the patient lies down. These basic symptoms are often accompanied by fatigue, which is often worst after any type of exertion, along with a loss of concentration, blurred or tunnel vision, difficulty sleeping or nausea. POTS is considered a syndrome rather than a disease because it has many possible causes. It can be transient — a side effect of certain medications or a result of loss of conditioning, acute blood loss or dehydration — and in these cases it resolves when the trigger is removed. Other types of POTS are more persistent — which turned out to be the case for this patient — lasting months or years. © 2015 The New York Times Company
Link ID: 20575 - Posted: 02.13.2015
By Siri Carpenter “I don’t look like I have a disability, do I?” Jonas Moore asks me. I shake my head. No, I say — he does not. Bundled up in a puffy green coat in a drafty Starbucks, Moore, 35 and sandy-haired, doesn’t stand out in the crowd seeking refuge from the Wisconsin cold. His handshake is firm and his blue eyes meet mine as we talk. He comes across as intelligent and thoughtful, if perhaps a bit reserved. His disability — autism — is invisible. That’s part of the problem, says Moore. Like most people with autism spectrum disorders, he finds relationships challenging. In the past, he has been quick to anger and has had what he calls “meltdowns.” Those who don’t know he has autism can easily misinterpret his actions. “People think that when I do misbehave I’m somehow intentionally trying to be a jerk,” Moore says. “That’s just not the case.” His difficulty managing emotions has gotten him into some trouble, and he’s had a hard time holding onto jobs — an outcome he might have avoided, he says, if his coworkers and bosses had better understood his intentions. Over time, things have gotten better. Moore has held the same job for five years, vacuuming commercial buildings on a night cleaning crew. He attributes his success to getting the right amount of medication and therapy, to time maturing him and to the fact that he now works mostly alone. Moore is fortunate. His parents help support him financially. He has access to good mental health care. And with the help of the state’s division of vocational rehabilitation, he has found a job that suits him. Many adults with autism are not so lucky. © Society for Science & the Public 2000 - 2015.
Link ID: 20574 - Posted: 02.13.2015
By David Tuller The Institute of Medicine on Tuesday proposed a new name and new diagnostic criteria for the condition that many still call chronic fatigue syndrome. Experts generally agree that the disease has a physical basis, but they have struggled for decades to characterize its symptoms. The new report may help improve diagnosis, but the recommendations are unlikely to end the long, contentious debate over who has the condition and what may be causing it. An institute panel recommended that the illness be renamed “systemic exertion intolerance disease,” a term that reflects what patients, clinicians and researchers all agree is a core symptom: a sustained depletion of energy after minimal activity, called postexertional malaise. The new name “really describes much more directly the key feature of the illness, which is the inability to tolerate both physical and cognitive exertion,” said Dr. Peter Rowe, a member of the panel and a pediatrician at Johns Hopkins who treats children with the condition. An alternate name for the illness, myalgic encephalomyelitis, meaning “brain and spinal cord inflammation with muscle pain,” was coined decades ago. Many experts now refer to the condition as M.E./C.F.S. About one million people in the United States are believed to have the syndrome. Many say they have been accused of imagining or exaggerating their symptoms, and many doctors have long viewed it as a psychological illness. The authors urged that doctors take patients’ physical complaints seriously. “This is not a figment of their imagination,” said Dr. Ellen Wright Clayton, the chairwoman of the Institute of Medicine panel and a professor of pediatrics and law at Vanderbilt University. Patients attribute much of their mistreatment to the name “chronic fatigue syndrome,” chosen by the Centers for Disease Control in 1988. © 2015 The New York Times Company
Link ID: 20573 - Posted: 02.13.2015
Scientists have uncovered more than 90 new gene regions that could help explain why some people are more likely to put on weight than others. The team scoured DNA libraries of more than 300,000 people, constructing the largest-ever genetic map of obesity. Looking for consistent patterns they found a link with genes involved in brain processes, suggesting obesity could partly have a neurological basis. The results are published in the journal Nature. Researchers from the international Giant consortium (Genetic Investigation of Anthropometric Trait), analysed the genetics behind body mass index (a ratio of weight and height ). And in a separate Nature paper they looked specifically at how genetics influence where fat is distributed around the body. Fat around the abdomen for example can cause more health problems than fat carried around the thighs. Some 33 newly pinpointed gene regions were linked to body fat distribution - giving further clues about why some people are pear-shaped while others put on weight more around the tummy. They also identified more than 60 genetic locations that influence body mass index - tripling the number previously known. And some of these regions have links with the nervous system. © 2015 BBC
Ewen Callaway A mysterious group of humans from the east stormed western Europe 4,500 years ago — bringing with them technologies such as the wheel, as well as a language that is the forebear of many modern tongues, suggests one of the largest studies of ancient DNA yet conducted. Vestiges of these eastern émigrés exist in the genomes of nearly all contemporary Europeans, according to the authors, who analysed genome data from nearly 100 ancient Europeans1. The first Homo sapiens to colonize Europe were hunter-gatherers who arrived from Africa, by way of the Middle East, around 45,000 years ago. (Neanderthals and other archaic human species had begun roaming the continent much earlier.) Archaeology and ancient DNA suggest that farmers from the Middle East started streaming in around 8,000 years ago, replacing the hunter-gatherers in some areas and mixing with them in others. But last year, a study of the genomes of ancient and contemporary Europeans found echoes not only of these two waves from the Middle East, but also of an enigmatic third group that they said could be from farther east2 (see 'Ancient European genomes reveal jumbled ancestry'). Ancient genes To further pin down the origins of this ghost lineage, a team led by David Reich, an evolutionary and population geneticist at Harvard Medical School in Boston, Massachusetts, analysed nuclear DNA from the bodies of 69 individuals who lived across Europe between 8,000 and 3,000 years ago. They also examined previously published genome data from another 25 ancient Europeans, including Ötzi, the 5,300-year-old 'ice man' who was discovered on the Italian-Austrian border. © 2015 Nature Publishing Group
Link ID: 20571 - Posted: 02.13.2015
By Devin Powell Dog owners may think their pets can tell a smile from a frown, but scientific evidence has been lacking. Now, researchers have trained dogs from a variety of breeds to look at a pair of photos arranged side by side—one showing the upper half of a woman’s face looking happy and the other showing the upper half of the same woman’s face looking angry—and pick out the happy expression by touching their snouts to it (pictured). When then shown the lower halves of the faces or pieces of other people’s faces, the perceptive pooches could still easily discern happy from angry. Another group of canines similarly learned to identify angry faces. Dogs in a previous study that distinguished expressions on whole faces could have done so using simple visual clues that reappeared in every face: the white of teeth in a smile, for instance, or creases in angry skin. Identifying emotions from photos of different parts of the face requires a more holistic understanding of expression, argue the authors of the new study, published online today in Current Biology. While primates are known to recognize faces, dogs may have been especially adapted for emotional sensitivity to humans during their domestication. The researchers plan to investigate how common this ability is by testing pigs and other animals. © 2015 American Association for the Advancement of Science.
By DENISE GRADY However bad you thought smoking was, it’s even worse. A new study adds at least five diseases and 60,000 deaths a year to the toll taken by tobacco in the United States. Before the study, smoking was already blamed for nearly half a million deaths a year in this country from 21 diseases, including 12 types of cancer. The new findings are based on health data from nearly a million people who were followed for 10 years. In addition to the well-known hazards of lung cancer, artery disease, heart attacks, chronic lung disease and stroke, the researchers found that smoking was linked to significantly increased risks of infection, kidney disease, intestinal disease caused by inadequate blood flow, and heart and lung ailments not previously attributed to tobacco. Even though people are already barraged with messages about the dangers of smoking, researchers say it is important to let the public know that there is yet more bad news. “The smoking epidemic is still ongoing, and there is a need to evaluate how smoking is hurting us as a society, to support clinicians and policy making in public health,” said Brian D. Carter, an epidemiologist at the American Cancer Society and the first author of an article about the study, which appears in The New England Journal of Medicine. “It’s not a done story.” In an editorial accompanying the article, Dr. Graham A. Colditz, from Washington University School of Medicine in St. Louis, said the new findings showed that officials in the United States had substantially underestimated the effect smoking has on public health. He said smokers, particularly those who depend on Medicaid, had not been receiving enough help to quit. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 20569 - Posted: 02.13.2015
By Michelle Roberts Health editor, BBC News online Women trying for a baby and those in the first three months of pregnancy should not drink any alcohol, updated UK guidelines say. The Royal College of Obstetricians and Gynaecologists (RCOG) had previously said a couple of glasses of wine a week was acceptable. It now says abstinence is the only way to be certain that the baby is not harmed. There is no proven safe amount that women can drink during pregnancy. The updated advice now chimes with guidelines from the National Institute for Health and Care Excellence (NICE). In the US, experts say there is no safe time to drink during pregnancy. But the RCOG highlights around the time of conception and the first three months of pregnancy as the most risky. Drinking alcohol may affect the unborn baby as some will pass through the placenta. Around conception and during the first three months, it may increase the chance of miscarriage, says the RCOG. After this time, women are advised to not drink more than one to two units, more than once or twice a week, it says. Drinking more than this could affect the development of the baby, in particular the way the baby's brain develops and the way the baby grows in the womb, which can lead to foetal growth restriction and increase the risk of stillbirth and premature labour, says the advice. © 2015 BBC
|By Stephani Sutherland More than half a billion people carry a genetic mutation that incapacitates the enzyme responsible for clearing alcohol from the body. The deficiency is responsible for an alcohol flush reaction, colloquially known as the “Asian glow” because the vast majority of carriers are descendants of the Han Chinese. Now research published last September in Science Translational Medicine suggests that the mutation might also compromise carriers' pain tolerance. The finding points to a new target for pharmaceutical pain relief and implies that drinking alcohol might exacerbate inflammatory conditions such as arthritis. When people consume alcohol, the body breaks it down into several by-products, including chemicals called aldehydes. These compounds are noxious if they remain in the system too long, causing flushing, nausea, dizziness and other symptoms of the alcohol flush reaction. In most people, aldehydes are immediately broken down by the enzyme aldehyde dehydrogenase (ALDH2), but in those with the genetic mutation, the enzyme is incapacitated. Researchers led by Daria Mochly-Rosen of Stanford University genetically modified some mice to carry the mutation seen in humans that disables ALDH2. When they injected those mice and normal mice in the paw with an inflammatory compound that turned it red and swollen, mice carrying the mutation showed increased sensitivity to a poke compared with those with functioning ALDH2. When the researchers treated all the rodents with a novel drug called Alda-1 that boosts ALDH2 activity, the pain symptoms were reduced regardless of whether they carried the gene mutation. © 2015 Scientific American
By Amy Ellis Nutt When we tell stories about our lives, most of us never have our memories questioned. NBC's Brian Williams, like other high-profile people in the past, is finding out what happens when questions arise. Williams's faux pas – retelling a story of his helicopter coming under fire in Iraq a dozen years ago when it was actually the helicopter flying ahead of him – was much like Hillary Rodham Clinton's during the 2008 presidential campaign. Her story was about coming under fire during a visit to an airfield in Bosnia 12 years earlier. George W. Bush also misremembered when, on several occasions, he told audiences that on 9/11 he watched the first plane fly into the north tower of the World Trade Center on TV, just before entering that classroom in Florida to read a book to school kids. In each case, these were highly emotional moments. Williams's helicopter made an emergency landing in the desert behind the aircraft that was hit; Clinton was made to don a flak jacket and was told her airplane might not be able to land at the airport in Bosnia because of sniper fire in the area; and Bush was told by an aide about the first crash into World Trade Center just before entering the classroom. That each of those memories was false created huge public relations headaches for Clinton and Williams. But the fact is that false memories are not that uncommon, especially when they involve highly emotional events. Scientists have been telling us for years that memory of autobiographical events, also known as episodic memory, is pliable and even unreliable. The consensus from neuroimaging studies and laboratory experiments is that episodic memory is not like replaying a film but more like reconstructing an event from bits and pieces of information. Memories are stored in clusters of neurons called engrams, and the proteins responsible for storing those memories, scientists say, are modified and changed just by the reconstruction process of remembering.
Keyword: Learning & Memory
Link ID: 20566 - Posted: 02.09.2015
Madeline Bonin Bats and moths have been evolving to one-up each other for 65 million years. Many moths can hear bats’ ultrasonic echolocation calls, making it easy for the insects to avoid this predator. A few species of bat have developed echolocation calls that are outside the range of the moths’ hearing, making it harder for the moths to evade them1. But humans short-circuit this evolutionary arms race every time they turn on a porch light, according to a study in the Journal of Applied Ecology2. In field experiments, ecologist Corneile Minnaar of the University of Pretoria and his colleagues examined the diet of Cape serotine bats (Neoromicia capensis) both in the dark and under artificial light in a national park near Pretoria. The bat, an insect-eating species common in South Africa, has an echolocation call that moths can hear. Minnaar and his team determined both the species and quantity of available insect prey at the test sites using a hand-held net and a stationary trap. Cape serotine bats do not normally eat many moths. As the scientists expected, they caught more during the lighted trials than in the dark. What was surprising, however, was the discovery that the insects formed a greater share of the bats' diet during the lighted trials. The percentage of moths eaten in bright areas was six times larger than in dark zones, even though moths represented a smaller share of the total insect population under the lights than in the shade. But surprisingly, though moths represented a smaller share of the total insect population in the lighted areas, they played a larger role in the bats' diet. © 2015 Nature Publishing Group