Researchers have found a brain mechanism that may calm you down in life or death situations and may give you a better chance at survival. The study was done in rats, but as this ScienCentral New video explains it may have important implications for people. In life or death situations, survival sometimes hangs on the threads of willpower. When British mountaineer and author of Touching the Void Joe Simpson crawled through the Peruvian Andees twenty years ago with broken bones and no food or water, death seemed certain. But he didn’t give up hope and he made it back to base camp. He told Climber Magazine he couldn’t "Just sit there." Now neuroscientists say a person’s belief in their ability to survive a life or death situation may be a function of brain circuitry. "It’s belief in control that really matters, not that you really can [survive] or not," says Steven Maier, director of the Center for Neuroscience at the University of Colorado at Boulder. By "control" Maier means having the presence of mind to handle life or death situations as opposed to just freezing or feeling helpless. (C) ScienCentral, 2000-2005.

Keyword: Stress
Link ID: 7237 - Posted: 06.24.2010

Bruce Bower A new scientific era may have dawned for light therapy, a potential depression fighter that has languished in the shadows of antidepressant medication and psychotherapy for the past 20 years. A research review commissioned by the American Psychiatric Association in Washington, D.C., concludes that in trials, daily exposure to bright light is about as effective as antidepressant drugs in quelling seasonal affective disorder (SAD), or winter depression, and other forms of depression. "I now tell my patients that light therapy is a reasonable depression treatment, even if the data base for this approach is relatively small," says psychiatrist Robert N. Golden of the University of North Carolina at Chapel Hill. Golden directed the new statistical review, which appears in the April American Journal of Psychiatry. Like many mainstream psychiatrists, Golden had been skeptical of studies reporting that depression diminishes in response to daily bright-light exposure, usually administered early in the morning for 30 minutes to 1 hour. These investigations often contain serious flaws, he says, such as few participants and no groups treated with dim lights or other placebos. Copyright ©2005 Science Service

Keyword: Depression; Biological Rhythms
Link ID: 7236 - Posted: 06.24.2010

Clues about how a suspect version of a gene may slightly increase risk for schizophrenia* are emerging from a brain imaging study by the National Institutes of Health's (NIH) National Institute of Mental Health (NIMH). The gene variant produced a telltale pattern of activity linked to production of a key brain messenger chemical. The study found that increased activity in the front of the brain predicted increases in the neurotransmitter dopamine in the middle of the brain in subjects with the suspected schizophrenia-related version of the gene. Yet, the opposite relationship held for subjects with the other of two common versions of the gene. "A tiny variation in the gene that makes the enzyme that breaks down dopamine causes a complete flipflop – not a mere difference in degree – in dopamine activity in these two brain areas," explained NIMH's Dr. Andreas Meyer-Lindenberg, who, along with Dr. Karen Berman and colleagues, reported their findings in the April 10, 2005 online edition of Nature Neuroscience. The NIMH study also for the first time confirms in living humans that activity of the front brain area, the prefrontal cortex, is regulated by dopamine production in the midbrain, which, in turn, is regulated by these two common gene variants.

Keyword: Schizophrenia; Genes & Behavior
Link ID: 7235 - Posted: 06.24.2010

A new mouse study suggests that a brain system that controls the sleep/wake cycle might also play a role in regulating appetite and metabolism. Mice with a mutation in a gene called "Clock," which helps drive circadian rhythm, ate significantly more and gained more weight. The finding could help explain why disrupted sleep patterns-particularly when combined with a high-fat diet--are associated with excessive weight gain and the onset of metabolic syndrome in some people, according to investigators supported by the National Institutes of Health (NIH). The study, by Fred W. Turek, Ph.D., and Joseph Bass, M.D., Ph.D., of Northwestern University in Evanston, Ill., and others will be available at the Science Express website, http://www.sciencemag.org/sciencexpress/recent.shtml, on April 21, 2005. At least 40 million Americans have chronic sleep problems, and an additional 20 million experience occasional sleeping problems. As many as 47 million Americans have metabolic syndrome, a cluster of conditions shown to increase a person's risk of heart disease and stroke. The National Cholesterol Education Program defines metabolic syndrome as having at least 3 of the following risk factors: high blood pressure, high glucose (sugar) levels which can indicate risk for diabetes, high triglyceride levels, low levels of good cholesterol, and a large waist. Scientists have found that circadian rhythms (which control the sleep/wake cycle and other biological processes), hunger, and satiety are all regulated by centers within a brain structure called the hypothalamus. And previous studies in humans have suggested that disrupted sleep patterns may contribute to the development of obesity, diabetes, and metabolic syndrome.

Keyword: Sleep; Biological Rhythms
Link ID: 7234 - Posted: 04.23.2005

Jessica Ebert It seems that mice can be coaxed into a hibernation-like state by a whiff of hydrogen sulphide, the gas found in rotten eggs. The discovery could improve the preservation of organs or tissues for transplants, and could lead to more effective treatments for illnesses as diverse as cancer and stroke. Hydrogen sulphide can be deadly in high concentrations, causing burns and interfering with respiration. But it is also produced in small quantities by animals, in which it is thought to play a vital role in controlling body temperature and metabolism. Mark Roth, a biochemist at the Fred Hutchinson Cancer Research Center, Seattle, and his colleagues tried exposing mice to air laced with relatively low concentrations of the gas: within minutes, the mice seemed to fall unconscious. Their core body temperature dropped by some 20ºC, and their breathing slowed from about 120 breaths a minute to fewer than 10, the team reports in Science1. When re-exposed to clean air after six hours, the mice bounced back without any evident side-effects, says Roth. "This indicates that it's possible to decrease metabolic rate on demand," says Roth. By shutting down metabolism, the body's need for oxygen diminishes, which could "revolutionize treatment for a host of human ills", says Roth. ©2005 Nature Publishing Group

Keyword: Sleep; Stroke
Link ID: 7233 - Posted: 06.24.2010

An article in the journal Epilepsia reviewed recent data on the risks associated with continuation of medical treatment of women with epilepsy during their pregnancies. While the general consensus is that use of antiepileptic drugs is associated with increased risk for birth defects, physicians weigh this risk against that of uncontrolled epileptic seizures, which can be more harmful to the fetus than the actual drugs. Most women with active epilepsy choose to continue with drug therapy during pregnancy and have more than 90% chance to give birth to a perfectly healthy child. It remains unsolved whether risks for birth defects vary with different drugs. One drug, valproate, has been associated with a higher risk of birth defects than some others although the reasons for this have not been completely clarified. However, for some patients, valproate is the most effective medication for controlling the seizures, which must be balanced against the risk. An additional concern could be possible postnatal effects of anti-epileptic drugs to the child which do not become apparent until school age.

Keyword: Epilepsy; Development of the Brain
Link ID: 7232 - Posted: 04.23.2005

Nervous system development requires billions of neurons to migrate to the appropriate locations in the brain and grow nerve fibers (axons) that connect to other nerve cells in an intricate network. Growth cones, structures in the tips of growing axons, are responsible for steering axons in the right direction, guided by a complex set of signals from cells they encounter along the way. Some signals lure the axons to extend and grow in a particular direction; others are inhibitory, making the axon turn away or stop growing. In two papers in the April 21 Neuron, researchers from Children's Hospital Boston reveal important insights into how inhibitory cues affect the growth cone, and identify possible targets within axons that could be blocked to overcome this inhibition. Such intervention could possibly enable damaged axons to regenerate (normally impossible in a mature nervous system) and ultimately restore nerve function. It's been known that cells synthesize an inhibitory protein called ephrin, which binds to a receptor called Eph on the axon's growth cone. But how this triggers the axon to change course or stop growing has been a mystery.

Keyword: Development of the Brain
Link ID: 7231 - Posted: 04.21.2005

DALLAS – – Why people get drowsy and fall asleep, and how caffeine blocks that process, are the subjects of a new study by researchers at UT Southwestern Medical Center. When cells in a certain part of the brain become overworked, a compound in the brain kicks in, telling them to shut down. This causes people to become drowsy and fall asleep. Alter that natural process by adding coffee or tea, and the brain compound – called adenosine – is blocked, and people stay awake. These findings, available online and in the April 21 issue of the journal Neuron, offer new clues regarding the function of the brain in the body's natural sleep process, as well as potential targets for future treatments for insomnia and other sleep problems. Prolonged increased neural activity in the brain's arousal centers triggers the release of adenosine, which in turn slows down neural activity in the arousal center areas. Because the arousal centers control activity throughout the entire brain, the process expands outward and causes neural activity to slow down everywhere in the brain. "Insomnia and chronic sleep loss are very common problems," said Dr. Robert W. Greene, professor of psychiatry and senior author of the study. "In addition, all the major psychiatric disorders, including depression, schizophrenia and post-traumatic stress disorder have sleep disruption as a prominent symptom.

Keyword: Sleep
Link ID: 7230 - Posted: 06.24.2010

Much research has been done on how "fear-conditioning" affects brain circuitry, but what about the flip side: "safety conditioning?" Now, researchers led by Michael T. Rogan and Eric R. Kandel of Columbia University Medical Center have discovered in mice how the brain responds to external stimuli that signal safety. Their findings, say the researchers, could aid in treating psychiatric disorders involving a feeling of loss of safety, as well as understanding why some people respond more resiliently to trauma than others. In their experiments, the scientists first safety-conditioned mice by teaching them to associate a series of beeps with the absence of a mildly uncomfortable foot shock. They found that the beeps reduced the classic "freeze" defensive response in the trained mice. They also found that when the safety-conditioned mice, compared to control mice, heard the beeps, they would increase adventurous exploration of an open space--abandoning their normal, protective, wall-hugging behavior. The mice showed the same adventurous behavior when exposed to an instinctive safety signal--dimmed light--indicating that the same neural response mechanisms were at work, said the researchers. When the safety-conditioned mice were given the choice of two rooms--one in which their entry triggered the safety signal--they overwhelmingly chose the "safety" room. Electrophysiological studies of the animals' brains revealed that the safety tones depressed activity in a region of the amygdala--the brain structure that processes emotions and that is activated in fear responses.

Keyword: Emotions
Link ID: 7229 - Posted: 04.21.2005

Boston, MA – Researchers from the Harvard School of Public Health (HSPH) recently discovered that cigarette smoking may contribute to the progression of multiple sclerosis (MS), suggesting that quitting smoking could limit or delay central nervous system deterioration. This is the first time that a modifiable risk factor for MS progression has been identified, providing a new strategy for patients hoping to control neurological damage from the disease. Study results appear in the March 9, 2005 issue of Brain. Miguel Hernán, lead author of the study and an assistant professor of epidemiology at HSPH, noted that "the findings are interesting because no modifiable risk factors for the progression of MS are known. This was the first prospective study that identified a potential intervention (quitting smoking) for reducing the risk of progression of MS." Analyzing over 2,000 medical records in the General Practice Research Database (GPRD), researchers identified 179 British patients who were originally diagnosed with relapsing-remitting MS, a form of the disease in which symptoms fade and recur in unpredictable patterns. Patients who were current or past smokers were 3.6 times as likely as patients who had never smoked to develop secondary progressive MS, a later stage of the disease marked by steady deterioration of the central nervous system. This disease progression also occurred more quickly in patients who were identified as current or past smokers. The study also supported earlier research showing that smoking may increase the risk of initial MS diagnosis. Current and past smokers were 30% more likely to be diagnosed with MS than those who had never smoked.

Keyword: Multiple Sclerosis; Drug Abuse
Link ID: 7228 - Posted: 06.24.2010

ANAHEIM, CALIFORNIA--People with glioblastoma multiforme (GBM)—the most common and aggressive form of primary brain tumor—nearly double their survival time after surgery and radiation treatment if they carry a version of a gene involved in cell immortalization, according to a new study. The findings could pave the way toward individualizing treatment for the cancer, say the researchers. Cancer cells achieve immortality in part by turning on production of the enzyme telomerase, which lengthens structures called telomeres that protect the ends of chromosomes. Telomerase is encoded by the hTERT gene, which is not active in most normal mature cells. Previous research has shown that a genetic variation in hTERT, known as MNS16A-S, increases the gene's activity, leading molecular biologist Luo Wang of the MD Anderson Cancer Center at the University of Texas in Houston to ask whether such variations affect survival rate in patients with GBM. To test the hypothesis, Wang and his team analyzed the available DNA samples of 301 GBM patients, ages 20 to 73, who had undergone surgery and radiation treatment at the same hospital between 1994 and 2003. Only 11 percent carried the MNS16A-S variation, while the rest carried longer versions of the gene known as MNS16A-L or MNS16A-LL. After analyzing the medical records, the researchers found that the S carriers survived for an average of 25 months after therapy, but the L and LL-allele carriers only lived an average of 14 months. The findings, presented here on April 18 at a meeting of the American Association for Cancer Research, still held true when the researchers controlled for severity of surgery and the fact that some patients had also received chemotherapy. Copyright © 2005 by the American Association for the Advancement of Science.

Keyword: Miscellaneous
Link ID: 7227 - Posted: 06.24.2010

By Jeff Wheelwright Pecos Road runs due west along the southern boundary of Phoenix. On the city side of the road, new subdivisions of retirement homes are pushing up their tile roofs like mushrooms that sprout with no rain. On the other side of the road lies the flat scrub of the Gila River Indian Community, some 600 square miles, most of it empty. The reservation shimmers out of the reach of the builders like a desert mirage. This land was no good to anyone in 1859, when it was allocated to the Pima Indians. Today it has 13,000 Native American residents, living in squat cinder-block houses in scattered, dusty hamlets; three casinos that have boosted the tribal income to $100 million annually from $4 million; irrigated cotton, alfalfa, and citrus, for Pimas were always farmers; and a hospital and two kidney-dialysis clinics, with another medical clinic in the planning stage. Kidney failure is a deadly complication of diabetes, and Pimas, so far as scientists can tell, have the world’s highest rate of type 2 diabetes. The Pimas have grown to hate this superlative perhaps more than the disease itself. Mary Thomas, the 60-year-old ex-governor of the tribe and presently its lieutenant governor, drove me around the community. A few miles south of Pecos Road, we came to the St. Johns Mission, a quiet, whitewashed church. There was once a Catholic boarding school for Indian children on the grounds. Thomas said that when she was 17 and in school here, she went for an eye test and was told she had diabetes. © 2004 The Walt Disney Company. All rights reserved

Keyword: Genes & Behavior; Obesity
Link ID: 7226 - Posted: 06.24.2010

A new study published online April 21, 2005 in the American Journal of Medical Genetics Part A examines whether the recent decline in neural tube defects in Chile was due to the addition of folic acid to wheat flour in that country or to pre-existing decreasing trends. The journal is available online via Wiley InterScience at http://www.interscience.wiley.com/journal/ajmg. Recent data in Chile have suggested that the incidence of the neural tube defects spina bifida and anencephaly (a fatal condition that results in malformation of the brain) have significantly declined since January 2000, when wheat flour began to be fortified with folic acid. In that time, Chile has been fortifying its foods at double the rate of the U.S. In order to determine if the decrease was directly attributable to the addition of folic acid as opposed to an independent trend, the study examined historical data from before the fortification and compared it to data from a two-year period after fortification began. Led by Eduardo E. Castilla, of the genetics department at the Instituto Oswaldo Cruz in Rio de Janeiro, Brazil, researchers performed a survey of maternity hospitals in the ECLAMC (Latin American Collaborative Study of Congenital Malformations) network in Chile between the years 1982 and 2002. The data were divided between the pre-fortification years 1982-1989 and 1990-2000 to provide a baseline, and 2001-2002, the period during which flour was fortified. While the prevalence rates of neural tube defects did not significantly change between the two pre-fortified periods, the rate of spina bifida decreased by 51 percent and the rate of anencephaly decreased by 46 percent in the 2001-2002 period. Because different hospitals might experience different rates in neural tube defects at different times, the study examined only those hospitals with data for two consecutive periods.

Keyword: Development of the Brain
Link ID: 7225 - Posted: 04.21.2005

Amazonian ants rig up gruesome traps to snare prey before stinging them to death and carving them up to eat, a new study reveals. Allomerus decemarticulatus is a tiny tree-dwelling ant which lives in the forests of the northern Amazon. Researchers examining the relationship between different ant species and their host plants noticed that this particular ant lived on only one plant - Hirtella physophora - and that they built galleries hanging under its stems. Many ant species build these galleries as hideouts to act as sanctuaries between their nests and foraging areas. But the team, led by Jérôme Orivel at the University of Toulouse, France, spotted that A. decemarticulatus were using these galleries as traps for prey. The traps are woven together using hairs stripped from the ants’ host plant and reinforced with fungus, producing a platform with pitted holes. “The ants are always hiding just under the holes, waiting with their mandibles open. When an insect arrives they immediately grab the legs and antennae,” says Orivel. This pulling immobilises the victim, stretching it out as though being tortured on a mediaeval rack. Worker ants then clamber over their helpless prey, biting and stinging until the victim is paralysed or dead. The carcass is then chopped into small pieces while still on the rack or, more likely, carried back to the leaf pouch where the ants nest to be devoured. The surprise-attack traps are “like something out of Edgar Allan Poe”, says Mike Kaspari, an ant expert at the University of Oklahoma, US. © Copyright Reed Business Information Ltd.

Keyword: Intelligence
Link ID: 7224 - Posted: 06.24.2010

Shares in GW Pharmaceuticals rose nearly 9.5% after the UK biotech firm's prescription cannabis drug was approved for use in Canada. Sativex is used to treat the central nervous system and alleviate the symptoms of multiple sclerosis (MS). The Salisbury-based company said this was the world's first approval of a medicine derived from cannabis. Delays in development of the product - its first to come to the market - has hit GW's stock price in the past. Shares in GW shares closed up 11.5 pence at 132.5p on the London Stock Exchange on Tuesday. Sativex, administered by a mouth spray, will be marketed in Canada by German company Bayer. GW said it hoped to launch Sativex in Canada in late spring. "The approval of Sativex reflects the urgent need for additional treatment options in the field of neuropathic pain in MS," said Dr Allan Gordon of Mount Sinai Hospital, Toronto, in a statement issued by regulators Health Canada. Some MS patients already smoke cannabis to relieve their symptoms. Satifex consists of a cannabis extract containing tetrahydrocannabinol and cannabidiol. GW had originally hoped to win UK approval for Sativex in 2003. (C)BBC

Keyword: Drug Abuse
Link ID: 7223 - Posted: 04.20.2005

By PETER D. KRAMER Shortly after the publication of my book ''Listening to Prozac,'' 12 years ago, I became immersed in depression. Not my own. I was contented enough in the slog through midlife. But mood disorder surrounded me, in my contacts with patients and readers. To my mind, my book was never really about depression. Taking the new antidepressants, some of my patients said they found themselves more confident and decisive. I used these claims as a jumping-off point for speculation: what if future medications had the potential to modify personality traits in people who had never experienced mood disorder? If doctors were given access to such drugs, how should they prescribe them? The inquiry moved from medical ethics to social criticism: what does our culture demand of us, in the way of assertiveness? It was the medications' extra effects -- on personality, not on the symptoms of depression -- that provoked this line of thought. For centuries, doctors have treated depressed patients, using medication and psychological strategies. Those efforts seemed uncontroversial. But authors do not determine the fate of their work. ''Listening to Prozac'' became a ''best-selling book about depression.'' I found myself speaking -- sometimes about ethics, more often about mood disorders -- with many audiences, in bookstores, at gatherings of the mentally ill and their families and at professional meetings. Invariably, as soon as I had finished my remarks, a hand would shoot up. A hearty, jovial man would rise and ask -- always the same question -- ''What if Prozac had been available in van Gogh's time?'' Copyright 2005 The New York Times Company

Keyword: Depression
Link ID: 7222 - Posted: 04.20.2005

Forgetting is bad. Remembering is always good. Or so I thought until I met patients with unexpected benefits of memory loss. "It will be a blessing if I lose my mind," one patient said. "I'll probably be happy not knowing I owe anybody!" Andy Rooney wrote, in his 1982 book, And More by Andy Rooney, "Sadness is one of the principal ingredients of memory, and there's just so much of that [that] anyone wants to bring on himself on purpose by sitting around remembering." All this raises an important question in my mind. Is forgetfulness nature's way of enforcing forgiveness, the letting go of past wrongs and sorrows, the memory of which can only sadden the ageing mind, with little chance for reconciliation and closure? In pondering this question I wonder whether the evolutionary reason for the high prevalence of Alzheimer's disease among those aged 80 or older is to shield ageing minds from the vagaries of the past, the company of friends and family severed, the sadness that comes with dreams unfulfilled. Was I being too picky in correcting the medical student who introduced his 91 year old patient as being "pleasantly demented with no complaints"? My premise—that there is nothing pleasant about Alzheimer's disease—conflicts with occasional sightings of apparently happy patients living with the disease. Maybe the medical student is right after all. Will memory enhancement therapy make these patients happier or more agitated and less functional? © 2005 BMJ Publishing Group Ltd

Keyword: Alzheimers; Learning & Memory
Link ID: 7221 - Posted: 06.24.2010

MADISON -- Unveiling a delivery method that may one day help surgeons treat the deadly neurodegenerative disease amyotrophic lateral sclerosis (ALS), researchers at the University of Wisconsin-Madison have inserted engineered human stem cells into the spinal cords of ALS-afflicted rats. Reporting their work today (April 19) in the journal Human Gene Therapy, the scientists directed certain types of neural stem cells to secrete a neuron-protecting protein before injecting them into the rat spinal cord where motor neurons reside. Motor neurons dictate muscle movement by relaying messages from the spinal cord and brain to the rest of the body. ALS causes the neurons to progressively decay and die. Notably, the UW-Madison stem cell researchers did not work with human embryonic stem cells, blank-slate cells that arise during the earliest stages of development and can develop into any of the 220 tissue and cell types in humans. Scientists have long regarded these cells as a crucial ingredient in the quest to cure spinal injuries and neurodegenerative disease. Rather, the scientists worked with more specialized neural stem cells -- known as neural progenitor cells -- that arise from primitive stem cells during the first few weeks of human brain development. Unlike embryonic stem cells, they can only develop into neural tissue and they are incapable of living forever, as embryonic stem cells can.

Keyword: ALS-Lou Gehrig's Disease ; Stem Cells
Link ID: 7220 - Posted: 04.20.2005

Although the omega-3 fatty acids found in fish are well known for their health benefits, many fish are also the primary source of mercury in the general population. Researchers from the Johns Hopkins Bloomberg School of Public Health recently completed the first study of mercury and cognitive function in urban, U.S. adults between the ages of 50 and 70 years. They found that blood mercury levels were not consistently associated with adverse performance on a broad range of tests of cognitive function. This study may help policy makers with future decisions about mercury emissions from power plants as well as fish consumption recommendations for older adults. The study is published in the April 20, 2005, issue of the Journal of the American Medical Association (JAMA). “Our study provides no evidence to challenge the government’s current recommendations for blood mercury levels, but neither does it indicate that they are safe. The key point is that the aging population may be more sensitive to toxic chemicals and this is the first study to examine mercury exposure in the older U.S. population,” said Megan Weil, MHS, lead author of the study and a PhD-candidate in the Bloomberg School of Public Health’s Department of Environmental Health Sciences. © 2005, Johns Hopkins University.

Keyword: Neurotoxins
Link ID: 7219 - Posted: 06.24.2010

The drug memantine can reduce cognitive deterioration and loss of everyday functions in patients with moderate to severe Alzheimer's disease, according to a new review of studies. Memantine's effects are small but "clinically noticeable" after patients take 20 milligrams of the drug daily for 28 weeks, according to Dr. Rupert McShane of the University of Oxford and colleagues. The effect of memantine was measured by a variety of tests that rate a patient's thinking skills, daily activity and mood. While there is no evidence that the drug can treat agitation in Alzheimer's patients, it does appear to prevent the onset of agitation, the review finds. The studies also hint at some cognitive benefits from the drug for patients with mild to moderate Alzheimer's and vascular dementia, which occurs when brain cells are starved of oxygen by blocked or diseased blood vessels. However, these changes were not clinically significant, and it remains unknown whether there is a true benefit in mild to moderate cases, McShane and colleagues write. The Food and Drug Administration approved memantine for the treatment of moderate to severe Alzheimer's dementia in 2003. The European Agency for the Evaluation of Medical Products approved the drug for similar indications in 2002. Manufacturers of the drug in Europe and the United States have applied for approval of the drug for mild to moderate Alzheimer's dementia.

Keyword: Alzheimers
Link ID: 7218 - Posted: 04.20.2005