By Janet Raloff A new study may explain how rising carbon dioxide concentrations — and the ocean acidification they induce — can cause topsy-turvy changes in the behavior of fish. Like a flipped switch, the normal response of nerve cells can reverse as acidifying seawater perturbs how a fish regulates acids and bases in its body, including the brain. “This could be a big deal,” says neurobiologist Andrew Dittman of the National Oceanic and Atmospheric Administration’s Northwest Fisheries Science Center in Seattle. Dittman, who was not affiliated with the study, says the new findings could go a long way toward explaining curious sensory changes observed in fish exposed to acidifying waters. The scary scent of predators, for example, can suddenly become alluring. For the new study, published online January 15 in Nature Climate Change, Göran Nilsson of the University of Oslo and his colleagues homed in on brain chemistry. The idea emerged after Philip Munday of James Cook University in Townsville, Australia, told Nilsson of behavioral quirks his laboratory fish were exhibiting in a high–carbon dioxide environment — conditions exemplifying ocean waters a half-century or more from now. Nilsson, a neurophysiologist, speculated that a connection between nerves and chemistry might be involved. “It was very much an ‘Aha’ moment,” Munday says. © Society for Science & the Public 2000 - 2012

Keyword: Drug Abuse
Link ID: 16257 - Posted: 01.16.2012

By DIANE ACKERMAN WHAT’S the quickest way to a man’s heart? No, not through the chest wall with a knife. According to Mom wisdom, it’s a cozy meal, in a penumbra of pleasure that mingles the fragrant food with the cook. If men are anything like common fruit flies — and who’s to say they’re not at times; heaven knows women are — Mom was right. Anyway, that’s the romantic ploy of female fruit flies, for whom a dinner date is the ultimate rush. And rush it literally is, since they live only about 25 days and can’t afford to be shy. Still, the males need to be in the right mood, and the females are surprisingly picky and manipulative, given their short careers. Did I mention that some fruit flies have come-hither eyes? I don’t mean the dozens of mosaic facets, so evocative of hippie sunglasses, but the zingy psychedelic eye colors lab folk like to breed into them, the better to study mutant genes. As a Cornell grad student, I often stopped by the fetid biology lab to admire the eggplant-blackness of the abdomens, the spiky hairs, the gaudy prisms of the eyes — some apricot, some teal, some purple, some the brick-red of Ming vases. A favorite of biologists, fruit flies have it all — they’re prowling for mates within 12 hours of birth, they’re easy to raise and they can lay 100 eggs a day. Plus, they share most of our genes, including about 70 percent of those we’ve linked to such diseases as Parkinson’s and Alzheimer’s. © 2012 The New York Times Company

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 16256 - Posted: 01.16.2012

By NICHOLAS BAKALAR A new study has found that among immigrants, younger age at the time of migration predicts a higher incidence of psychotic disorders. The study, published in December in The American Journal of Psychiatry, was conducted from 1997 to 2005 in The Hague, where there are detailed records on almost everyone ages 15 to 54 who has made contact with the health care system for a possible psychotic disorder. The researchers found 273 immigrants, 119 second-generation citizens and 226 Dutch citizens who fit the criteria. In four ethnic groups — people from Suriname, the Netherlands Antilles, Turkey and Morocco — the risk of psychosis was most elevated among those who immigrated before age 4. There was no association of psychosis with age among immigrants from Western countries. The researchers, led by Dr. Wim Veling of the Parnassia Psychiatric Institute in The Hague, investigated various possible explanations — that social factors may be involved, that people may migrate because they are prone to psychosis, that a decision to migrate is influenced by the early appearance of psychosis, among many others. But the correlation between younger age of migration and the development of psychosis persisted. “We don’t know the reason,” said Dr. Ezra Susser, the senior author and a professor of epidemiology at Columbia University, “but it might be related to early social context, which we know has an important influence on later health and mental health.” © 2012 The New York Times Company

Keyword: Schizophrenia; Development of the Brain
Link ID: 16255 - Posted: 01.14.2012

Using MR spectroscopy, a team of researchers has developed a way to measure whether brain tumors have a mutation in a gene called IDH. The tissue being analyzed is inside the red boxes. The tumor on the left has the mutation, while the tumor on the right does not. A team of researchers from MIT, Harvard University, Massachusetts General Hospital, and Agios Pharmaceuticals are using MR spectroscopy to measure whether brain tumors have a mutation in the IDH gene. Scientists are now targeting isocitrate dehydrogenase (IDH) in a hope to slow tumor growth and find new ways to treat gliomas. Gliomas, the most common types of brain tumor, are also among the deadliest cancers: Their mortality rate is nearly 100 percent, in part because there are very few treatments available. A team of researchers from MIT, Harvard University, Massachusetts General Hospital (MGH) and Agios Pharmaceuticals has now developed a way to identify a particular subset of brain tumors, which may help doctors choose treatments and create new drugs that target the disease’s underlying genetic mutation. Scientists have known for several years that many brain tumors involve a mutation in the gene for an enzyme called isocitrate dehydrogenase (IDH). This enzyme is involved in cell metabolism — the process of breaking down sugar molecules to extract energy from them. IDH mutations are found in up to 86 percent of low-grade gliomas, which have a better prognosis than high-grade gliomas, also called glioblastomas. Patients with low-grade gliomas can survive for years, though the tumors almost always prove fatal. SciTechDaily Copyright © 1998 - 2012

Keyword: Brain imaging; Genes & Behavior
Link ID: 16254 - Posted: 01.14.2012

By msnbc.com staff and news services A 9-year-old Detroit-area girl whose battle with Huntington's disease drew attention after she was taunted online in 2010 by her grandmother's former neighbor has died. Michigan Memorial Funeral Home in Flat Rock, which is handling arrangements, says Kathleen Edward died Wednesday. One Facebook posting was of her doctored photo placed above a set of crossbones and another included a photo of her mother in the arms of the grim reaper. The conflict with the neighbor reportedly stemmed from a misunderstanding with the girl's family. After the Facebook taunts appeared, people worldwide voiced their support of the young girl on Facebook and raised money to send her on a shopping spree in 2010, according to the Detroit Free Press. Huntington's disease is a genetic, incurable brain disorder which, in children, can cause tremors, slow, rigid movements and seizures. Kathleen's mother also died from the degenerative disease in 2009, the newspaper reported. If one parent has Huntington's disease, a child has a 50 percent chance of getting it. Most people with Huntington's disease develop symptoms in their 40s or later, but when younger people get it, the disease tends to progress more quickly, according to the Mayo Clinic. "She suffered with this disease for a while, and she never complained," her grandmother, Rebecca Rose, told the Detroit Free Press. "She was always happy, always smiling." © 2012 msnbc.com

Keyword: Huntingtons
Link ID: 16253 - Posted: 01.14.2012

Caitlin Stier, video intern Don't believe your eyes as you watch this video: although the rectangles moving in sync suddenly seem to shuffle, their motion hasn't actually changed. Keep watching when a backdrop of morphing stripes appears and a caterpillar-like motion can be seen. Created by graduate student Sebastiaan Mathôt from VU University of Amsterdam, the brain trick occurs when the background is striped rather than solid, an illusion originally developed by researcher Stuart Anstis from University of California, San Diego. The effect is caused by the influence of contrast on motion. When there is a big difference in contrast between a moving object and its background, it appears to move faster than when brightness levels are similar. In this case, the top rectangle is brighter than the maroon one below it. So when their front edges are superimposed on a dark stripe, the top block seems to move faster than the bottom one. Similarly, the speed effect is reversed when they cover the lighter stripe. In the second version of the illusion with morphing stripes, the front and back edges of the blocks sit on different colours. Since the motion of each edge is perceived independently, the front and back of the blocks appear to move at different speeds, creating a caterpillar-like sashay. According to Anstis, the contrast effect is also experienced by drivers. On a foggy day, the difference in brightness between an object and its surroundings is generally less than on a sunny day. This can cause drivers to underestimate how fast they're travelling and speed up, sometimes with disastrous consequences. © Copyright Reed Business Information Ltd.

Keyword: Vision
Link ID: 16252 - Posted: 01.14.2012

By Susana Martinez-Conde and Stephen L. Macknik Our brains are exquisitely tuned to perceive, recognize and remember faces. We can easily find a friend’s face among dozens or hundreds of unfamiliar faces in a busy street. We look at each other’s facial expressions for signs of appreciation and disapproval, love and contempt. And even after we have corresponded or spoken on the phone with somebody for a long time, we are often relieved when we meet him or her in person and are able to put “a face to the name.” The neurons responsible for our refined “face sense” lie in a brain region called the fusiform gyrus. Trauma or lesions to this brain area result in a rare neurological condition called prosopagnosia, or face blindness. Prosopagnostics fail to identify celebrities, close relatives and even themselves in the mirror. But even those of us with normal face-recognition skills are subject to many illusions and biases in face perception. This illusion, created by psychologist Richard Russell, won third prize in the 2009 Best Illusion of the Year Contest. The side-by-side faces are perceived as female and male. Yet both are versions of the same androgynous face (see http://illusioncontest.neuralcorrelate.com/2009/the-illusion-of-sex). The two images are identical, except that the contrast between the eyes and mouth and the rest of the face is higher for the face on the left than for the face on the right. This illusion shows that contrast is an important cue for determining the sex of a face, with low-contrast faces appearing male and high-contrast faces appearing female. It may also explain why females in many cultures darken their eyes and mouths with cosmetics: a made-up face looks more feminine than a fresh face. © 2012 Scientific American,

Keyword: Vision
Link ID: 16251 - Posted: 01.14.2012

By Laura Beil When Lewis Carroll sent Alice down the rabbit hole, she encountered a strange and twisted land with distortions of size and time. Some headache experts see something else — the possible ghosts of the author’s migraines, which can leave victims temporarily blinded, nauseated, hallucinatory, numb, unable to concentrate or seeking shelter from painful stings of light and sound. People with migraines travel between two worlds: one in which they are having a migraine and one in which they are not. “I’m very brave generally,” Tweedledum tells Alice, “only today I happen to have a headache.” But even after the headache is gone, migraine sufferers live with the dread of its return. For more than a century, researchers have been trying to step through the looking glass to find clues to the mystery of migraines, with little success. Treatments that can prevent or end migraine attacks exist only because drugs for something else were found, often by accident, to quiet the migraine’s neurological storm. “All of the major things we use were not designed for migraine at all,” says Peter Goadsby, a neurologist at the University of California, San Francisco. “It’s not good enough that one of the commonest of medical problems has treatment developed by serendipity.” A major barrier to relief, it turns out, has been that migraines, which affect 36 million people in the United States, have no known cause. But researchers now think that they are, at least, looking for the culprits in the right places. © Society for Science & the Public 2000 - 2012

Keyword: Pain & Touch
Link ID: 16250 - Posted: 01.14.2012

Arran Frood Has a cheap and effective treatment for chronic pain been lying under clinicians' noses for decades? Researchers have found that a very high dose of an opiate drug that uses the same painkilling pathways as morphine can reset the nerve signals associated with continuous pain — at least in rats. If confirmed in humans, the procedure could reduce or eliminate the months or years that millions of patients spend on pain-managing prescription drugs. The results of the study are described today in Science1. “We have discovered a new effect of opiates when they are given, not constantly at a low dose, but at a very high dose,” says Jürgen Sandkühler, a neurophysiologist at the Center for Brain Research of the Medical University of Vienna, and a co-author of the paper. Chronic pain is a nerve condition that lingers long after the immediate, or acute, pain-causing stimulus has receded. It can follow surgery or injury, and is also associated with conditions such as rheumatoid arthritis and cancer. Sandkühler says that the original stimulus changes how the central nervous system deals with pain over time. In a model known as long-term potentiation, nerves carrying pain signals fire repeatedly, turning on a cellular pain amplifier that causes anything from exaggerated pain to outright agony on a long-term basis. © 2012 Nature Publishing Group

Keyword: Pain & Touch; Drug Abuse
Link ID: 16249 - Posted: 01.14.2012

By Helen Briggs Health editor, BBC News website Web addicts have brain changes similar to those hooked on drugs or alcohol, preliminary research suggests. Experts in China scanned the brains of 17 young web addicts and found disruption in the way their brains were wired up. They say the discovery, published in Plos One, could lead to new treatments for addictive behaviour. Internet addiction is a clinical disorder marked by out-of-control internet use. A research team led by Hao Lei of the Chinese Academy of Sciences in Wuhan carried out brain scans of 35 men and women aged between 14 and 21. Seventeen of them were classed as having internet addiction disorder (IAD) on the basis of answering yes to questions such as, "Have you repeatedly made unsuccessful efforts to control, cut back or stop Internet use?" Specialised MRI brain scans showed changes in the white matter of the brain - the part that contains nerve fibres - in those classed as being web addicts, compared with non-addicts. BBC © 2012

Keyword: Drug Abuse; Brain imaging
Link ID: 16248 - Posted: 01.14.2012

By Christoph W. Korn Ask a bride before walking down the aisle “How likely are you to get divorced?” and most will respond “Not a chance!” Tell her that the average divorce rate is close to 50 percent, and ask again. Would she change her mind? Unlikely. Even law students who have learned everything about the legal aspects of divorce, including its likelihood, state that their own chances of getting divorced are basically nil. How can we explain this? Psychologists have documented human optimism for decades. They have learned that people generally overestimate their likelihood of experiencing positive events, such as winning the lottery, and underestimate their likelihood of experiencing negative events, such as being involved in an accident or suffering from cancer. Informing people about their statistical likelihood of experiencing negative events, such as divorce, is surprisingly ineffective at altering their optimistic predictions, and highlighting previously unknown risk factors for diseases fails to engender realistic perceptions of medical vulnerability. How can people maintain their rose-colored views of the future in the face of reality? Which neural processes are involved in people’s optimistic predictions? To answer these questions we have investigated optimism by using a recent, burgeoning approach in neuroscience: Describing neural activity related to complex behavior with the simple concept of “prediction errors.” Prediction errors are the brain’s way of keeping track of how well it is doing at predicting what is going to happen in the future. © 2012 Scientific American,

Keyword: Emotions
Link ID: 16247 - Posted: 01.14.2012

By GRETCHEN REYNOLDS A newly discovered hormone produced in response to exercise may be turning people’s white fat brown, a groundbreaking new study suggests, and in the process lessening their susceptibility to obesity, diabetes and other health problems. The study, published on Wednesday in Nature and led by researchers at the Dana-Farber Cancer Institute and Harvard Medical School, provides remarkable new insights into how exercise affects the body at a cellular level. For the study, the researchers studied mouse and human muscle cells. Scientists have believed for some time that muscle cells influence biological processes elsewhere in the body, beyond the muscles themselves. In particular, they have suspected that muscle cells communicate biochemically with body fat. But how muscle cells “talk” to fat, what they tell the fat and what role exercise has in sparking or sustaining that conversation have been mysteries — until, in the new study, scientists closely examined the operations of a substance called PGC1-alpha, which is produced in abundance in muscles during and after exercise. “It seems clear that PGC1a stimulates many of the recognized health benefits of exercise,” said Bruce Spiegelman, the Stanley J. Korsmeyer professor of cell biology and medicine at the Dana-Farber Cancer Institute and Harvard Medical School, who led the study. Mice bred to produce preternaturally large amounts of PGC1a in their muscles are typically resistant to age-related obesity and diabetes, much as people who regularly exercise are. © 2012 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 16246 - Posted: 01.12.2012

by Elsa Youngsteadt The temperature of a nest can affect a hatchling lizard's size, speed, and sex. Now, the reptiles can add smarts to the list. Researchers have found that lizards incubated in warmer environments may learn faster than others. The results are preliminary, but they suggest that a hotter climate could give some lizards a cognitive edge, potentially helping them escape predators. Among the species poised to sharpen up is the three-lined skink (Bassiana duperreyi), a small, bug-eating lizard native to southeast Australia. The female skinks lay clusters of eggs under sunny rocks and logs, and their nests are heating up. University of Sydney herpetologist Richard Shine and his colleagues found that between 1997 and 2006, the lizards' nest temperatures increased by about 1.5°C—despite females' tendency to dig deeper nests and lay eggs earlier in the spring. Lizard moms might do well to accept the climbing temperatures—at least for now. Nests at the hot end of normal are more likely to produce fast-running hatchlings with an even sex ratio. (Cooler nests have more males, which are hardier in the cold—but an equal ratio could lead to more baby lizards overall.) Joshua Amiel, a Ph.D. student in Shine's lab, wondered if the warmer embryos' brains might develop differently, too. He collected wild females and nestled their eggs in individual glass dishes of sand and vermiculite (a common potting mix ingredient). Half went to a warm chamber with an average temperature of 22°C, the others to an incubator averaging 16°C, until they hatched. © 2010 American Association for the Advancement of Science.

Keyword: Learning & Memory; Evolution
Link ID: 16245 - Posted: 01.12.2012

By Jason G. Goldman Classical conditioning is one of those introductory psychology terms that gets thrown around. Many people have a general idea that it is one of the most basic forms of associative learning, and people often know that Ivan Pavlov’s 1927 experiment with dogs has something to do with it, but that is often where it ends. The most important thing to remember is that classical conditioning involves automatic or reflexive responses, and not voluntary behavior (that’s operant conditioning, and that is a different post). What does this mean? For one thing, that means that the only responses that can be elicited out of a classical conditioning paradigm are ones that rely on responses that are naturally made by the animal (or human) that is being trained. Also, it means that the response you hope to elicit must occur below the level of conscious awareness – for example, salivation, nausea, increased or decreased heartrate, pupil dilation or constriction, or even a reflexive motor response (such as recoiling from a painful stimulus). In other words, these sorts of responses are involuntary. The basic classical conditioning procedure goes like this: a neutral stimulus is paired with an unconditional stimulus (UCS). The neutral stimulus can be anything, as long as it does not provoke any sort of response in the organism. On the other hand, the unconditional stimulus is something that reliably results in a natural response. For example, if you shine a light into a human eye, the pupil will automatically constrict (you can actually see this happen if you watch your eyes in a mirror as you turn on and off a light). Pavlov called this the “unconditional response.” (UCR) © 2012 Scientific American

Keyword: Learning & Memory
Link ID: 16244 - Posted: 01.12.2012

By Ferris Jabr At the backs of your eyeballs, on the living projector screens called retinas, your corneas display upside-down 2-D images of the world around you. With some complex mental origami, your brain transforms those flat worlds into a beautiful 3-D model of everything you see. In a new study, researchers changed how monkeys perceived 3-D optical illusions by stimulating particular clusters of neurons in their brains. The researchers think the region they tweaked is where 3-D modeling happens. Peter Janssen of Katholieke Universiteit Leuven in Belgium and his colleagues trained two rhesus macaques to recognize 3-D shapes created by an arrangement of dots on a computer screen—somewhat like the illusions in the popular Magic Eye book series, except that the monkeys wore goggles called stereoscopes to make the images pop. Sometimes the 3-D image seemed to bend into the computer screen, as though the monkeys were peering into the mouth of a gramophone speaker (a concave image); other times the image bulged out toward the monkeys like the protruding end a traffic cone (a convex image). Janssen made it easier or more difficult to recognize the 3-D images by changing the density of dots on the screen, sharpening or blurring the images. First, Janssen trained the monkeys to move their eyes to the left when they saw a concave image and to the right when they saw a convex image. Then he probed their brains with microelectrodes while they completed their visual tasks, searching for groups of neurons that fired in response to either a convex or a concave image. Previously, Janssen and others had found that neurons in a brain region called the inferotemporal cortex respond to complex features of images and objects, like their shape, so Janssen probed this region specifically. Sure enough, he found clusters of neurons that fired when the monkeys saw a concave image, and others that responded to a convex shape, and Janssen stimulated those clusters with a mild electric current. © 2012 Scientific American

Keyword: Vision
Link ID: 16243 - Posted: 01.12.2012

By Nathan Seppa People who smoke marijuana for recreational or medical purposes might now breathe easier. Scientists report in the Jan. 11 Journal of the American Medical Association that occasional cannabis users don’t experience any loss of lung function. In a 20-year study that included lung tests and a specific accounting of marijuana use, scientists also found that people who smoke more than 20 times a month and accumulate many years of use might have a slight drop in lung capacity over time. But the researchers are unsure of that finding since it was based on scant data. The study is the longest ever conducted that measures cannabis smoking and lung function, uses standard lung measurements and includes thousands of volunteers, says Donald Tashkin, a pulmonologist at UCLA who wasn’t involved in the study. “That makes it important,” he says. The data, he says, also suggest that marijuana is not a significant risk factor for chronic obstructive pulmonary disease, which includes emphysema. COPD is marked by loss of lung function and is typically caused by tobacco smoking. The researchers tapped into a health study of 5,115 young adults recruited in 1985 and given lung tests periodically until 2006. The volunteers revealed whether and how often they smoked tobacco, marijuana or both. Most marijuana users in the study reported light use — a few times a month on average during the two decades. © Society for Science & the Public 2000 - 2012

Keyword: Drug Abuse
Link ID: 16242 - Posted: 01.12.2012

Erin Allday, Chronicle Staff Writer It's no big secret that alcohol makes most people feel pretty good, but scientists at UCSF and UC Berkeley have for the first time found evidence that liquor triggers the release of pleasure-inducing endorphins in the brain - and that heavy drinkers are especially influenced by those endorphins. Studies of alcohol's effect on animal brains have shown for decades that endorphins - the body's tiny, natural proteins that behave like opiates - play a key role in the appeal of alcohol and why it can be addictive. But the UC study is the first to demonstrate, using brain-imaging technology, what actually happens in human brains while a person is drunk, or at least tipsy. The findings, while not necessarily shocking, could help researchers develop more focused drug treatments for fighting alcoholism, said scientists involved with the study released Wednesday. "Over the years, people have come up with a variety of hypotheses about how alcohol works in the brain. We know that it induces this endorphin release, and that's sort of unequivocal now," said Jennifer Mitchell, clinical project director of UCSF's Ernest Gallo Clinic and Research Center and lead author of the study. "Heavy drinkers report a lot of pleasure from a drink of alcohol," she said. "That's why we think drug treatment could be effective - if we can block that high, eventually they'll learn that drink isn't worth it anymore." © 2012 Hearst Communications Inc

Keyword: Drug Abuse
Link ID: 16241 - Posted: 01.12.2012

By Susan Milius CHARLESTON, S.C. — The greeneye fish views its stygian home through fluorescent lenses that turn one color into another, researchers propose, making glowing green images of hard-to-see violet objects. “Crazy” is what Yakir Gagnon of Duke University cheerfully called the fish-vision idea he and his colleagues presented January 4 at the annual meeting of Society for Integrative and Comparative Biology. Fluorescent materials known to science so far, he explained, respond to incoming light by glowing in a different color in all directions. Yet lenses on the bulging, upward-looking Chlorophthalmus fish appear to have materials that direct that fluorescent glow in the same direction and pattern as incoming light. Like many deep-sea fishes, greeneyes have only one kind of light-detecting pigment in the retina, the surface at the back of the eye that catches images. That pigment is optimized to pick up a particular wavelength of green light. Alone, the pigment doesn’t even detect blue-violet light. Yet greeneyes’ fluorescent, glowing lenses appear to translate blue-violet light into a more detectable green color. The Duke team has found that incoming blue-violet light (with a short wavelength of 410 nanometers) zaps lens substances into fluorescing a blue-green that’s just a twinkle away from the color the retinal pigment sees best. The lens glow peaks mostly at 485 nanometers, and the retinal pigment picks up light best at 488 nanometers. © Society for Science & the Public 2000 - 2012

Keyword: Vision; Evolution
Link ID: 16240 - Posted: 01.12.2012

by Kai Kupferschmidt Those palm readers predicting your age from your lifeline are making it up. But now scientists say they have found a true lifeline in the cells of Zebra finches. The birds with the longest telomeres—the protective caps at the ends of chromosomes—live the longest, according to a new study. "It is the first time this has been shown for any species," says María Blasco, a telomere researcher at the Spanish National Cancer Research Centre in Madrid, who was not involved in the work. Telomeres are repetitive DNA sequences that, together with some proteins, sit at the ends of chromosomes to keep them from fraying. They have long been known to shorten with age, and when they reach a critical length, cells stop dividing. While abnormally short telomeres have been implicated in some diseases, studies investigating whether longer telomeres lead to a longer life have shown mixed results. Now biologist Pat Monaghan and her colleagues at the University of Glasgow in the United Kingdom have come up with the best evidence yet that telomere length correlates with life span. The scientists measured telomere length in red blood cells of 99 captive zebra finches (Taeniopygia guttata). The birds resemble long-lived animals in that there is little restoration of telomeres in body cells as they age. The first measurement was taken at 25 days; the researchers then followed the birds over their natural life span, ranging from less than a year to nearly 9 years, and measured telomeres again at various time points. They found a highly significant correlation between telomere length at 25 days and life span; birds with longer telomeres lived longer. Length measured at 1 year also predicted life span, but the relationship was weaker, whereas at later time points (after 3, 4, 6, and 7 years) there was no correlation, the team reports online today in the Proceedings of the National Academy of Sciences. © 2010 American Association for the Advancement of Science.

Keyword: Genes & Behavior
Link ID: 16239 - Posted: 01.10.2012

By Alice Reid Well before sunup, Chuck Linderman launches his daily workout at the Alexandria boat house: 30 minutes pulling hard on a Concept 2 rowing machine, an equal stint lifting free weights and 30 minutes pedaling a stationary bike. He drives himself to sweaty, breathless exhaustion, for Linderman is training for the race of his life — a race against Parkinson’s disease. Linderman is one of a million Americans afflicted by this neurodegenerative disease that kills off the brain cells responsible for the body’s ability to move. His diagnosis came six years ago, when his wife noticed that his right arm was moving weirdly and that he was having trouble fastening the top button on his dress shirts. His doctor recommended seeing a neurologist. “It took the guy less than 15 minutes to make the diagnosis,” said Linderman, 64. Rowing already played a role in his life. For nearly a decade, he had been active in Alexandria Community Rowing’s masters program. So his response to Parkinson’s was immediate. Fight back with what he knew best: strenuous exercise. “What is the alternative? A descent into invalidism?” said Linderman, who retired two years ago from his job as director of a power company association. Exercise of any sort has long been known to be helpful for Parkinson’s. Before the development of effective drug therapy in the ’60s, patients often improved with any exercise, even the act of folding laundry, according to Michael Okun, national medical director of the Parkinson’s Foundation, which emphasizes exercise as an important tool to fight the disease. © 1996-2012 The Washington Post

Keyword: Parkinsons
Link ID: 16238 - Posted: 01.10.2012