By ROBERT PEAR WASHINGTON — Psychiatrists are significantly less likely than doctors in other specialties to accept insurance, researchers say in a new study, complicating the push to increase access to mental health care. The study, published Wednesday in the journal JAMA Psychiatry, found that 55 percent of psychiatrists accepted private insurance, compared with 89 percent of other doctors. Likewise, the study said, 55 percent of psychiatrists accept patients covered by Medicare, against 86 percent of other doctors. And 43 percent of psychiatrists accept Medicaid, which provides coverage for low-income people, while 73 percent of other doctors do. The lead author of the study, Dr. Tara F. Bishop of Weill Cornell Medical College in New York, said: “In the wake of the school killings in Newtown, Conn., and other recent mass shootings, the need for increased mental health services is now recognized. But unless patients have deep pockets, they may have a hard time finding a psychiatrist who will treat them.” Mental health care is one of 10 types of “essential health benefits” that must be provided by insurers under the new health care law. A federal rule issued last month requires insurers to cover care for mental health and addiction on the same terms as treatments for physical illnesses, without charging higher co-payments or deductibles or imposing stricter limits on services. Starting next year, Medicare will end a discriminatory policy that for decades has required people to pay a larger share of the bill for mental health care than for other outpatient services. However, the study suggests that expanding coverage may not by itself guarantee access to psychiatrists. “Even if you have good insurance that covers mental health care, you may still have a problem if there’s no doctor who accepts your insurance,” Dr. Bishop said. © 2013 The New York Times Company

Keyword: Depression; Schizophrenia
Link ID: 19031 - Posted: 12.12.2013

Smoking tobacco or marijuana, taking prescription painkillers, or using illegal drugs during pregnancy is associated with double or even triple the risk of stillbirth, according to research funded by the National Institutes of Health. Researchers based their findings on measurements of the chemical byproducts of nicotine in maternal blood samples; and cannabis, prescription painkillers and other drugs in umbilical cords. Taking direct measurements provided more precise information than did previous studies of stillbirth and substance use that relied only on women’s self-reporting. The study findings appear in the journal Obstetrics & Gynecology. “Smoking is a known risk factor for stillbirth, but this analysis gives us a much clearer picture of the risks than before,” said senior author Uma M. Reddy, M.D., MPH, of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the NIH institute that supported the study. “Additionally, results from the latest findings also showed that likely exposure to secondhand smoke can elevate the risk of stillbirth.” Dr. Reddy added, “With the legalization of marijuana in some states, it is especially important for pregnant women and health care providers to be aware that cannabis use can increase stillbirth risk.” The study enrolled women between March 2006 and September 2008 in five geographically defined areas delivering at 59 hospitals participating in the Stillbirth Collaborative Research Network External Web Site Policy. Women who experienced a stillbirth and those who gave birth to a live infant participated in the study. The researchers tested blood samples at delivery from the two groups of women and the umbilical cords from their deliveries to measure the exposure to the fetus. They also asked participants to self-report smoking and drug use during pregnancy.

Keyword: Development of the Brain; Drug Abuse
Link ID: 19030 - Posted: 12.12.2013

by Rowan Hooper BIOENGINEERS dream of growing spare parts for our worn-out or diseased bodies. They have already succeeded with some tissues, but one has always eluded them: the brain. Now a team in Sweden has taken the first step towards this ultimate goal. Growing artificial body parts in the lab starts with a scaffold. This acts as a template on which to grow cells from the patient's body. This has been successfully used to grow lymph nodes, heart cells and voice boxes from a person's stem cells. Bioengineers have even grown and transplanted an artificial kidney in a rat. Growing nerve tissue in the lab is much more difficult, though. In the brain, new neural cells grow in a complex and specialised matrix of proteins. This matrix is so important that damaged nerve cells don't regenerate without it. But its complexity is difficult to reproduce. To try to get round this problem, Paolo Macchiarini and Silvia Baiguera at the Karolinska Institute in Stockholm, Sweden, and colleagues combined a scaffold made from gelatin with a tiny amount of rat brain tissue that had already had its cells removed. This "decellularised" tissue, they hoped, would provide enough of the crucial biochemical cues to enable seeded cells to develop as they would in the brain. When the team added mesenchymal stem cells – taken from another rat's bone marrow – to the mix, they found evidence that the stem cells had started to develop into neural cells (Biomaterials, doi.org/qfh). The method has the advantage of combining the benefits of natural tissue with the mechanical properties of an artificial matrix, says Alex Seifalian, a regenerative medicine specialist at University College London, who wasn't involved in the study. © Copyright Reed Business Information Ltd.

Keyword: Development of the Brain
Link ID: 19029 - Posted: 12.12.2013

By Janelle Weaver Children with a large vocabulary experience more success at school and in the workplace. How much parents talk to their children plays a major role, but new research shows that it is not just the quantity but also the quality of parental input that matters. Helpful gestures and meaningful glances may allow kids to grasp concepts more easily than they otherwise would. In a study published in June in the Proceedings of the National Academy of Sciences USA, Erica Cartmill of the University of Chicago and her collaborators videotaped parents in their homes as they read books and played games with their 14- or 18-month-old children. The researchers created hundreds of 40-second muted video clips of these interactions. Another set of study participants watched the videos and used clues from the scenes to guess which nouns the parents were saying at various points in the sequences. The researchers used the accuracy of these guesses to rate how well a parent used nonverbal cues, such as gesturing toward and looking at objects, to clarify a word's meaning. Cartmill and her team found that the quality of parents' nonverbal signaling predicted the size of their children's vocabulary three years later. Surprisingly, socioeconomic status did not play a role in the quality of the parents' nonverbal signaling. This result suggests that the well-known differences in children's vocabulary size across income levels are likely the result of how much parents talk to their children, which is known to differ by income, rather than how much nonverbal help they offer during those interactions. © 2013 Scientific American

Keyword: Language; Development of the Brain
Link ID: 19028 - Posted: 12.12.2013

Ian Sample, science correspondent Differences in children's exam results at secondary school owe more to genetics than teachers, schools or the family environment, according to a study published yesterday. The research drew on the exam scores of more than 11,000 16-year-olds who sat GCSEs at the end of their secondary school education. In the compulsory core subjects of English, maths and science, genetics accounted for on average 58% of the differences in scores that children achieved. Grades in the sciences, such as physics, biology and chemistry, were more heritable than those in humanities subjects, such as art and music, at 58% and 42% respectively. The findings do not mean that children's performance at school is determined by their genes, or that schools and the child's environment have no influence. The overall effect of a child's environment – including their home and school life – accounted for 36% of the variation seen in students' exam scores across all subjects, the study found. "The question we are asking is why do children differ in their GCSE scores? People immediately think it's schools. But if schools accounted for all the variance, then children in one classroom would all be the same," said Robert Plomin, an expert in behavioural genetics who led the study at King's College London. To tease out the genetic contribution to children's school grades, the researchers studied GCSE scores of identical twins (who share 100% of their genes) and non-identical twins (who share on average half of the genes that normally vary between people). Both groups share their environments to a similar extent. © 2013 Guardian News and Media Limited

Keyword: Intelligence; Genes & Behavior
Link ID: 19027 - Posted: 12.12.2013

By Sanaz Majd MD Scientific American presents House Call Doctor by Quick & Dirty Tips. Scientific American and Quick & Dirty Tips are both Macmillan companies. Have you been told by your spouse that you “fidget” in the middle of the night? Or have you noticed your legs or feet may have a mind of their own when you’re trying to fall asleep? Do you have an urge to move your legs a lot at bedtime? You may very well be one of the many people who remain undiagnosed with the condition called Restless Legs Syndrome, or RLS. For those who have never experienced RLS, it may seem like a very odd and peculiar phenomenon. But if you’ve ever had these symptoms, you may be surprised to learn that this is an actual medical condition. Maybe you’ve already mentioned it to your doctor, or maybe you never realized it was real until now. Either way, let’s find out more about Restless Legs Syndrome and how it’s treated. What Is RLS? I’ve actually discussed RLS in a previous episode on insomnia, and you may want to revisit that episode before moving on to this one. But in a nutshell, here are the symptoms that up to 10% of the American population are estimated to be suffering from: © 2013 Scientific American

Keyword: Sleep
Link ID: 19026 - Posted: 12.12.2013

By MAGGIE KOERTH-BAKER More than a decade ago, a 43-year-old woman went to a surgeon for a hysterectomy. She was put under, and everything seemed to be going according to plan, until, for a horrible interval, her anesthesia stopped working. She couldn’t open her eyes or move her fingers. She tried to breathe, but even that most basic reflex didn’t seem to work; a tube was lodged in her throat. She was awake and aware on the operating table, but frozen and unable to tell anyone what was happening. Studies of anesthesia awareness are full of such horror stories, because administering anesthesia is a tightrope walk. Too much can kill. But too little can leave a patient aware of the procedure and unable to communicate that awareness. For every 1,000 people who undergo general anesthesia, there will be one or two who are not as unconscious as they seem — people who remember their doctors talking, and who are aware of the surgeon’s knife, even while their bodies remain catatonic and passive. For the unlucky 0.13 percent for whom anesthesia goes awry, there’s not really a good preventive. That’s because successful anesthetization requires complete unconsciousness, and consciousness isn’t something we can measure. There are tools that anesthesiologists use to get a pretty good idea of how well their drugs are working, but these systems are imperfect. For most patients receiving inhaled anesthesia, they’re no better at spotting awareness than dosing metrics developed half a century ago, says George Mashour, a professor of anesthesiology at the University of Michigan Medical School. There are two intertwined mysteries at work, Mashour told me: First, we don’t totally understand how anesthetics work, at least not on a neurological basis. Second, we really don’t understand consciousness — how the brain creates it, or even what, exactly, it is. © 2013 The New York Times Company

Keyword: Consciousness; Sleep
Link ID: 19025 - Posted: 12.11.2013

By Graham Lawton Patricia Churchland, a neurophilosopher at the University of California at San Diego, says our hopes, loves and very existence are just elaborate functions of a complicated mass of grey tissue. Accepting that can be hard, but what we know should inspire us, not scare us. Her most recent book is Touching a Nerve: The Self as Brain. Graham Lawton: You compare revelations in neuroscience with the discoveries that the Earth goes around the sun and that the heart is a pump. What do you think these ideas have in common? Patricia Churchland: They challenge a whole framework of assumptions about the way things are. For Christians, it was very important that the Earth was at the center of the universe. Similarly, many people believed that the heart was somehow what made us human. And it turned out it was just a pump made of meat. I think the same is true about realizing that when we're conscious, when we make decisions, when we go to sleep, when we get angry, when we're fearful, these are just functions of the physical brain. Coming to terms with the neural basis of who we are can be very unnerving. It has been called "neuroexistentialism," which really captures the essence of it. We're not in the habit of thinking about ourselves that way. GL: Why is it so difficult for us to see the reality of what we actually are? PC: Part of the answer has to do with the evolution of nervous systems. Is there any reason for a brain to know about itself? We can get along without knowing, just as we can get along without knowing that the liver is in there filtering out toxins. The wonderful thing, of course, is that science allows us to know. © 2013 The Slate Group, LLC.

Keyword: Consciousness
Link ID: 19024 - Posted: 12.11.2013

by Chelsea Whyte For chameleons, war paint isn't just an accessory, it is a battle flag. The brightness of the colours these lizards display and how rapidly they change are good indicators of which animal will win in a fight. Chameleons are famous for changing colour to hide from predators by blending into their surroundings, but they also use colour for social communication. One of the most diversely coloured species is the veiled chameleon (Chamaeleo calyptratus), which lives in parts of Saudi Arabia and Yemen. "At their brightest, they have vertical yellow stripes, blue-green bellies, black speckles that provide contrast and make their stripes stand out, and orange around the corner of their mouths," says Russell Ligon, a behavioural ecologist at Arizona State University in Tempe. To see if individual variations in these colours and patterns influenced the outcome of a fight, Ligon and his colleague Kevin McGraw staged a round-robin tournament in which 10 male veiled chameleons were pitted against each other. Using a high-speed camera, they were able to capture the brightness and colour changes from 28 points on each animal, taking into account how the colours would look to a chameleon's eye – which sees both visible and ultraviolet light. They found that males with the brightest side stripes were more likely to instigate a fight, whereas those with brighter heads that changed colour most rapidly were more likely to win. This suggests that different colours and patterns may signal different aspects of competitive behaviour – how motivated the chameleon is versus its strength. © Copyright Reed Business Information Ltd.

Keyword: Aggression; Sexual Behavior
Link ID: 19023 - Posted: 12.11.2013

By Ben Thomas 2013’s Nobel prize in Physiology or Medicine honors three researchers in particular – but what it really honors is thirty-plus years of work not only from them, but also from their labs, their graduate students and their collaborators. Winners James Rothman, Randy Schekman and Thomas Südhof all helped assemble our current picture of the cellular machinery that enables neurotransmitter chemicals to travel from one nerve cell to the next. And as all three of these researchers agree, that process of understanding didn’t catalyze until the right lines of research, powered by the right tools, happened to converge at the right time. Long before that convergence, though, these three scientists began by seeking the answers to three different questions – none of which seemed to have anything to do with the others. When James Rothman started out as a researcher at Harvard in 1978, his goal was to find out exactly how vesicle transmission worked. Vesicles – Latin for “little vessels” – are the microscopic capsules that carry neurotransmitter molecules like serotonin and dopamine from one brain cell to another. By the late 1960s, the old-guard biochemist George Palade, along with other researchers, had already deduced that synaptic vesicles are necessary for neurotransmission – but the questions of which proteins guided these tiny vessels on their journey, and how they docked with receiving neurons, remained mysterious. Yale University's James Rothman set out to break down the process of vesicle transmission, chemical-by-chemical, reaction-by-reaction. Courtesy of Yale University. In other words, although researchers had established the existence of this vesicle transmission process, no one knew exactly what made it work, or how. © 2013 Scientific American

Keyword: Miscellaneous
Link ID: 19022 - Posted: 12.11.2013

by Bethany Brookshire When neurons throughout the brain and body send messages, they release chemical signals. These chemicals, neurotransmitters, pass into the spaces between neurons, or synapses, binding to receptors to send a signal along. When they are not in use, neurotransmitters are stored within the cell in tiny bubbles called vesicles. During signaling, these vesicles head to the membrane of the neuron, where they dump neurotransmitter into the synapse. And after delivering their cargo, most vesicles disappear. But more vesicles keep forming, filling with neurotransmitters so neurons can keep sending signals. What goes up must come down. When vesicles go out, they must come back. But how fast to the vesicles re-appear? Must faster, it turns out, than we first thought. Neurotransmission happens fast. An electrical signal comes down a neuron in your brain and triggers vesicles to move to the cell membrane. When the vesicles merge into the membrane and release their chemical cargo, the neurotransmitters float across the open synapse to the next neuron. This happens every time the neuron “fires.” This needs to happen very quickly, as neurons often fire at 100 hertz, or 100 times per second. Some neurons perform a “kiss-and-run,” opening up a temporary pore in the membrane, releasing a little bit of neurotransmitter and darting away again. Other vesicles need to merge with the synapse entirely. With the assistance of docking proteins, these vesicles fuse with the membrane of the neuron to release the neurotransmitters, a process called exocytosis. © Society for Science & the Public 2000 - 2013.

Keyword: Miscellaneous
Link ID: 19021 - Posted: 12.11.2013

By Jeanene Swanson Depression strikes some 35 million people worldwide, according to the World Health Organization, contributing to lowered quality of life as well as an increased risk of heart disease and suicide. Treatments typically include psychotherapy, support groups and education as well as psychiatric medications. SSRIs, or selective serotonin reuptake inhibitors, currently are the most commonly prescribed category of antidepressant drugs in the U.S., and have become a household name in treating depression. The action of these compounds is fairly familiar. SSRIs increase available levels of serotonin, sometimes referred to as the feel-good neurotransmitter, in our brains. Neurons communicate via neurotransmitters, chemicals which pass from one nerve cell to another. A transporter molecule recycles unused transmitter and carries it back to the pre-synaptic cell. For serotonin, that shuttle is called SERT (short for “serotonin transporter”). An SSRI binds to SERT and blocks its activity, allowing more serotonin to remain in the spaces between neurons. Yet, exactly how this biochemistry then works against depression remains a scientific mystery. In fact, SSRIs fail to work for mild cases of depression, suggesting that regulating serotonin might be an indirect treatment only. “There’s really no evidence that depression is a serotonin-deficiency syndrome,” says Alan Gelenberg, a depression and psychiatric researcher at The Pennsylvania State University. “It’s like saying that a headache is an aspirin-deficiency syndrome.” SSRIs work insofar as they reduce the symptoms of depression, but “they’re pretty nonspecific,” he adds. © 2013 Scientific American

Keyword: Depression
Link ID: 19020 - Posted: 12.11.2013

Taking some heartburn medications for more than two years is linked to a higher risk of vitamin B12 deficiency in adults, a U.S. study suggests. Left untreated, vitamin B12 deficiency can lead to dementia, neurological damage, anemia, and other complications. Knowing that stomach acid aids in vitamin B12 absorption, researchers set out to test whether suppressing the acids can lead to vitamin deficiency. The drugs in question are known as proton pump inhibitors and they include such well known brands as Losec, Nexium, Prabacid and Pariet. Doses of more than 1.5 pills per day were more strongly associated with vitamin D deficiency than doses of less than 0.75 pills per day, Dr. Douglas Corley, a gastroenterologist and research scientist with the Kaiser Permanente Division of Research in Broadway, Calif. and his co-authors said in Wednesday's issue of the Journal of the American Medical Association. "This research raises the question of whether people who are taking acid-depressing medications long term should be screened for vitamin B12 deficiency," Corley said in a release. "It's a relatively simple blood test, and vitamin supplements are an effective way of managing the vitamin deficiency, if it is found." For the study, researchers looked at electronic health records of 25,956 adults diagnosed with vitamin B12 deficiency in Northern California between January 1997 and June 2011, and compared them with 184,199 patients without B12 deficiency during the same time period. Among the 25,956 patients who had vitamin B12 deficiency, 12 per cent used proton pump inhibitors for at least two years, compared with 7.2 per cent of those in the control group. © CBC 2013

Keyword: Alzheimers; Learning & Memory
Link ID: 19019 - Posted: 12.11.2013

By Ingfei Chen The way doctors diagnose Alzheimer's disease may be starting to change. Traditionally clinicians have relied on tests of memory and reasoning skills and reports of social withdrawal to identify patients with Alzheimer's. Such assessments can, in expert hands, be fairly conclusive—but they are not infallible. Around one in five people who are told they have the neurodegenerative disorder actually have other forms of dementia or, sometimes, another problem altogether, such as depression. To know for certain that someone has Alzheimer's, doctors must remove small pieces of the brain, examine the cells under a microscope and count the number of protein clumps called amyloid plaques. An unusually high number of plaques is a key indicator of Alzheimer's. Because such a procedure risks further impairing a patient's mental abilities, it is almost always performed posthumously. In the past 10 years, however, scientists have developed sophisticated brain scans that can estimate the amount of plaque in the brain while people are still alive. In the laboratory, these scans have been very useful in studying the earliest stages of Alzheimer's, before overt symptoms appear. The results are reliable enough that last year the Food and Drug Administration approved one such test called Amyvid to help evaluate patients with memory deficits or other cognitive difficulties. Despite the FDA's approval, lingering doubts about the exact role of amyloid in Alzheimer's and ambivalence about the practical value of information provided by the scan have fueled debate about when to order an Amyvid test. Not everyone who has an excessive amount of amyloid plaque develops Alzheimer's, and at the moment, there is generally no way to predict whom the unlucky ones will be. Recent studies have shown that roughly one third of older citizens in good mental health have moderate to high levels of plaque, with no noticeable ill effects. And raising the specter of the disorder in the absence of symptoms may upset more people than it helps because no effective treatments exist—at least not yet. © 2013 Scientific American

Keyword: Alzheimers; Brain imaging
Link ID: 19018 - Posted: 12.11.2013

By Dan Hurley Darwin and Freud walk into a bar. Two alcoholic mice — a mother and her son — sit on two bar stools, lapping gin from two thimbles. The mother mouse looks up and says, “Hey, geniuses, tell me how my son got into this sorry state.” “Bad inheritance,” says Darwin. “Bad mothering,” says Freud. For over a hundred years, those two views — nature or nurture, biology or psychology — offered opposing explanations for how behaviors develop and persist, not only within a single individual but across generations. And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life experiences, but those of your mother’s, grandmother’s and beyond. The bar was in Madrid, where the Cajal Institute, Spain’s oldest academic center for the study of neurobiology, was holding an international meeting. Moshe Szyf, a molecular biologist and geneticist at McGill University in Montreal, had never studied psychology or neurology, but he had been talked into attending by a colleague who thought his work might have some application. Likewise, Michael Meaney, a McGill neurobiologist, had been talked into attending by the same colleague, who thought Meaney’s research into animal models of maternal neglect might benefit from Szyf’s perspective.

Keyword: Epigenetics
Link ID: 19017 - Posted: 12.11.2013

Three lawsuits filed last week that attempted to achieve “legal personhood” for four chimpanzees living in New York have been struck down. The suits, brought by the animal rights group the Nonhuman Rights Project (NhRP), targeted two chimps on private property and two in a research lab at Stony Brook University in New York. They were the first step in a nationwide campaign to grant legal rights to a variety of animals. NhRP had spent 5 years honing its legal strategy. It picked what it thought would be the most favorable jurisdictions and petitioned the judges with a writ of habeas corpus, which allows a person being held captive to have a say in court. Suffolk County Supreme Court Justice W. Gerard Asher denied the writ for the Stony Brook chimpanzees, writing in a brief decision that the animals did not qualify for habeas corpus because they were not “persons.” Both chimps are used in locomotion research at the university in work that is attempting to shed light on the origin of bipedalism in humans. Asher did not meet with NhRP lawyers; he issued his decision via a court clerk. The other judges were more accommodating. Fulton County Supreme Court Justice Joseph Sise and Niagara County Supreme Court Justice Ralph Boniello both allowed NhRP lawyers to make oral arguments in the courtroom. “As an animal lover, I appreciate your work,” said Sise, who handled the case of a chimpanzee named Tommy living in cage on his owner’s property in Gloversville, according to an NhRP press release. The group made “a very strong argument,” Sise said, according to the release, but he did not agree that habeas corpus applied to chimpanzees. Boniello, who oversaw the case of a chimp named Kiko living on his owner’s property in Niagara Falls, said he did not want to be the first “to make that leap of faith” equating chimpanzees with human beings. © 2013 American Association for the Advancement of Science.

Keyword: Animal Rights
Link ID: 19016 - Posted: 12.11.2013

Someday, a smart phone app that asks what you’re feeling 10 times a day may be able to tell you if you’re edging closer to depression—and recommend that you seek preventive therapy or drugs. Scientists have discovered that how quickly someone bounces back from negative feelings, over hours or days, can predict whether that person is at risk of an episode of major depressive disorder. “The holy grail of depression epidemiology is that we want to intervene early to prevent people from having depressive episodes,” says social scientist Stephen Gilman of Harvard University, who was not involved in the study. “Where this work is headed is making an advance in that direction, toward early detection and therefore early intervention.” Researchers asked more than 600 people—some healthy and some with a diagnosis of depression—to track their emotions for 5 or 6 days. Ten times a day, at random intervals, a watch would beep and the subjects would record how strongly they identified with each of four emotions: cheerful, content, sad, and anxious. Six to 8 weeks later, participants filled out a more detailed questionnaire that rated their levels of clinical depression. By the end of the follow-up period, about 13% of the subjects had experienced a shift toward being more depressed, a number consistent with what would be expected in the general population. Trends in the daily mood records, the team discovered, could predict whether a previously healthy person would make that shift toward depression. © 2013 American Association for the Advancement of Science

Keyword: Depression
Link ID: 19015 - Posted: 12.10.2013

By JAMES GORMAN Sometimes the scientists who study animal behavior solve puzzles and other times they uncover new ones. The war between mockingbirds and cowbirds is a case in point. Cowbirds are brood parasites, meaning they lay their eggs in the nests of other bird species, thus unloading the messy and demanding business of chick-rearing. They also peck holes in the eggs of the host birds, destroying as many as they can. Mockingbirds are a favorite target of this plan, and it seems to make perfect sense for them to viciously attack cowbirds when they catch them in the nest. But when Ros Gloag, then a doctoral student at Oxford, and her colleagues in Argentina looked closely at the war between chalk-browed mockingbirds and shiny cowbirds, they found something unexpected, as they reported in the November issue of Animal Behaviour. They stationed small video cameras near the nests of 40 pairs of chalk-browed mockingbirds. Over two breeding seasons they recorded more than 200 attacks on intruding cowbirds. They were surprised to find that these attacks, which their videos show to be quite vicious, did not stop the cowbirds from laying eggs. The cowbirds would hunker down and let the much large mockingbirds deliver hammer blows to the head, but in matter of seconds they would lay an egg and flee. How could such a failed strategy persist in evolution? © 2013 The New York Times Company

Keyword: Aggression; Sexual Behavior
Link ID: 19014 - Posted: 12.10.2013

Brian Owens Fruitflies know exactly how much alcohol will be good for their young. Larvae living on a food source with the right concentration of ethanol will grow into heavy, healthy adults and will be protected against parasites — which explains why the insects are attracted to rotting fruit or the crate of empty beer bottles in your kitchen but not to the vodka or gin. Now researchers have uncovered the neural mechanism that allows the fruitfly Drosophila melanogaster to choose the best place to lay its eggs. The work is published today in Proceedings of the National Academy of Sciences1. A team led by Ulrike Heberlein, a molecular biologist at the Howard Hughes Medical Institute’s Janelia Farm Research Campus in Ashburn, Virginia, found that clusters of neurons, working in opposition to each other, help the flies to choose the place with the most beneficial concentration of ethanol in which to lay their eggs. The neurons all release the neurotransmitter dopamine, a key player in the brain's reward circuitry. Neurons of the PAM and PPM3 clusters encourage the flies to seek out ethanol, whereas PPL1 neurons apply the brakes, preventing the flies from laying their eggs on food containing high levels of ethanol that could harm the larvae. “They can discriminate among ethanol concentrations that are very similar — 3% versus 5% — so the system evolved to have great sensitivity,” says Heberlein. Their favourite booze strength is 5%, similar to that of a typical beer. Heberlein's team also traced the neurons involved in ethanol preference to specific brain regions. Both the pro-ethanol PAM and anti-ethanol PPL1 neurons were active in the mushroom body, whereas the pro-ethanol PPM3 ones were active in the ellipsoid body. Both of these brain structures are involved in decision-making and memory, and mushroom body neurons also play a part in ethanol-reward memory. © 2013 Nature Publishing Group,

Keyword: Chemical Senses (Smell & Taste)
Link ID: 19013 - Posted: 12.10.2013

Researchers striving to understand the origins of dementia are building the case against a possible culprit: lead exposure early in life. A study spanning 23 years has now revealed that monkeys who drank a lead-rich formula as infants later developed tangles of a key brain protein, called tau, linked to Alzheimer's disease. Though neuroscientists say more work is needed to confirm the connection, the research suggests that people exposed to lead as children—as many in America used to be before it was eliminated from paint, car emissions, water, and soil—could have an increased risk of the common, late-onset form of Alzheimer’s disease. Even in small doses, lead can wreak havoc on the heart, intestines, kidneys, and nervous system. Children are especially prone to its pernicious effects, as it curbs brain development. Many studies have linked early lead exposure with lower IQs. Researchers estimate that one in 38 children in the United States still have harmful levels of the metal in their systems, but evidence linking this exposure to dementia later in life has been tenuous. A team led by toxicologist Nasser Zawia, however, has vigorously pursued the lead hypothesis. In one early study, from 2008, the group showed that plaques, insoluble globs of a protein called β-amyloid, marred the brains of five macaques that had consumed a lead-enriched formula as infants. The researchers had compared the preserved brain tissues from those macaques, sacrificed in 2003 at age 23 in a National Institutes of Health lab, with four similarly aged monkeys who had had lead-free formula. The amyloid plaques closely resembled those in the brains of adults with Alzheimer's disease that are thought to contribute to the dementia. © 2013 American Association for the Advancement of Science.

Keyword: Alzheimers; Neurotoxins
Link ID: 19012 - Posted: 12.10.2013