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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.
Carl Zimmer In 1998, Dr. Philip A. Starr started putting electrodes in people’s brains. A neurosurgeon at the University of California, San Francisco, Dr. Starr was treating people with Parkinson’s disease, which slowly destroys essential bits of brain tissue, robbing people of control of their bodies. At first, drugs had given his patients some relief, but now they needed more help. After the surgery, Dr. Starr closed up his patients’ skulls and switched on the electrodes, releasing a steady buzz of electric pulses in their brains. For many patients, the effect was immediate. “We have people who, when they’re not taking their meds, can be frozen,” said Dr. Starr. “When we turn on the stimulator, they start walking.” First developed in the early 1990s, deep brain stimulation, or D.B.S., was approved by the Food and Drug Administration for treating Parkinson’s disease in 2002. Since its invention, about 100,000 people have received implants. While D.B.S. doesn’t halt Parkinson’s, it can turn back the clock a few years for many patients. Yet despite its clear effectiveness, scientists like Dr. Starr have struggled to understand what D.B.S. actually does to the brain. “We do D.B.S. because it works,” said Dr. Starr, “but we don’t really know how.” In a recent experiment, Dr. Starr and his colleagues believe they found a clue. D.B.S. may counter Parkinson’s disease by liberating the brain from a devastating electrical lock-step. The new research, published on Monday in Nature Neuroscience, may help scientists develop better treatments for Parkinson’s disease. It may also help researchers adapt D.B.S. for treatment of such brain disorders as depression and obsessive compulsive disorder. © 2015 The New York Times Company
Link ID: 20817 - Posted: 04.18.2015
|By Julie Hecht Unlike porcupines, dogs are a relatively hands-on (actually, paws-on) species, both with one another and with us. YouTube has numerous videos of dogs essentially saying, “Just keep petting me, please. Yes, that’s it…more.” But this relationship is not one-sided. Many studies find that positive interactions between people and dogs can be beneficial for both species. Increases in β-endorphin (beta-endorphin), oxytocin and dopamine—neurochemicals associated with positive feelings and bonding—have been observed in both dogs and people after enjoyable interactions like petting, play and talking. Essentially, interacting with a dog, particularly a known dog, can have some of the same psychophysiological markers as when two emotionally attached people spend time together. But do certain types of interactions have an outsized impact? Dogs are incredibly attentive to human faces and, in some cases, even specific facial expressions. This seemingly routine, benign behavior—your dog turning to gaze on your beautiful face as you do his or hers—could actually hold a very important piece of the puzzle in our relationship with dogs, suggests a study published this week in Science. The new study, by Miho Nagasawa of Azabu University in Japan and colleagues, builds on Nagasawa’s previous work, published in Hormones and Behavior in 2009, that found owners and dogs sharing a long mutual gaze had higher levels of oxytocin in their urine than owners of dogs giving a shorter gaze. (Oxytocin, a humble peptide of nine amino acids that is sometimes called the “cuddle hormone,” has been implicated in social bonding and is instrumental to the cascade of hormonal changes leading up to and following birth.) Nagasawa and her colleagues concluded that their finding was “a manifestation of attachment behavior.” © 2015 Scientific American
By Chris Cesare The beautiful color of a sunset might be more than just a pretty picture. It could be a signal to our bodies that it’s time to reset our internal clock, the biological ticktock that governs everything from sleep patterns to digestion. That’s the implication of a new study in mice that shows these small rodents use light’s changing color to set their own clocks, a finding that researchers expect will hold for humans, too. “I think this work opens up how we're just starting to scratch the surface and look at the environmental adaptations of clocks,” says Carrie Partch, a biochemist at the University of California, Santa Cruz, who was not involved in the new study. Scientists have long known about the role light plays in governing circadian rhythms, which synchronize life’s ebb and flow with the 24-hour day. But they weren’t sure how different properties of light, such as color and brightness, contributed to winding up that clock. “As a sort of common sense notion people have assumed that the clock somehow measures the amount of light in the outside world,” says Tim Brown, a neuroscientist at the University of Manchester in the United Kingdom and an author of the new study. “Our idea was that it might be doing something more sophisticated than that.” To find out, Brown and his colleagues targeted an area in the brain called the suprachiasmatic nucleus, or SCN, a region common to all vertebrates. It’s where the body keeps time using chemical and electrical rhythms that last, on average, 24 hours. The team wanted to know if color signals sent from the eyes reached the SCN and whether that information affected the timing of the clock. © 2015 American Association for the Advancement of Science
By KATIE THOMAS Last fall, an article in the American Journal of Psychiatry caught the attention of specialists who treat borderline personality disorder, an intractable condition for which no approved drug treatment exists. The article seemed to offer a glimmer of hope: The antipsychotic drug Seroquel XR reduced some of the disorder’s worst symptoms in a significant number of patients. “It was an exciting development,” recalled Mark F. Lenzenweger, a professor at Binghamton University and Weill Cornell Medical College and an expert in borderline personality disorder. In the realm of clinical trials, however, reality is sometimes far messier than the tidy summaries in medical journals. A closer look at the Seroquel XR study shows just how complicated things can get when a clinical trial involves psychiatric disorders and has its roots in intersecting and sometimes competing interests: a drug company looking to hold onto sales of a best-selling drug, a prominent academic with strong ties to the pharmaceutical industry and a university under fire for failing to protect human study subjects. The trial was paid for by AstraZeneca, the maker of Seroquel XR, and was conducted by Dr. S. Charles Schulz, the head of psychiatry at the University of Minnesota. Two of the study participants were living in a residential treatment facility for sex offenders and may have lied about their diagnosis to qualify for the trial. One of those men slipped the drugs to unwitting treatment center residents and staff, an alarming development that nevertheless did not seem to ruffle the university oversight board that is charged with looking into such episodes. The University of Minnesota’s clinical trial practices are now under intense scrutiny. In February, a panel of outside experts excoriated the university for failing to properly oversee clinical trials and for paying inadequate attention to the protection of vulnerable subjects. The review, commissioned by the university after years of criticism of its research practices, singled out Dr. Schulz and his department of psychiatry, describing “a culture of fear” that pervaded the department. © 2015 The New York Times Company
Link ID: 20814 - Posted: 04.18.2015
Mothers may influence the mood and behaviour of their babies through their breast milk, researchers say. There's growing evidence that mother's milk doesn't just affect the growth of a baby's body "but also areas of their brain that shape their motivations, their emotions, and therefore their behavioural activity," says Katie Hinde, an assistant professor of human evolutionary biology at Harvard University. In a paper published in the journal Evolution, Medicine and Public Health, Hinde and two other researchers propose a way in which the composition of breast milk could influence a baby's brain and behaviour. If food is scarce or there are a lot of predators around, it may be better for a mother to have a baby that is calmer and focuses on growing rather than one that is very active and playful, Hinde told CBC Radio's Quirks & Quarks in an interview that airs Saturday. It may be possible to influence a baby's activity level by changing the composition of the milk to affect the bacteria in the infant's gut, she added. Breast milk contains a lot of sugars that infants can't digest, but that feed bacteria that live in human intestines. Those bacteria don't just help digest food, said Hinde. "They can release chemical signals that travel to the infant's brain and shape neurodevelopment." ©2015 CBC/Radio-Canada
Michaeleen Doucleff It began with anxiety and depression. A few months later, hallucinations appeared. Then the Texas man, in his 40s, couldn't feel the left side of his face. He thought the symptoms were because of a recent car accident. But the psychiatric problems got worse. And some doctors thought the man might have bipolar disorder. Cattle feeding practices have been changed in an effort to halt the spread of mad cow disease. Eventually, he couldn't walk or speak. He was hospitalized. And about 18 months after symptoms began, the man died. An autopsy confirmed what doctors had finally suspected: the human version of mad cow disease, called variant Creutzfeldt-Jakob disease.* The case, published Wednesday in the journal Emerging Infectious Diseases, is only the fourth one diagnosed in the U.S. In those previous cases, people caught the disease in another country. Right away the man's diagnosis raised a new question: How did a rare disease linked to contaminated beef in the U.K. more than a decade ago get to a Texas man? Back in the early '80s, British ranchers noticed some of their cows were dying of a strange neurological disease. The cows became aggressive. They couldn't walk. Eventually, scientists figured out the culprit. A rogue protein formed large clumps in the brain and spinal cord. Over time, the clumps spread throughout the brain and damaged tissue. © 2015 NPR
Link ID: 20812 - Posted: 04.18.2015
By SABRINA TAVERNISE E-cigarettes have arrived in the life of the American teenager. Use of the devices among middle- and high school students tripled from 2013 to 2014, according to federal data released on Thursday, bringing the share of high school students who use them to 13 percent — more than smoke traditional cigarettes. About a quarter of all high school students and 8 percent of middle school students — 4.6 million young people altogether — used tobacco in some form last year. The sharp rise of e-cigarettes, together with a substantial increase in the use of hookah pipes, led to 400,000 additional young people using a tobacco product in 2014, the first increase in years, though researchers pointed out the percentage of the rise fell within the report’s margin of error. But the report also told another story. From 2011 to 2014, the share of high school students who smoked traditional cigarettes declined substantially, to 9 percent from 16 percent, and use of cigars and pipes ebbed too. The shift suggested that some teenage smokers may be using e-cigarettes to quit. Smoking is still the single-biggest cause of preventable death in the United States, killing more than 480,000 Americans a year, and most scientists agree that e-cigarettes, which deliver the nicotine but not the dangerous tar and other chemicals, are likely to be far less harmful than traditional cigarettes. The numbers came as a surprise and seemed to put policy makers into uncharted territory. The Food and Drug Administration took its first tentative step toward regulating e-cigarettes last year, but the process is slow, and many experts worry that habits are forming far faster than rules are being written. Because e-cigarettes are so new, scientists are still gathering evidence on their long-term health effects, leaving regulators scrambling to gather data. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 20811 - Posted: 04.18.2015
By Lenny Bernstein The dangers associated with night-time breathing disturbances, such as obstructive sleep apnea, are well known: increased risk of high blood pressure, heart attack, stroke and diabetes, not to mention sometimes dangerous daytime drowsiness, according to the National Heart, Lung and Blood Institute. Now a study suggests that such sleep conditions can hasten the onset of both Alzheimer's disease and "moderate cognitive impairment," such as memory loss, by quite a few years. But in a bit of good news, it concludes that using a continuous positive airway pressure (CPAP) machine, the treatment of choice for sleep apnea, can prevent or delay cognitive problems. A team of researchers led by Ricardo Osorio, an assistant professor of psychiatry at NYU Langone Medical Center determined that the sleep disturbances brought on mild cognitive impairment at least 11 years earlier in groups of people enrolled in a long-term Alzheimer's disease study, even when they controlled for other factors. In the largest group, that meant self-reported or family-reported cognitive problems, such as memory loss, at about 72 instead of 83. The same was true for Alzheimer's disease itself, which started in one group at a little older than 83, instead of about 88, when other factors were ruled out. The study was published online in the journal Neurology. It could be that the intermittent cutoff of oxygen to the brain is responsible for the problems, or the sleep disruption itself may be affecting cognition, Osorio said. Studies are underway to determine the cause.
Link ID: 20810 - Posted: 04.18.2015
by Beth Mole Small doses of lead may have big impacts on reading and math scores, scientists report April 7 in Environmental Health. Researchers looked at third grade test scores and levels of lead in blood samples from 58,650 students in Chicago public schools. As little as 2 micrograms of lead per deciliter of blood was associated with lower reading and math scores. The Centers for Disease Control and Prevention recommends that anything above 5 micrograms per deciliter is of concern. The researchers estimate that childhood lead levels at or above 5 micrograms per deciliter of blood accounted for as many as 25 percent of the children in the study failing reading and math standardized tests. The findings confirm that lead exposure, even at low doses, is associated with poor school performance. © Society for Science & the Public 2000 - 2015
By Virginia Morell Like many newborn mammals, baby mice cry to get their mother’s attention. But the mother doesn’t instinctively recognize these calls; she must learn the sounds of her offspring—just as human parents must learn the cries of their infants. Now, a team of researchers has discovered that the hormone oxytocin, which has been tied to trust and maternal bonding, holds the key to how this learning occurs. Only after oxytocin tweaks the brain of a female mouse does she respond with a mother’s concern and attentiveness to crying pups. “It’s an exciting study with implications that … could be helpful to certain disorders, such as autism,” says Larry Young, a neuroscientist at Emory University in Atlanta who was not involved in the work. To understand the role oxytocin plays in a mother mouse’s brain, scientists at New York University School of Medicine first investigated how female mice in general respond to the distress calls of baby mice. Pups emit ultrasonic cries when they are separated from the nest, which sometimes happens when a mother carries her babies to a new location. (Moms change nest locations regularly to elude predators.) When a mother hears these cries, she runs to the lost pup, picks it up, and carries it back to her nest. Other scientists have shown that moms respond even to the distress cries of pups that aren’t their own, readily approaching loudspeakers that broadcast the calls. Most virgin female mice, though, couldn’t care less; they seem completely indifferent to the pups’ cries for help. And yet, some virgin females that have either been housed with a mother and her litter or have been injected with oxytocin will retrieve crying infants. © 2015 American Association for the Advancement of Science.
Angus Chen A common pain medication might make you go from "so cute!" to "so what?" when you look at a photo of an adorable kitten. And it might make you less sensitive to horrifying things too. It's acetaminophen, the active ingredient in Tylenol. Researchers say the drug might be taking the edge off emotions – not just pain. "It seems to take off the highs of your daily highs and the lows off your daily lows," says Baldwin Way, a psychologist at Ohio State University and the principal investigator on the study, "It kind of flattens out the vicissitudes of your life." The idea that over-the-counter pain pills might affect emotions has been circulating since 2010, when two psychologists, Naomi Eisenberger and Nathan DeWall, led a study showing that acetaminophen seemed to be having both a psychological and a neurological effect on people. They asked volunteers to play a rigged game that simulated social rejection. Not only did the acetaminophen appear to be deflecting social anxieties, it also seemed to be dimming activity in the insula, a region of the brain involved in processing emotional pain. A brain that can let other thoughts bubble up despite being in pain might help its owner benefit from meditation or other cognitive therapies. "But [the insula] is a portion of the brain that seems to be involved in a lot of things," Way says. In older studies, scientists saw that people with damage in their insula didn't react as strongly to either negative or positive images. So Way and one of his students, Geoffrey Durso, figured that if acetaminophen is doing something to the insula, then it might be having a wider effect, too. © 2015 NPR
By Nicholas Bakalar Breathing problems during sleep may be linked to early mental decline and Alzheimer’s disease, a new study suggests. But treating apnea with a continuous positive airway pressure machine can significantly delay the onset of cognitive problems. In a group of 2,470 people, average age 73, researchers gathered information on the incidence of sleep apnea, a breathing disorder marked by interrupted breathing and snoring, and the incidence of mild cognitive impairment and Alzheimer’s disease. After adjusting for a range of variables, they found that people with disordered breathing during sleep became cognitively impaired an average of about 10 years sooner than those without the disorder. But compared with those whose sleep disorder was untreated, those using C.P.A.P. machines delayed the appearance of cognitive impairment by an average of 10 years — making their age of onset almost identical to those who had no sleep disorder at all. The lead author, Dr. Ricardo S. Osorio, a research professor of psychiatry at New York University, said the analysis, published online in Neurology, is an observational study that does not prove cause and effect. “But,” he added, “we need to increase the awareness that sleep disorders can increase the risk for cognitive impairment and possibly for Alzheimer’s. Whether treating sleep disorders truly slows the decline is still not known, but there is some evidence that it might.” © 2015 The New York Times Company
by Jessica Hamzelou An exoskeleton that enables movement and provides tactile feedback has helped eight paralysed people regain sensation and move previously paralysed muscles "I FELT the ball!" yelled Juliano Pinto as he kicked off the Football World Cup in Brazil last year. Pinto, aged 29 at the time, lost the use of his lower body after a car accident in 2006. "It was the most moving moment," says Miguel Nicolelis at Duke University in North Carolina, head of the Walk Again Project, which developed the thought-controlled exoskeleton that enabled Pinto to make his kick. Since November 2013, Nicolelis and his team have been training Pinto and seven other people with similar injuries to use the exoskeleton – a robotic device that encases the limbs and converts brain signals into movement. The device also feeds sensory information to its wearer, which seems to have partially reawakened their nervous system. When Nicolelis reassessed his volunteers after a year of training, he found that all eight people had regained sensations and the ability to move muscles in their once-paralysed limbs. "Nobody expected it at all," says Nicolelis, who presented the results at the Brain Forum in Lausanne, Switzerland, on 31 March. "When we first saw the level of recovery, there was not a single person in the room with a dry eye." When a person's spinal cord is injured, the connection between body and brain can be damaged, leaving them unable to feel or move parts of their body. If a few spinal nerves remain, people can sometimes regain control over their limbs, although this can involve years of rehabilitation. © Copyright Reed Business Information Ltd.
Link ID: 20805 - Posted: 04.16.2015
|By Cari Nierenberg and LiveScience Women who develop gestational diabetes early in their pregnancy have a higher chance of having a child with autism than women who don't develop the condition, a new study suggests. Researchers found that mothers-to-be who developed gestational diabetes — high blood sugar during pregnancy in women who have never had diabetes — by their 26th week of pregnancy were 63 percent more likely to have a child diagnosed with an autism spectrum disorder (ASD) compared with women who did not have gestational diabetes at any point during their pregnancy (and who also did not have type 2 diabetes prior to pregnancy). The finding does not mean that autism is common among children born to women who had gestational diabetes. "Autism is still rare," said study co-author Anny Xiang, a research scientist at Kaiser Permanente Southern California in Pasadena. The findings show that, although the risk of having a child with autism is still low among women who have gestational diabetes early in pregnancy (before 26 weeks), the study did find a relationship between these women and an increased risk that the child would have autism, Xiang said. The study, published today (April 14) in the Journal of the American Medical Association, looked at more than 320,000 children born in Southern California between 1995 and 2009. About 8 percent of the kids were born to mothers who had pregnancy-related diabetes, and 2 percent had mothers with type 2 diabetes. © 2015 Scientific American
By Neuroskeptic According to a large study just published in the Journal of Autism and Developmental Disorders, there’s no correlation between brain anatomy and self-reported autistic traits. Dutch researchers P. Cedric M. P. Koolschijn and colleagues looked at two samples of young Dutch adults: an ‘exploration’ sample of 204, and a separate ‘validation’ group of 304 individuals. Most of the participants did not have autism. The researchers looked for associations between various aspects of brain structure and autistic traits, using the AQ questionnaire, a popular self-report measure. Autistic traits are personality or behavior features similar to (but generally milder than) autism symptoms. For example, the first item on the AQ is “I prefer to do things with others rather than on my own.” If you disagree with that, you get a point. More points means more autistic traits. Koolschijn et al. used VBM, vertex-based cortical thickness analysis, and diffusion weighted imaging to explore different aspects of brain grey and white matter anatomy. However, although AQ scores were weakly correlated with the volume of a few brain areas in the exploration sample, none of these correlations were confirmed in the larger validation sample, suggesting that they were just false positives caused by the large number of multiple comparisons.
A study using mice has uncovered a possible cause of Alzheimer’s disease, and suggests that a drug currently being investigated in human clinical trials to treat cancer could prevent the illness. The research has been heralded as offering hope of finding new treatments for dementia, an illness that affects 850,000 people in the UK. The findings, by Duke University in America and published in the Journal of Neuroscience, are surprising, according to one of the authors, as they contradict current thinking on the disease. The research suggests that in mice with Alzheimer’s disease certain immune cells that normally protect the brain begin abnormally to consume an important nutrient called arginine. By blocking this process using the drug difluoromethylornithine (DFMO), memory loss and a buildup of sticky proteins known as brain plaques were prevented. The study used a type of mouse in which a number of important genes had been swapped to make the animal’s immune system more similar to a human’s. Senior author Carol Colton, professor of neurology at the Duke University School of Medicine, and a member of the Duke Institute for Brain Sciences, said: “If indeed arginine consumption is so important to the disease process, maybe we could block it and reverse the disease.” It was previously thought the brain releases molecules that ramp up the immune system, apparently damaging the brain, but the study found a heightened expression of genes associated with the suppression of the immune system. Author Matthew Kan said: “It’s surprising because [suppression of the immune system is] not what the field has been thinking is happening in AD [Alzheimer’s disease].” © 2015 Guardian News and Media Limited
Link ID: 20802 - Posted: 04.15.2015
Jon Hamilton There's new evidence that the brain's activity during sleep isn't random. And the findings could help explain why the brain consumes so much energy even when it appears to be resting. "There is something that's going on in a very structured manner during rest and during sleep," says Stanford neurologist Dr. Josef Parvizi, "and that will, of course, require energy consumption." For a long time, scientists dismissed the brain's electrical activity during rest and sleep as meaningless "noise." But then studies using fMRI began to reveal patterns suggesting coordinated activity. To take a closer look, Parvizi and a team of researchers studied three people awaiting surgery for epilepsy. These people spent several days with electrodes in their brains to help locate the source of their seizures. And that meant Parvizi's team was able to monitor the activity of small groups of brain cells in real time. "We wanted to know exactly what's going on during rest," Parvizi says, "and whether or not it reflects what went on during the daytime when the subject was not resting." In the study published online earlier this month in Neuron, the team first studied the volunteers while they were awake and answering simple questions like: Did you drive to work last week? "In order to answer yes or no, you retrieve a lot of facts; you retrieve a lot of visualized memories," Parvizi says. © 2015 NPR
By JAMES GORMAN Studies of hunters and gatherers — and of chimpanzees, which are often used as stand-ins for human ancestors — have cast bigger, faster and more powerful males in the hunter role. Now, a 10-year study of chimpanzees in Senegal shows females playing an unexpectedly big role in hunting and males, surprisingly, letting smaller and weaker hunters keep their prey. The results do not overturn the idea of dominant male hunters, said Jill D. Pruetz of Iowa State University, who led the study. But they may offer a new frame of reference on hunting, tools and human evolution. “We need to broaden our perspective,” she said. Among the 30 or so chimps Dr. Pruetz and her colleagues observed, called the Fongoli band, males caught 70 percent of the prey, mostly by chasing and running it down. But these chimps are very unusual in one respect. They are the only apes that regularly hunt other animals with tools — broken tree branches. And females do the majority of that hunting for small primates called bush babies. Craig Stanford, an anthropologist at the University of Southern California who has written extensively on chimp hunting and human evolution, said the research was “really important” because it solidified the evidence for chimps hunting with tools, which Dr. Pruetz had reported in earlier papers. It also clearly shows “the females are more involved than in other places,” he said, adding that it provides new evidence to already documented observations that female chimps are “much more avid tool users than males are.” All chimpanzees eat a variety of plant and animal foods, including insects like termites. And all chimpanzees eat some other animals. The most familiar examples of chimpanzee hunting are bands of the apes chasing red colobus monkeys through the trees in the rain forests of East Africa. © 2015 The New York Times Company
By Laura Sanders To drive a rat to drink, make it smoke first. Rats dependent on nicotine escalate their drinking more quickly than rats that haven’t been exposed to nicotine, researchers report in the April 15 Journal of Neuroscience. The results help explain why alcohol and tobacco addictions in people often go hand in hand. After nicotine injections, rats that had previously been exposed to alcohol dosed themselves with more alcohol than rats unexposed to nicotine did. Scientists were able to curb this booziness: Rats injected with a compound that made brain cells ignore nicotine did not boost their intake of alcohol. The double whammy of nicotine and alcohol dependence may be due to a select group of nerve cells throughout the rat brain that respond to this nicotine-aided drinking, Olivier George of the Scripps Research Institute in La Jolla, Calif., and colleagues found. If a similar response happens in humans, studying these particular nerve cells might ultimately lead to better ways to curb both alcohol and tobacco dependencies, the researchers write. R. Leão et al. Chronic nicotine activates stress/reward-related brain regions and facilitates the transition to compulsive alcohol drinking. Journal of Neuroscience. Vol. 35, April 15, 2015. doi:10.1523/JNEUROSCI.3302-14.2015. © Society for Science & the Public 2000 - 2015.
Keyword: Drug Abuse
Link ID: 20799 - Posted: 04.15.2015
Daniel Cressey Experiments that use only a small number of animals are common, but might not give meaningful results. Replace, refine, reduce: the 3 Rs of ethical animal research are widely accepted around the world. But now the message from UK funding agencies is that some experiments use too few animals, a problem that leads to wastage and low-quality results. On 15 April, the research councils responsible for channelling government funding to scientists, and their umbrella group Research Councils UK, announced changes to their guidelines for animal experiments. Funding applicants must now show that their work will provide statistically robust results — not just explain how it is justified and set out the ethical implications — or risk having their grant application rejected. The move aims to improve the quality of medical research, and will help to address widespread concerns that animals — mostly mice and rats — are being squandered in tiny studies that lack statistical power. “If the study is underpowered your results are not going to be reliable,” says Nathalie Percie du Sert, who works on experimental design at the National Centre for the Replacement, Refinement and Reduction (NC3Rs) of Animals in Research in London. “These animals are going to be wasted.” © 2015 Nature Publishing Group
Keyword: Animal Rights
Link ID: 20798 - Posted: 04.15.2015