By Christof Koch There is ample evidence that men and women think, express themselves and even experience emotions differently (for more details, read on through this issue). But in the area of sensory perception, psychologists are hard-pressed to identify major discrepancies. By and large, the way the two genders experience the sounds, sights and smells of life is quite similar. The most striking exception may be found, at least for some, in the perception of colors. Seeing in color is a complex process, as you may remember from your school days. It starts with the delicate lining of the eyes, a structure called the retina. Retinal tissue contains light-sensitive cells that absorb wavelengths in the visible spectrum and convert them into electrical signals. The brain interprets this information as the riot of colors we consciously experience. The retinal cells called cones come in three varieties. The S-type cone is maximally sensitive to light in the short-wavelength (blue) part of the visible spectrum, the M-type cone responds best to medium wavelengths, and the L-type to long, reddish wavelengths. People with normal color vision are known as trichromats because they possess these three kinds of photosensitive cone cells. About 8 percent of men, but fewer than 1 percent of women, have impoverished color vision, typically because they lack the gene for either the L- or the M-type photopigment. While their vision is normal in every other way, they suffer from what is often called red-green color blindness. Depending on the specific genetic omission involved, such people—who are known as dichromats because they have only two types of cone cells—are unable to distinguish between violet, lavender and purple or between red, orange, yellow and green. © 2010 Scientific American,

Keyword: Vision; Genes & Behavior
Link ID: 13973 - Posted: 06.24.2010

by Wendy Zukerman Smoking could predispose people to dementia, not protect them as has been suggested in the past. This is the conclusion from lab experiments in which rats with brain plaques developed further symptoms of Alzheimer's when given nicotine. In Alzheimer's disease, the brain becomes riddled with amyloid protein plaques and tangles of tau proteins. Low doses of nicotine have been shown to reduce the number of plaques in rats, but till now little was known about the effect of nicotine on the protein tangles. To find out, Yan-Jiang Wang's team at the Third Military Medical University in Chongqing, China, injected amyloid plaques into the brains of healthy rats and gave some the equivalent of a smoker's daily dose of nicotine for two weeks, while others received nothing. All the rats showed early signs of tau tangles and had difficulty navigating a maze, but the rats that were on nicotine did worse than those that were not. Smokers take note Jürgen Goetz, of the Brain and Mind Research Institute at the University of Sydney, Australia, says the results are likely to have implications for humans. Some previous studies, many of them funded by tobacco companies, have indicated that smokers are less likely to develop Alzheimer's. But when a team of researchers re-examined 43 studies earlier this year, discounting the industry-funded ones, they concluded that smoking actually increases the risk of Alzheimer's Journal reference: European Journal of Pharmacology , DOI: 10.1016/j.ejphar.2010.03.029 © Copyright Reed Business Information Ltd.

Keyword: Alzheimers; Drug Abuse
Link ID: 13972 - Posted: 06.24.2010

By Anne Miller Glass shards glistened sharply in a pool of water on the kitchen floor. My mom assured my fiance, Michael Davoli, that the old cheap glass didn't matter, but he still looked shell-shocked. He was always so careful to place drinks safely in front of himself: Anything too near his hands could be toppled. He helped my mother pick up the pieces and said he hadn't knocked over a glass in years. Such is life with Tourette's syndrome. Most people know the stereotype of unpredictable and uninhibited cursing or barking. Those symptoms do exist, for some people. But the truth is much more complicated. Michael, who has been my husband since August, doesn't curse unless he wants to. But as with the majority of people with Tourette's, there are myriad ways his inability to control some of his movements affects how he navigates his days. How and why people develop Tourette's remains a mystery. Research indicates a genetic tie: Those with Tourette's have a 50 percent chance of passing it to their children, and it's not unusual for someone with Tourette's to have a relative who also has the syndrome. The condition typically manifests in grade school, often with rapid eye blinks, and more often in boys than in girls. Medical experts estimate that as many as one in 100 people suffer from Tourette's. It is also associated with creative personalities: Composer Wolfgang Amadeus Mozart, writer Samuel Johnson and jazz great Thelonious Monk may have had it. In the sports world, Jim Eisenreich, who won a World Series with the Florida Marlins in 1997, and Tim Howard, a goalie on the U.S. national soccer team, live with Tourette's. © 2010 The Washington Post Company

Keyword: Tourettes
Link ID: 13971 - Posted: 06.24.2010

By Katie Moisse A little stress can do us good—it pushes us to compete and innovate. But chronic stress can increase the risk of diseases such as depression, heart disease and even cancer. Studies have shown that stress might promote cancer indirectly by weakening the immune system's anti-tumor defense or by encouraging new tumor-feeding blood vessels to form. But a new study published April 12 in The Journal of Clinical Investigation shows that stress hormones, such as adrenaline, can directly support tumor growth and spread. For normal cells to thrive in the body, "they need to be attached to their neighbors and their surroundings," says the study's lead author Anil Sood from The University of Texas M. D, Anderson Cancer Center in Houston. Cells that detach from their environment undergo a form of programmed cell death called anoikis. "But cancer cells have come up with way to bypass this effect—they avoid anoikis," Sood says. This allows cancer cells to break off from tumors, spread throughout the body (in blood or other fluid) and form new tumors at distant sites—a process called metastasis. So Sood wondered: Could stress affect anoikis? "It surprised us that this biology hadn't been studied before," he notes. "Stress influences so many normal physiological processes. Why wouldn't it be involved in tumor progression?" Sood and his team first studied the effects of stress hormones on human ovarian cancer cell anoikis in culture. Cells that were exposed to stress hormones were protected from self destruction—meaning they could survive without being anchored to their surroundings. The stress hormone treatment activated a protein called FAK (focal adhesion kinase), which is known to protect cells from anoikis. Inhibiting FAK reversed the effects. © 2010 Scientific American,

Keyword: Stress
Link ID: 13970 - Posted: 06.24.2010

By Nathan Seppa Losing weight on purpose in old age may provide a survival edge, at least for obese people, a new analysis shows. Writing in an upcoming issue of the Journal of Gerontology: Medical Sciences, researchers tackled a long-held assumption that weight loss in old age is uniformly unhealthy. The idea stems from overpowering data linking rapid, unintentional weight loss in the elderly to a hidden underlying problem, such as the onset of type 2 diabetes. “The loss of weight over six months without a specific cause is a very bad prognostic sign,” says study coauthor Stephen Kritchevsky, an epidemiologist at Wake Forest University School of Medicine in Winston-Salem, N.C. That has ingrained the notion among doctors that any weight loss in the elderly is risky, he says. “I’ve been at meetings on nutrition in the elderly, and there have been reputable geriatricians who have said in public that if you ask an older person to lose weight you’re committing malpractice,” he says. To assess the effects of intended weight loss, Kritchevsky and his colleagues analyzed data collected by a long-term trial in the 1990s. In the study 316 obese people, average age 70, were randomly assigned in roughly equal numbers to one of four interventions: a dieting program, dieting plus exercise, exercise only or health education only. The people had arthritic knees but were otherwise free of major health problems. © Society for Science & the Public 2000 - 2010

Keyword: Obesity
Link ID: 13969 - Posted: 06.24.2010

by Cassandra Willyard Two genetic studies involving thousands of participants suggest that age-related macular degeneration, an eye disease common among the elderly, is tied to a gene that helps regulate “good” cholesterol. The studies present the first genetic evidence of a link between cholesterol and the disease, and they may lead scientists to identify new targets for therapy. Age-related macular degeneration is the leading cause of blindness in older adults in the United States. Lesions form behind the retina, impeding the center of an individual’s field of vision. A link between cholesterol and an eye disease might sound strange, but scientists have known for years that cholesterol can accumulate at the back of the eye as part of aging. Moreover, cholesterol is a major component of the macular lesions. What role cholesterol plays in the eye, however, remains unclear. In the new work, scientists compared the genomes of people who have macular degeneration with the genomes of healthy individuals to search for genetic variants that occur more frequently among one group or the other. In the first study, Johanna Seddon, a genetic epidemiologist at Tufts University in Boston and colleagues scanned the genomes of 979 people with advanced degeneration and 1709 healthy people. The researchers found a strong association with a variant of the hepatic lipase gene (LIPC). LIPC codes for an enzyme involved in the metabolism of HDL, or “good,” cholesterol. People with this variant had an 18% reduced risk of having the disease. A scan of 4337 other cases and 2077 controls yielded the same result. The researchers also found weaker associations with three other genes involved in the HDL pathway: ABCA1, CETP, and LPL. These weaker associations did not meet the strict criteria necessary in this type of study to achieve statistical significance. © 2010 American Association for the Advancement of Science

Keyword: Vision; Genes & Behavior
Link ID: 13968 - Posted: 06.24.2010

By Bruce Bower Nearly 2 million years ago, an adult and a child walking through the South African landscape somehow fell through openings in a partly eroded, underground cave and died. Today, that fatal plunge has led to their identification as representatives of a new hominid species — and a contentious debate among paleoanthropologists over the pair’s evolutionary relationship to modern humans. In the April 9 Science, anthropologist Lee Berger of the University of the Witwatersrand in Johannesburg and his colleagues assign newly discovered fossils from these ancient individuals to the species Australopithecus sediba. They propose that the species served as an evolutionary bridge from apelike members of Australopithecus to the Homo genus, which includes living people. In a local African tongue, sediba means fountain or wellspring, a reference to this species as a candidate ancestor of the Homo line. “Australopithecus sediba could be a Rosetta Stone for anatomically defining the Homo genus,” Berger says. Despite the importance of finding hominid fossils from the poorly understood period between 2 million and 1.7 million years ago, paleoanthropologists familiar with the finds doubt that they will illuminate Homo origins. “There’s no compelling evidence that this newly proposed species was ancestral to Homo,” remarks Bernard Wood of George Washington University in Washington, D.C. © Society for Science & the Public 2000 - 2010

Keyword: Evolution
Link ID: 13967 - Posted: 06.24.2010

by Michael Balter Children with a genetic condition that quells their fear of strangers don't stereotype based on race, according to a new study. The findings support the idea that prejudice stems from fear of people from different social groups, although some researchers question how well the new study supports that conclusion. Even individuals who profess not to be racist often harbor racist attitudes on an unconscious level, implying that racial prejudice is socially or biologically ingrained. In a 2005 paper in Science, New York University psychologist Elizabeth Phelps and her colleagues exposed black subjects and white subjects to pictures of both black and white faces, first in conjunction with a mild electric shock and then without the shock. Once the shock was gone, the volunteers' fear reactions, as measured by electrical reactions in the skin, soon disappeared when exposed to pictures of their own race, but remained to a limited extent when exposed to pictures of the opposite race. Phelps’s team concluded that racial bias was linked to a deep-seated fear of people perceived as members of a different social group, a connection that some researchers had suspected but for which solid data was lacking. The researchers also found that this fear was diminished in people who had more contact with members of other races, such as those who dated interracially. To further explore the role of social fear in racial prejudice, a team led by Andreas Meyer-Lindenberg, a psychiatrist at the Central Institute of Mental Health in Mannheim, Germany, examined the attitudes of a group notably lacking it: children with a genetic disorder called Williams syndrome. Caused by the deletion of genes on chromosome 7, Williams syndrome often leads to mild to moderate mental and growth retardation as well as an intense sociability and lack of social fear, especially of strangers. “If I come into a Williams Syndrome Association meeting, 50 kids will crawl all over me and rejoice at seeing me even though they have never met me,” Meyer-Lindenberg says. © 2010 American Association for the Advancement of Science

Keyword: Emotions; Genes & Behavior
Link ID: 13966 - Posted: 06.24.2010

A new genetic fault which may account for some cases of inherited deafness has been revealed by Dutch researchers. It means that parents with the hereditary condition may be able to predict more accurately the chances of passing it on to their children. The new find, documented in the American Journal of Human Genetics, could even one day contribute to treatments, say the scientists. One child in 750 is born with severe hearing loss or profound deafness. The gene in question, labelled PTPRQ, appears to play a role in the development of the inner ear "hair cell" before the birth of the child. A genetic fault here means that these cells will not form properly or in sufficient numbers, leading to profound deafness or extremely poor hearing. This can lead to problems throughout childhood, including behavioural and developmental difficulties, and low academic achievement. The latest gene was tracked down by scientists at Radboud University Nijmegen Medical Centre who looked closely at the DNA of families prone to the condition, looking for shared genetic traits. There are now more than 60 known locations in our DNA which can contain faulty genes contributing to this form of deafness, although only half the genes in these locations which actually cause the problem are yet to be identified. Dr Hannie Kremer, who led the research, said: "Our approach is identifying more genes for congenital deafness. "This knowledge will help improve treatments for patients, genetic counselling, molecular diagnosis and the development of advanced therapeutic strategies." (C)BBC

Keyword: Hearing; Genes & Behavior
Link ID: 13965 - Posted: 04.12.2010

Jim Schnabel Of all the ways that proteins can go bad, becoming an amyloid is surely one of the worst. In this state, sticky elements within proteins emerge and seed the growth of sometimes deadly fibrils. Amyloids riddle the brain in Alzheimer's disease and Creutzfeldt–Jakob disease. But until recently it has seemed that this corrupt state could threaten only a tiny fraction of proteins. Research is now hinting at a more unsettling picture. In work reported in February, a team led by David Eisenberg at the University of California, Los Angeles, sifted through tens of thousands of proteins looking for segments with the peculiar stickiness needed to form amyloid1. They found, says Eisenberg, that "effectively all complex proteins have these short segments that, if exposed and flexible enough, are capable of triggering amyloid formation". Not all proteins form amyloids, however. The 'amylome', as Eisenberg calls it, is restricted because most proteins hide these sticky segments out of harm's way or otherwise keep their stickiness under control. His results and other work suggest that evolution treats amyloids as a fundamental threat. Amyloids have been found in some of the most common age-related diseases, and there is evidence that ageing itself makes some amyloid accumulation inevitable. It now seems as though the human body is perched precariously above an amyloidal abyss. "The amyloid state is more like the default state of a protein, and in the absence of specific protective mechanisms, many of our proteins could fall into it," says Chris Dobson, a structural biologist at the University of Cambridge, UK. © 2010 Nature Publishing Group,

Keyword: Prions; Alzheimers
Link ID: 13964 - Posted: 06.24.2010

By ANNE EISENBERG ERIC JONES sat in a middle seat on a recent flight from the New York area to Florida, but he wasn’t complaining. Instead, he was quietly enjoying actions that many other people might take for granted, like taking a cup of coffee from the flight attendant or changing the channel on his video monitor. These simple movements were lost to Mr. Jones when the fingers and thumb on his right hand were amputated three years ago. But now he has a prosthetic replacement: a set of motorized digits that can clasp cans, flimsy plastic water bottles or even thin slips of paper. “Pouring a can of soda into a cup — that is a mundane daily action for most people, but to me it is a very big deal,” said Mr. Jones, who lives with his family in Mamaroneck, N.Y. “I slip my bionic fingers on like a glove, and then I have five moveable fingers to grasp things. It’s wonderful to have regained these functions.” Mr. Jones’s prosthesis, called ProDigits, is made by Touch Bionics in Livingston, Scotland. The device can replace any or all fingers on a hand; each replacement digit has a tiny motor and gear box mounted at the base. Movement is controlled by a computer chip in the prosthesis. ProDigits was released commercially last December, said Stuart Mead, the chief executive of Touch Bionics. About 60 patients have been fitted worldwide, he said, and some have been wearing it for three or four years. The cost is $60,000 to $75,000, including fitting and occupational therapy. Copyright 2010 The New York Times Company

Keyword: Pain & Touch; Robotics
Link ID: 13963 - Posted: 06.24.2010

By JOHN TIERNEY As a retired clinical psychologist, Clark Martin was well acquainted with traditional treatments for depression, but his own case seemed untreatable as he struggled through chemotherapy and other grueling regimens for kidney cancer. Counseling seemed futile to him. So did the antidepressant pills he tried. Nothing had any lasting effect until, at the age of 65, he had his first psychedelic experience. He left his home in Vancouver, Wash., to take part in an experiment at Johns Hopkins medical school involving psilocybin, the psychoactive ingredient found in certain mushrooms. Scientists are taking a new look at hallucinogens, which became taboo among regulators after enthusiasts like Timothy Leary promoted them in the 1960s with the slogan “Turn on, tune in, drop out.” Now, using rigorous protocols and safeguards, scientists have won permission to study once again the drugs’ potential for treating mental problems and illuminating the nature of consciousness. After taking the hallucinogen, Dr. Martin put on an eye mask and headphones, and lay on a couch listening to classical music as he contemplated the universe. “All of a sudden, everything familiar started evaporating,” he recalled. “Imagine you fall off a boat out in the open ocean, and you turn around, and the boat is gone. And then the water’s gone. And then you’re gone.” Copyright 2010 The New York Times Company

Keyword: Depression; Drug Abuse
Link ID: 13962 - Posted: 06.24.2010

By LISA SANDERS, M.D. Dr. Kurtland Ma found the young man lying on the stretcher in the quiet of the predawn night. He was surprised by how healthy the patient looked: he had learned over the first year of his residency training that those who came to the Jacobi Medical Center emergency room in the Bronx at that hour were often the very sickest patients. The thin chart reported that the patient came to the E.R. because he was having trouble walking. He had a headache; he felt weak and dizzy, and yet his vitals and initial blood work were completely normal. He was a puzzle, the senior resident told him as she handed Dr. Ma the chart. “I have no idea what’s going on with this guy,” she told Dr. Ma. “But he is probably going to need a head CT.” The patient was 28 and said he was healthy until three days ago, when he and his girlfriend went to the Bahamas to celebrate his birthday. After a long day of swimming and snorkeling, they decided to try a restaurant they had heard good things about. They both ordered seafood — she had the red snapper, he the barracuda — and then went out dancing. Out on the dance floor the patient doubled over, caught off guard by an intense pain that knifed through his gut and took away his breath. He stumbled to the bathroom. The abdominal cramps and diarrhea came in waves. He kept thinking it would pass, but it didn’t. Finally he decided to go back to the hotel. As they walked through the streets crowded with other vacationers, his girlfriend teased him for letting a little bug ruin his birthday. But by then all he wanted was to lie down and go to sleep. Copyright 2010 The New York Times Company

Keyword: Pain & Touch
Link ID: 13961 - Posted: 06.24.2010

Obstructive sleep apnea is associated with an increased risk of stroke in middle-aged and older adults, especially men, according to new results from a landmark study supported by the National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health. Overall, sleep apnea more than doubles the risk of stroke in men. Obstructive sleep apnea is a common disorder in which the upper airway is intermittently narrowed or blocked, disrupting sleep and breathing during sleep. Researchers from the Sleep Heart Health Study (SHHS) report that the risk of stroke appears in men with mild sleep apnea and rises with the severity of sleep apnea. Men with moderate to severe sleep apnea were nearly three times more likely to have a stroke than men without sleep apnea or with mild sleep apnea. The risk from sleep apnea is independent of other risk factors such as weight, high blood pressure, race, smoking, and diabetes. They also report for the first time a link between sleep apnea and increased risk of stroke in women. Obstructive Sleep Apnea Hypopnea and Incident Stroke: The Sleep Heart Health Study, was published online March 25 ahead of print in the American Journal of Respiratory and Critical Care Medicine. Stroke is the second leading cause of death worldwide. "Although scientists have uncovered several risk factors for stroke — such as age, high blood pressure and atrial fibrillation, and diabetes — there are still many cases in which the cause or contributing factors are unknown, " noted NHLBI Acting Director Susan B. Shurin, M.D. "This is the largest study to date to link sleep apnea with an increased risk of stroke. The time is right for researchers to study whether treating sleep apnea could prevent or delay stroke in some individuals. "

Keyword: Sleep; Stroke
Link ID: 13960 - Posted: 06.24.2010

by Wendy Zukerman GRUMPY old people may be bad-tempered because their brains react differently to chronic stress. At least that's what happens to elderly rats. Elderly humans are more vulnerable to stress than their youthful counterparts. "There is more low-level anxiety and depression," says Nancy Pachana of the University of Queensland in Brisbane, Australia. To investigate why, Hirotaka Shoji of the National Centre for Geriatrics and Gerontology in Obu, Japan, put 3-month-old and 24-month-old rats under stress by placing them inside a wire-mesh container for 1 hour every day for two weeks. Before this treatment began, the two sets of rats had similar levels of the stress hormone, corticosterone. All the rats had higher levels of the hormone after two weeks, but the old rats had significantly more. The old rats also showed increased activity in areas of the brain associated with anxiety and decreased activity in regions linked with controlling emotions (Behavioural Brain Research, DOI: 10.1016/j.bbr.2010.03.025). Shoji suggests that ageing may reduce the brain's ability to damp down the release of corticosterone in response to repeated stress. When another group of rats were put in the cage just once, for an hour, stress hormone levels were similar in old and young rats, suggesting that ageing increases vulnerability to repeated stress rather than one-off episodes. © Copyright Reed Business Information Lt

Keyword: Stress
Link ID: 13959 - Posted: 06.24.2010

By Bruce Bower Data, like children, can be raised wrong. Then they become an embarrassment. Consider the retraction on February 2 of a study suggesting that the measles-mumps-rubella vaccine had caused a small number of children to develop autism. The now-debunked study, published in 1998 in a major medical journal, fueled parents’ fears about vaccinating children. So it stands to reason that reluctant parents, upon reading about the retraction, will drag their kids to the doctor for a shot and a lollipop. Don’t bet on it. A growing body of research indicates that people making decisions interpret the chances of encountering rare events, such as a child developing tragic complications from a vaccine, in dramatically different ways. “There’s an explosion of interest in studying how people acquire the information on which they base risky decisions,” says psychologist Craig Fox of the University of California, Los Angeles, who helped generate an influential model that predicts how people will make gambling decisions depending on descriptions of the odds. People who learn about the like­lihood of encountering a low-probability, high-impact event via descriptions that include precise probabilities tend to overestimate, by a lot, the chances of that event actually occurring. Vaccine-o-phobic parents have typically never seen a child sink into autism after an MMR injection and never will (SN Online: 2/3/10). But they have heard scary secondhand accounts, read celebrity-penned tales of vaccine horrors and scanned government statistics on the minuscule but still real chances of side effects unrelated to autism. © Society for Science & the Public 2000 - 2010

Keyword: Autism; Attention
Link ID: 13958 - Posted: 06.24.2010

by Mark Cohen Hey, Mom! Mom! Watch me! Look, Mom!” I could hear the excited cries through the closed door of the examining room, even though I was still 20 feet down the hall. The happy shouts were followed by a loud thump and then a cascade of muted crashes. As I headed toward the commotion, my medical assistant smiled and handed me the chart for this patient. “You’d better get in to see this little guy quickly, Dr. Cohen, before he totally wrecks your room!” The brief information on the consultation request said, “Tyler Winters, 3-year-old boy, hyperactive.” As I often tell medical students, nearly all 3-year-olds are hyperactive at least some of the time. Often the parents of a child whose development and behavior are perfectly normal insist on a referral to a developmental pediatrician like myself because they are sure there is something wrong—or someone has told them as much. I generally look forward to those consultations; it’s enjoyable to reassure an anxious parent that her child is developing normally. Before leaving my office I had briefly looked through Tyler’s medical record on the computer. Other than his having been adopted at birth, there was nothing that stood out as unusual. When I knocked and opened the door, Tyler was clambering onto the exam table while his mother, Sandi, was attempting to move a pile of books from the floor back onto the book rack. They had apparently been knocked off (the crashes) when he jumped from the table to the floor (the loud thump). Sandi glanced at me with a nervous smile, then quickly turned to scoop her child off the table.

Keyword: ADHD
Link ID: 13957 - Posted: 06.24.2010

By TERRY SEJNOWSKI Is there anything good about insomnia? Could there possibly be any upside to a long, torturous sleepless night? To answer the question, let’s look at another condition entirely. Postpartum depression affects between 5 percent and 25 percent of new mothers. Symptoms — including sadness, fatigue, appetite changes, crying, anxiety and irritability — usually occur in the first few months after child birth. There is a simple way to alleviate postpartum depression in just a few hours: sleep deprivation. If a depressed mother stays up all night, or even the last half of the night, it is likely that by morning the depression will lift. Although this sounds too good to be true, it has been well documented in over 1,700 patients in more than 75 published papers during the last 40 years.[1] Sleep deprivation used as a treatment for depression is efficacious and robust: it works quickly, is relatively easy to administer, inexpensive, relatively safe and it also alleviates other types of clinical depression. Sleep deprivation can elevate your mood even if you are not depressed, and can induce euphoria. This throws a new light on insomnia. This remarkable result is not well known outside a small circle of sleep researchers for three good reasons. First, sleep deprivation is not as convenient as taking a pill. Second, prolonged sleep deprivation is not exactly a desirable state; it leads to cognitive defects, such as reduced working memory and impaired decision making. Finally, depression recurs after the mother, inevitably, succumbs to sleep, even for a short nap. Nonetheless this is an incredibly important observation; it shows that depression can be rapidly reversed and suggests that something is happening in the sleeping brain to bring on episodes of depression. All this offers hope that studying sleep deprivation may lead to new, unique and rapid treatments for depression. Copyright 2010 The New York Times Company

Keyword: Depression; Sleep
Link ID: 13956 - Posted: 06.24.2010

The use of anti-psychotic drugs in the elderly doubles the risk of potentially fatal pneumonia, say Dutch researchers. A study of almost 2,000 patients found the increased risk starts soon after treatment begins and concluded that patients should be closely monitored. An expert review published in 2009 found the drugs are overused in many cases and are responsible for up to 1,800 deaths in the UK every year. Ministers have said they want to see a significant cut in their use. The latest research published in the Annals of Internal Medicine compared the health records of 258 over-65s with pneumonia with 1,686 patients without the infection. Of those with pneumonia, a quarter died within a month. When they looked at prescribed drugs, they found current use of anti-psychotics was associated with a roughly two-fold increase in the risk of pneumonia. Those on the newer types of anti-psychotic drugs were slightly less likely to have the infection than those on the older class of drugs but were still at significant increased risk. The risk was found to start soon after treatment and increased the higher the dose of drugs the patient was prescribed. The researchers from Erasmus University Medical Center in Rotterdam said: "Clinicians who start treatment with anti-psychotic drugs should closely monitor patients, particularly at the start of therapy and if high doses are given." (C)BBC

Keyword: Schizophrenia
Link ID: 13955 - Posted: 04.08.2010

WASHINGTON - Smoking may increase the risk of multiple sclerosis in people who have other risk factors for the neurological disorder, researchers said Wednesday. The findings suggest that smokers who have high levels of a protein that protects against the Epstein-Barr virus, a common herpes virus, were twice as likely as nonsmokers to get multiple sclerosis (MS), the researchers wrote in the online edition of the journal Neurology. Previous studies have suggested that smoking and the virus-fighting protein were independent risk factors and this research looked at how they may be associated with each other, Claire Simon of Harvard University said in a telephone interview. "We found that that association was stronger in people who reported smoking compared with people who did not report smoking," Simon said. The study found no association between smoking and a gene related to the immune system gene called HLA-DR15, which is thought to be another risk factor for MS, she said. Studying the potential risk factors simultaneously might provide clues about why some people get MS and others do not, Simon said. MS is an incurable condition that affects more than 1 million people worldwide. The disease can cause mild symptoms in some people and permanent disability in others. Symptoms may include numbness or weakness in one or more limbs, partial or complete loss of vision, tingling or pain, electric-shock sensation with certain head movements, tremors and an unsteady gait. Copyright 2010 Reuters

Keyword: Multiple Sclerosis; Drug Abuse
Link ID: 13954 - Posted: 04.08.2010