By Tina Hesman Saey HONOLULU — Humans may owe the gift of gab to a newly discovered gene that helps keeps vocal pipes limber. Researchers discovered the gene, dubbed tospeak, in an Australian family with a speaking disorder. Many of the women in the family have weak, husky voices, while several of their male relatives cannot speak above a whisper, reported Raymond Clarke of the University of New South Wales’ St. George Hospital in Kogarah, Australia, October 21 at the annual meeting of the American Society of Human Genetics. Clarke and his colleagues traced the source of the family’s disorder to a region of chromosome 8. Part of the chromosome had been rearranged, causing a break in the tospeak gene. Tospeak probably doesn’t code for a protein, Clarke says. The gene is sprinkled with stop signals and its RNA product doesn’t resemble other RNAs that have specific functions in the cell. But production of the tospeak RNA seems to be important for proper development of the larynx. Members of the family who have the speaking problem have short, thick vocal cords that don’t vibrate properly. Some of the family members also have fused bones in the wrists and feet, known as the carpals and tarsals, and fused vertebrae in their spines. All of the defects may be linked to a breakdown in relations between tospeak and a neighboring gene, known as GDF6, the researchers report. © Society for Science & the Public 2000 - 2009

Keyword: Language; Genes & Behavior
Link ID: 13393 - Posted: 06.24.2010

An international team led by a National Institutes of Health researcher has found that carriers of a rare, genetic condition called Gaucher disease face a risk of developing Parkinson’s disease more than five times greater than the general public. The findings were published today in the New England Journal of Medicine. In previous studies, several genes have been linked to Parkinson's disease. However, researchers say their work conclusively shows that mutations in the gene responsible for Gaucher disease are among the most significant risk factors found to date for Parkinson's disease. The discovery was made by investigators from the National Human Genome Research Institute (NHGRI) and the National Institute on Aging (NIA), both parts of the National Institutes of Health, in collaboration with scientists from 16 research centers across four continents. Parkinson's disease, a neurological condition that typically causes tremors and stiffness in movement, affects about 1 to 2 percent of people over the age of 60. The chance of developing Parkinson's disease increases with age and involves a combination of environmental risk factors and genetic susceptibility. Gaucher disease occurs when an individual inherits two defective copies of the GBA gene, which codes for an enzyme called glucocerebrosidase. This enzyme breaks down a fatty substance called glucocerebroside, which, when not properly disposed of, can harm the spleen, liver, lungs, bone marrow and, in some cases, the brain. The enzyme functions in a part of the cell called the lysosome, where cellular components are broken down, or metabolized, for recycling.

Keyword: Parkinsons; Genes & Behavior
Link ID: 13392 - Posted: 06.24.2010

Susan Milius, Science News -- Like a songbird calling another out, one male humpback whale may make another change his tune. Studying humpbacks with methods adapted from bird research has uncovered the first known instances of what look like whales responding musically to each other's songs, says Danielle Cholewiak, a researcher for the Stellwagen Bank National Marine Sanctuary based in Scituate, Mass. Cholewiak and colleagues detected melodic adjustments when a solo singer encountered another singer nearby and when researchers played their song remixes for whales. Male whales may be using music to tell another male, "Hey, I'm talking to you," Cholewiak reported Oct. 14 at the Society of Marine Mammology's biennial conference. Cholewiak "showed short-term acoustic interactions between males -- that was the new thing," said Adam S. Frankel of Marine Acoustics Inc., an independent consulting firm in Arlington, Va. Among humpback whales, only males boom out long strings of repeating phrases of hums and whups and chirps. The sounds can make a boat vibrate, said Salvatore Cerchio of the Wildlife Conservation Society in New York City, who worked with Cholewiak on the new study. Scientists use the word song to describe this patterned male vocalization, just as they do for elaborate bird serenades. © 2009 Discovery Communications, LLC.

Keyword: Language; Sexual Behavior
Link ID: 13391 - Posted: 06.24.2010

(HealthDay News) -- Exposure to too much light at night may cause depression, suggests a new study. Ohio State University researchers found that mice kept in a lighted room 24 hours a day had more depressive symptoms than mice that had a normal day-night cycle. The study also found that mice that lived in a constantly lit room, but could take refuge in a dark tube when they desired, had fewer depressive symptoms than mice that couldn't get away from the 24-hour light. "The ability to escape light seemed to quell the depressive effects," lead author Laura Fonken, a graduate student in psychology, said in a news release from Ohio State University. The findings indicate the need to learn more about how artificial light affects humans, said study co-author Randy Nelson, a professor of neuroscience and psychology. "Constant light with no chance of escape increased depressive symptoms," Nelson said in the news release. "The increasing rate of depressive disorders in humans corresponds with the increasing use of light at night in modern society. Many people are now exposed to unnatural light cycles, and that may have real consequences for our health," he added. The study, presented at the annual meeting of the Society for Neuroscience held Oct. 17 to 21 in Chicago, is scheduled to be published in the Dec. 28 issue of the journal Behavioural Brain Research. © 2009 ScoutNews, LLC.

Keyword: Biological Rhythms; Depression
Link ID: 13390 - Posted: 06.24.2010

(HealthDay News) -- While adult male monkeys exposed to cocaine in the womb have poor impulse control, the same is not true for female monkeys, new research has found. The male monkeys continued to have poor impulse control 15 years after birth. Impulsivity is a risk factor for drug abuse, said the researchers, who added that their findings could help improve understanding of human drug abuse. "This is the first time that so many different measures of impulsivity, which is considered a risk factor for drug abuse, have been looked at in the same group of animals," lead investigator Lindsey Hamilton, of Wake Forest University School of Medicine, said in a university news release. "We're looking for ways to predict which individuals are going to take drugs during their lives. It was very surprising to see that, even more than a decade after the prenatal cocaine exposure, the monkeys ended up being more impulsive and possibly more susceptible to drug use. It was particularly interesting, however, that this effect was only seen in the males. Something is either protecting the females from the effects of the cocaine exposure in the womb or making the males more susceptible to the lasting effects," Hamilton explained. Hamilton and colleagues conducted four impulse control tests with male and female monkeys exposed to cocaine in the womb and monkeys with no cocaine exposure. © 2009 U.S.News & World Report LP

Keyword: Drug Abuse; ADHD
Link ID: 13389 - Posted: 06.24.2010

By Frederik Joelving When you've spent the weekend splurging on greasy fast foods, your bathroom scale isn't alone in reeling from the impact. Your brain does, too. New research shows just how saturated fat tricks us into eating more and elucidates the evolutionary basis for the propensity for poundage in developed nations. Our brain physiology, it seems, is glaringly out-of-date in the modern world. Researchers have long known that the hormones leptin and insulin play key roles in appetite and food intake. In healthy people leptin, which is secreted by fat tissue, acts as a molecular measuring tape for our waistlines, quashing feelings of hunger. Insulin spikes when the pancreas gets a whiff of the blood sugar increase after a meal; once the brain detects the spike, it knows to tamp down the desire for food. Certain foods and metabolic disorders, however, can disrupt our ability to respond appropriately to these hormonal signals. In a study published in the September issue of The Journal of Clinical Investigation, scientists report unraveling a central biochemical mechanism behind fat's effect on the mammalian brain . They found that after only three days on a diet high in saturated fat—a common ingredient in beef and cheese—the brains of rats and mice became resistant to leptin and insulin. In contrast, unsaturated fats, such as those found in olive oil, did not trigger resistance. As a result of the hormone resistance, a meal high in saturated fat can crank up our appetite well after dessert. "Taking time off from a healthy diet to eat most fast foods may have consequences that last for some days, even after one resumes the healthy diet," says University of Cincinnati behavioral neuroscientist Stephen Benoit, who led the study. He believes the findings are likely to apply to humans, too. © 1996-2009 Scientific American Inc.

Keyword: Obesity
Link ID: 13388 - Posted: 06.24.2010

By Vilayanur S. Ramachandran and Diane Rogers-Ramachandran Humans enjoy stereoscopic vision. As we mentioned in our essay last issue, because our eyes are separated horizontally images we see in the two eyes are slightly different and the difference is proportional to the relative depth. The visual areas in the brain measure these differences, and we experience the result as stereo—what we all have enjoyed as children playing with View-Master toys. Visual-image processing from the eye to the brain happens in stages. Rudimentary features such as the orientation of edges, direction of motion, color, and so on are extracted early on in areas called V1 and V2 before reaching the next stages in the visual-processing hierarchy for a progressively more refined analysis. This stage-by-stage description is a caricature; many pathways go “back” from stage to stage—allowing the brain to play a kind of 20-questions game to arrive at a solution after successive iterations. Returning to the concept of stereo, we can ask: At what stage is the comparison of the two eyes’ images made? If you are looking at a scene with hundreds of features, how do you know which feature in one eye matches with which feature in the other eye? How do you avoid false matches? Until the correct matching is achieved, you cannot measure differences. In stereopsis, this conundrum is called the correspondence problem. © 1996-2009 Scientific American Inc.

Keyword: Vision
Link ID: 13387 - Posted: 06.24.2010

Jennifer Viegas, Discovery News -- Females of the Australian redback spider, one of the world's most poisonous spiders and a close relative to the black widow, demand 100 minutes of courting or else they usually cannibalize their male suitors, research finds. Proving that bigger isn't always better in the mating game, the tiniest of males sometimes approach female redbacks after offering the critical 100 minutes of wooing and successfully mate without being eaten, according to the paper in the latest Proceedings of the Royal Society B. The study shows that puny males of this species can win at love without exerting much effort and begins to explain the extreme size differences between males and females among some spider species. "Based upon our data of the timing of premature lethal cannibalism, it appears as though females are not tuned to select male size, but rather the duration of courtship," co-author Jeffrey Stoltz told Discovery News. Females don't even discriminate once the 100 minutes are up, Stoltza added, so other males can even scramble in at that point and win her favor. Stoltz, a University of Toronto researcher, and colleague Maydianne Andrade analyzed Australian redback spiders bred from a population collected in Sydney. They focused on the spider's unique mating ritual. © 2009 Discovery Communications, LLC.

Keyword: Sexual Behavior; Evolution
Link ID: 13386 - Posted: 06.24.2010

by Ewen Callaway Creating chimeras with the higher brain of a songbird and the hindbrain of a non-singer may one day shed light on the evolution of birdsong, and even human speech. "The goal is to get a non-singing animal that can actually learn how to imitate sounds," says Erich Jarvis, a neuroscientist at Duke University in Durham, North Carolina. The chimera would have the hindbrain of a quail and the forebrain of the zebra finch. "I knew when I started this project that it was one of those crazy ones." Both people and songbirds learn how to communicate in infancy by listening to adults and imitating their sounds. In the embryo, neurons from learning centres in the higher brain, or forebrain, connect up with neurons in the hindbrain that control vocal muscles in the throat. These connections are absent in non-singing birds such as quails, which simply squawk. A quail's call is innate and is not learned from a parent. Jarvis's team is investigating how forebrain neurons are normally guided to the hindbrain in a songbird by doing brain transplants on bird embryos that are 2 days old – the size of a pen tip. Jarvis announced his first results at the Society for Neuroscience's annual meeting in Chicago last week. The team has removed the tissue from a quail embryo that gives rise to the forebrain and replaced it with the same tissue from a finch embryo. They found that some of the finch neurons make a beeline for the quail's hindbrain. © Copyright Reed Business Information Ltd

Keyword: Language; Animal Communication
Link ID: 13385 - Posted: 06.24.2010

By Laura Sanders CHICAGO — The Halle Berry fan club is expanding one brain cell at a time. By eavesdropping on the activity of single neurons in the human brain, scientists have figured out which brain cells go wild for superstars such as the popular actress. And the newest research shows that people can activate those cells selectively. “This study is the first demonstration of humans’ ability to control the activity of single neurons,” the researchers wrote in a summary of their study. The results, presented October 19 at the Society for Neuroscience’s annual meeting by Moran Cerf of the California Institute of Technology in Pasadena, may help researchers understand how each cell in the brain sees and responds to the world. “This type of work gives us some clues about what’s going on in the brain,” comments Christoph Weidemann of the University of Pennsylvania, who studies how the brain processes information. “It’s quite an amazing feat for the brain to make sense of its input and reliably recognize people and objects.” The new study was conducted on people with epilepsy. Doctors had implanted electrodes in these patients’ brains to track where seizures originate. The researchers used these same electrodes to eavesdrop on the activity of single brain cells in a part of the brain called the medial temporal lobe, which is important for “memory, attention, perception — the things that we care about the most,” Cerf said in his presentation. © Society for Science & the Public 2000 - 2009

Keyword: Vision; Attention
Link ID: 13384 - Posted: 06.24.2010

By Michael Torrice Red-eye flights, all-night study sessions, and extra-inning playoff games all deprive us of sleep and can leave us forgetful the next day. Now scientists have discovered that lost sleep disrupts a specific molecule in the brain's memory circuitry, possibly leading to treatments for tired brains. Neuroscientists studying rodents and humans have found that sleep deprivation interrupts the storage of episodic memories: information about who, what, when, and where. To lay down these memories, neurons in our brains form new connections with other neurons or strengthen old ones. This rewiring process, which occurs over a period of hours, requires a rat's nest of intertwined molecular pathways within neurons that turn genes on and off and fine-tune how proteins behave. Neuroscientist Ted Abel of the University of Pennsylvania and colleagues wanted to untangle these molecular circuits and pinpoint which one sleep deprivation disrupts. The researchers started by studying electrical signals in slices of the hippocampus--the brain's memory center--from sleep-deprived mice. They tested for long-term potentiation (LTP), a strengthening of connections between neurons that neuroscientists think underlies memory. When the scientists tried to trigger LTP in these brain slices with electrical stimulation or chemicals, they found that methods that fired up cellular pathways involving the molecule cyclic adenosine monophosphate (cAMP) didn't work. Brain cells from sleep-deprived mice also held about 50% less cAMP than did cells from well-rested mice. In the brain, cAMP acts as a molecular messenger, passing signals between proteins that regulate activity of genes responsible for memory formation. © 2009 American Association for the Advancement of Science.

Keyword: Sleep; Learning & Memory
Link ID: 13383 - Posted: 06.24.2010

by Clare Wilson A US jury's decision that an antidepressant caused heart defects in an unborn baby is highlighting the painful dilemma facing pregnant women with depression. The most common antidepressants have been linked to birth defects and miscarriage, yet some doctors fear that letting depressive symptoms go untreated may have long-term consequences for the mother and her unborn baby. On 15 October, a jury in Philadelphia, Pennsylvania, ordered manufacturer GlaxoSmithKline to pay $2.5 million to the family of 3-year-old Lyam Kilker, who was born with serious heart defects. While pregnant, Kilker's mother took the antidepressant paroxetine (Seroxat or Paxil), which belongs to the most commonly prescribed class of antidepressants, known as selective serotonin reuptake inhibitors (SSRIs). Doctors try to avoid giving drugs to pregnant women, but Kilker's mother is not unusual. Antidepressants are increasingly being prescribed during pregnancy, particularly in the US, where 13 per cent of pregnant women took them in 2003. The trend reflects an increase in their use in the general population: often a woman is already taking antidepressants when she becomes pregnant. Awareness is also growing of the potential risks of not treating depression during pregnancy, on the child as well as the mother. Last year, a large study showed that children whose mothers had been depressed while pregnant took longer to start smiling, talking and developing motor skills (BJOG, vol 115, p 1043). © Copyright Reed Business Information Ltd

Keyword: Depression; Development of the Brain
Link ID: 13382 - Posted: 06.24.2010

by Douglas Fox THE MAN dangles on a cable hanging from an eight-storey-high tower. Suspended in a harness with his back to the ground, he sees only the face of the man above, who controls the winch that is lifting him to the top of the tower like a bundle of cargo. And then it happens. The cable suddenly unclips and he plummets towards the concrete below. Panic sets in, but he's been given an assignment and so, fighting his fear of death, he stares at the instrument strapped to his wrist, before falling into the sweet embrace of a safety net. A team of scientists will spend weeks studying the results. The experiment was extreme, certainly, but the neuroscientist behind the study, David Eagleman at Baylor College of Medicine in Houston, Texas, is no Dr Strangelove. When we look back at scary situations, they often seem to have occurred in slow motion. Eagleman wanted to know whether the brain's clock actually accelerates - making external events appear abnormally slow in comparison with the brain's workings - or whether the slo-mo is just an artefact of our memory. It's just one of many mysteries concerning how we experience time that we are only now beginning to crack. "Time," says Eagleman, "is much weirder than we think it is." By understanding the mechanisms of our brain's clock, Eagleman and others hope to learn ways of temporarily resetting its tick. This might improve our mental speed and reaction times. What's more, since time is crucial to our perception of causality, a faulty internal clock might also explain the delusions suffered by people with schizophrenia. © Copyright Reed Business Information Ltd

Keyword: Attention; Learning & Memory
Link ID: 13381 - Posted: 06.24.2010

By Gisela Telis If your ears are still ringing from that last Metallica concert, scientists can't help you--but they may have figured out what's going on in your head. A type of small neuron in the inner ear, it seems, may help process painfully loud sounds. The discovery solves a 70-year-old mystery about what these neurons do--and may deepen understanding of hearing loss and impairment. Humans and other mammals owe their hearing to a forest of hairlike cells in the inner ear. As sound waves move into the ear, the hair cells sway along, and their motion releases electrical and chemical signals that the brain interprets as sound. Two kinds of neurons transmit those signals. Type I is the standard: It makes up 90% to 95% of all neurons in the inner ear and tells the brain about a sound's frequency, volume, and timing--all the ingredients of hearing as we know it. The remaining 5% of the neurons are type II, which were first described in 1937 and are smaller and harder to study. In fact, just a single study has reported success in connecting a type II neuron to an electrode, which is the main method for studying hearing cells. Hearing researcher Paul Fuchs and his colleagues at the Johns Hopkins University School of Medicine in Baltimore, Maryland, came up with a different way to isolate the elusive neurons. Instead of trying to find them within an intact ear, they dissected the inner ears of rats. During a window of only a few hours before the tissue samples died, the researchers tracked down the type II neurons, hooked them up to electrodes, and recorded what they did in the presence of a chemical that provokes the same reaction as sound in hearing cells. © 2009 American Association for the Advancement of Science

Keyword: Hearing
Link ID: 13380 - Posted: 06.24.2010

By Laura Sanders CHICAGO — Junk food elicits addictive behavior in rats similar to the behaviors of rats addicted to heroin, a new study finds. Pleasure centers in the brains of rats addicted to high-fat, high-calorie diets became less responsive as the binging wore on, making the rats consume more and more food. The results, presented October 20 at the Society for Neuroscience’s annual meeting, may help explain the changes in the brain that lead people to overeat. “This is the most complete evidence to date that suggests obesity and drug addiction have common neurobiological underpinnings,” says study coauthor Paul Johnson of the Scripps Research Institute in Jupiter, Fla. To see how junk food affects the brain’s natural reward system — the network of nerve cells that release feel-good chemicals — Johnson started at the grocery store. He loaded up on typical Western fare, including Ho Hos, sausage, pound cake, bacon and cheesecake. Johnson fed rats either a standard diet of high-nutrient, low-calorie chow, or unlimited amounts of the palatable junk food. Rats that ate the junk food soon developed compulsive eating habits and became obese. “They’re taking in twice the amount of calories as the control rats,” says Johnson’s coauthor Paul Kenny, also of Scripps. Johnson and Kenny wanted to know if this overeating affected the pleasure centers of the rats’ brains, the regions responsible for drug addiction. The researchers used electrical stimulations to activate these reward centers and induce pleasure. Rats could control the amount of feel-good stimulation by running on a wheel — the more they ran, the more stimulation they got. The rats fed junk food ran more, indicating that they needed more brain stimulation to feel good. © Society for Science & the Public 2000 - 2009

Keyword: Obesity; Drug Abuse
Link ID: 13379 - Posted: 06.24.2010

By JANE E. BRODY If you have ever slept on an arm and awakened with a “dead” hand, or sat too long with your legs crossed and had your foot fall asleep, you have some inkling of what many people with peripheral neuropathy experience day in and day out, often with no relief in sight. And numbness and tingling are hardly the worst symptoms of this highly variable condition, which involves damage to one or more of the myriad nerves outside the brain and spinal cord. Effects may include disabling pain, stinging, swelling, burning, itching, muscle weakness, twitching, loss of sensation, hypersensitivity to touch, lack of coordination, difficulty breathing, digestive disorders, dizziness, impotence, incontinence, and even paralysis and death. I realize now that I had a mild, reversible bout of peripheral neuropathy several decades ago when a misplaced shot of morphine damaged a sensory nerve in my thigh. It took three years for the nerve to recover, and for much of that time I could not tolerate anything brushing against my leg. One of my sons, too, was afflicted when a nerve behind his knee was injured during a basketball game. He had no feeling or mobility in his foot for nine months, but after several years the nerve healed and he regained full use of his foot. And a good friend was nearly paralyzed, also temporarily, following a flu shot, by a far more serious form of peripheral neuropathy — an autoimmune affliction called Guillain-Barré syndrome, in which one’s own antibodies attack the myelin sheath that protects nerves throughout the body. Copyright 2009 The New York Times Company

Keyword: Neuroimmunology; Movement Disorders
Link ID: 13378 - Posted: 06.24.2010

By NICHOLAS BAKALAR The first time the words “amyotrophic lateral sclerosis” appeared in The New York Times was in 1876, in an advertisement for a medical text; the disease had first been described by a French doctor in 1869. The Times did not mention it again until Arthur Daley, a Pulitzer Prize-winning sports columnist, reported on Lou Gehrig’s diagnosis in June 1939. The end of Gehrig’s record streak of 2,130 straight games came on May 2, but the explanation in The Times the next day was that Gehrig had “recognized his competitive decline” and that his withdrawal from the lineup “does not necessarily mean the end of his playing career.” A column by John Kieran the same day expressed certainty that “with a little rest he should begin to feel his oats again,” that all he really needed was “a breathing spell.” On June 2, a 120-word article on the sports page reported that Gehrig would be examined at the Mayo Clinic. Yet on June 12, with no public report about the results of the examination, Gehrig was back in the lineup for three innings in an exhibition game against the Kansas City Blues, a Yankee farm club. Finally on June 22, Daley, quoting Dr. H. C. Habein of the Mayo Clinic, wrote that the Iron Horse had amyotrophic lateral sclerosis, the first mention of the illness in the newspaper in 63 years. An Associated Press release printed below the article quoted the editor of the Journal of the American Medical Association saying that A.L.S. was “a well-established scientific diagnosis of a condition in which there is a hardening of the tissues in the spinal column and a wasting of the muscles dependent upon it,” but although the doctor must have known the facts, he said nothing of a fatal prognosis. Copyright 2009 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 13377 - Posted: 06.24.2010

By TARA PARKER-POPE Dementia is often viewed as a disease of the mind, an illness that erases treasured memories but leaves the body intact. But dementia is a physical illness, too — a progressive, terminal disease that shuts down the body as it attacks the brain. Although the early stages can last for years, the life expectancy of a patient with advanced dementia is similar to that of a patient with advanced cancer. The lack of understanding about the physical toll of dementia means that many patients near the end of life are subjected to aggressive treatments that would never be considered with another terminal illness. People with advanced dementia are often given dialysis and put on ventilators; they may even get preventive care that cannot possibly help them, like colonoscopies and drugs for osteoporosis or high cholesterol. “You can go to an intensive-care unit in most places,” said Dr. Greg A. Sachs, chief of general internal medicine and geriatrics at Indiana University School of Medicine, “and you’ll find people with dementia getting very aggressive treatment.” The continued focus on treatment to prolong life often means that pain relief is inadequate, and symptoms like confusion and anxiety are worsened. A new study suggests that family members would be far less likely to subject their loved ones to such treatment if they had a better understanding of dementia as progressive, debilitating illness that ultimately shuts down the body after years of mental deterioration. Copyright 2009 The New York Times Company

Keyword: Alzheimers
Link ID: 13376 - Posted: 06.24.2010

By SEAN B. CARROLL I have long suspected that fish are smarter than we give them credit for. As a child, I had an aquarium with several pet goldfish. They certainly knew it was feeding time when my hand appeared over their tank, and they excitedly awaited their delicious fish flakes. They also exhibited a darker, disturbing behavior. Evidently, a safe life with abundant food was not fulfilling. From time to time, either sheer ennui or the long gray Toledo winter got to one of the fish and it ended its torment with a leap to my bedroom floor. Maybe my anthropomorphizing is a bit over the top. But, really, just how smart are fish? Can they learn? A 10-gallon tank with a plastic sunken pirate ship is certainly not the most stimulating habitat. But in the colorful, diverse and dangerous world of coral reefs, fish must be able to recognize not only food, but also to discriminate friends from foes, and mates from rivals, and to take the best action. In such a complex and dynamic environment, it would pay to be flexible and able to learn. A series of studies has recently revealed that reef fish are surprisingly adaptable. Freshly caught wild fish quickly learn new tasks and can learn to discriminate among colors, patterns and shapes, including those they have never encountered. These studies suggest that learning and interpreting new stimuli play important roles in the lives of reef fish. Copyright 2009 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 13375 - Posted: 06.24.2010

by Irving Kirsch ARE we too quick to prescribe psychotropic medication for emotional and behavioural problems? Take Alzheimer's disease. In an attempt to reduce their aggressive behaviour, up to 60 per cent of people with Alzheimer's in Europe and North America are prescribed antipsychotic medications such as Risperdal (risperidone) and Zyprexa (olanzapine). The estimated cost of these drugs is £80 million a year in the UK alone. People given antipsychotics are sedated and become less aggressive or agitated, but compared with placebo the benefits seem modest at best. In 2006, a 42-centre trial in the US found no significant differences between antipsychotic drugs and placebo after 12 weeks. Other trials showed some advantages of drugs over placebo, but these were "modest" (Cochrane Database of Systematic Reviews, DOI: 10.1002/14651858.CD003012.pub2). The risks, however, are large. According to the UK Medicines and Healthcare Products Regulatory Agency, the medication produces a threefold increase in the risk of stroke (www.bit.ly/NN8p0). The drugs also double the risk of dying over a three-year period, according to a study funded by the UK's Alzheimer's Research Trust (The Lancet, Neurology, vol 8, p 151). Last week, 10 dementia groups, including the trust, demanded the UK government publish a long-delayed review of the use of antipsychotic drugs in dementia. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers; Schizophrenia
Link ID: 13374 - Posted: 06.24.2010