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By SUSAN CAMPBELL, Courant Staff Writer A Connecticut scientist who helped chart the frontal lobe of the human brain died Thursday after she was hit by a car. Patricia Goldman-Rakic, Yale University School of Medicine professor of neuroscience, neurology, psychiatry and psychology, was crossing Whitney Avenue in Hamden Tuesday about 5 p.m. when she was struck by a car driven by Christopher Cawley, 19, of Hamden, police said. She was taken to Yale-New Haven Hospital with a broken leg and head injuries. She was 66. Goldman-Rakic was the first researcher to find that certain brain cells are dedicated to specific memory tasks. Her research has helped doctors understand schizophrenia, Alzheimer's disease and Parkinson's disease. She was recognized by a variety of professional organizations for her work. Copyright © 2003 by The Hartford Courant
Keyword: Miscellaneous
Link ID: 4115 - Posted: 06.24.2010
A burst of brain activity recorded by scientists could offer clues to a baby's level of understanding of the world around it. The researchers involved, from Birkbeck College, and University College London, believe their finding could begin to settle a controversial argument on baby brain development. When an object is shown to six-month-old babies, then hidden, they often behave as if it is no longer present. It appears to be "out of sight, out of mind", as far as their level of understanding is concerned. But scientists still suspect the baby, to some extent, does understand the object is still around, just hidden, even if it shows no physical signs of awareness. The London team wired up their babies to a harmless "hair-net" of sensors which measured electrical activity in the brain. (C) BBC
Keyword: Development of the Brain
Link ID: 4114 - Posted: 08.02.2003
For years researchers believed that the brain's ability to detect light relied solely on specialized nerve cells in the eyes, termed rods and cones. But now recent studies suggest otherwise. Although rods and cones are the light detectors that help us visualize images, another set of detectors appears to form a second eye system that monitors levels of brightness in the environment and aids a variety of different brain functions, including the control of our daily sleep and waking rhythms. Continued study could lead to the development of treatments that help people recover from problems tied to changes in environmental lighting such as jet lag. The sun seeps through the shades, radiating brighter and brighter. You lift your head from the pillow. Rise and shine. Researchers have long assumed that structures in the eyes known as rods and cones were crucial to this scenario. They believed that we relied solely on these specialized nerve cells for all of our light sensing, including the detection of the sun’s glare through the bedroom window, which has a knack for waking us up. It’s common knowledge that the rods and cones detect light information so we can visualize the window itself as well as other contents of the world, so the theory made sense. Copyright © 2003 Society for Neuroscience
Keyword: Vision; Biological Rhythms
Link ID: 4113 - Posted: 06.24.2010
Earlier studies suggesting that painkillers might also double as "brain pills" for Alzheimer's disease are being called into question. As this ScienCentral News video reports, new research has lessened the hope that painkillers can slow the disease's progress. Dashed Hopes: Alzheimer's disease, a progressive, degenerative disease of the brain, devastates roughly 4 million people in the U.S. today. One in 10 people over 65 and nearly half of those over 85 have the disease. "Because this is a disease of aging, and our population is getting older, we project 14 to 15 million cases by mid century," says Paul Aisen, professor of neurology and medicine and director of the Memory Disorders Program at the Georgetown University School of Medicine . "The annual estimated cost of this disease today is 100 billion dollars per year. This is one of the three most important healthcare problems that we face, along with cancer and cardiovascular disease." © ScienCentral, 2000-2003.
Keyword: Alzheimers
Link ID: 4112 - Posted: 06.24.2010
Study Involving 4,023 Adolescents Finds That Exposure To Interpersonal Violence Increases The Risk For PTSD WASHINGTON — The carefree days of youth apparently aren’t so carefree anymore – if they ever were – according to the results of a new study of America’s adolescents. The study, involving 4,023 youth (ages 12-17) interviewed by telephone, finds that roughly 16 percent of boys and 19 percent of girls met the criteria for at least one of the following diagnosis: posttraumatic stress disorder (PTSD), major depressive episode and substance abuse/dependence. The findings appear in the August issue of the Journal of Consulting and Clinical Psychology, published by the American Psychological Association (APA). Study lead author Dean G. Kilpatrick, Ph.D. and colleagues from the National Crime Victims Research and Treatment Center at the Medical University of South Carolina were particularly struck by the prevalence of PTSD in the national sample of adolescents. “Nearly four percent of the boys (3.7%) and over six percent of the girls (6.3%) reported PTSD symptoms during the preceding six months, indicating that a high percentage of youth in the United States encounter traumatic events and experience significant emotional responses associated with these events,” according to Dr. Kilpatrick. © 2003 American Psychological Association
Keyword: Stress
Link ID: 4111 - Posted: 06.24.2010
Biologists look into DNA for the secrets of long life John Travis For more than a decade, Cynthia Kenyon has watched microscopic worms of the species Caenorhabditis elegans live far longer than they should. She has seen mutant strains of this worm, which is normally dead and gone after a mere 2 or 3 weeks, last well into their second month. It's as if a person lived to be 200 years old. Kenyon's long-lived worms are a result of mutations in individual genes. That's a radical notion to many scientists who have long thought of aging as an uncontrollable process of deterioration that isn't regulated by single genes. "There have to be genes that affect life span," counters Kenyon of the University of California, San Francisco. Noting the dramatic differences in life span among various animals—a mouse may last for 2 years while a bat can live for half a century—Kenyon has become convinced that longevity has evolved in animals many times. She argues that her long-lived nematodes can reveal some of the fundamental molecular biology that controls longevity in more-complex organisms, even people. In 1993, Kenyon and her colleagues jump-started the field of aging genetics when they reported on a mutant strain of C. elegans that lives twice as long as normal. It showed the largest proportional lifespan extension of any animal known at the time. Researchers eventually determined that this long-lived nematode strain arose from a defect in a hormone-triggered cascade of molecular signals that resembles one in people that is prompted by the hormone insulin. Mutations affecting a similar hormone-driven cascade in fruit flies can lengthen the lives of these insects as well. Copyright ©2003 Science Service.
Keyword: Hormones & Behavior
Link ID: 4110 - Posted: 06.24.2010
John Travis An enzyme prevents brain cells in aging mice from developing knots of proteins resembling those that are a hallmark of Alzheimer's disease, scientists report. Known as Pin1, the enzyme could form the basis of new treatments for the memory-stealing disorder. In 1995, Kun Ping Lu of Beth Israel Deaconess Medical Center in Boston and Tony Hunter of the Salk Institute for Biological Studies in La Jolla, Calif., discovered Pin1. They subsequently showed that it interacts with a protein called tau, an important component of one of the two brain lesions seen in Alzheimer's disease. Known as tangles, these snarls of tau filaments turn up inside nerve cells. In contrast, the other lesion consists of an abnormal buildup outside nerve cells of a protein fragment known as beta-amyloid. Most neuroscientists favor the hypothesis that beta-amyloid triggers the brain-cell loss in Alzheimer's disease, but some argue that tau is equally, if not more, important. Tau protein normally shapes a cell's interior skeleton, but in Alzheimer's disease, molecular tags called phosphates get added to tau. This embellishment seems to promote tangle formation. Copyright ©2003 Science Service.
Keyword: Alzheimers
Link ID: 4109 - Posted: 06.24.2010
A ubiquitous signaling molecule, nitric oxide (NO), turns off the production of new neurons in the adult brain, researchers have discovered. By shutting down this off switch, doctors may one day be able to generate new neurons in the brains of patients suffering from neurological diseases or traumatic injury. Most neurons in the human brain are born while the fetus is still tucked inside its mother's womb. But in recent years, researchers have discovered that adult brains have stem cells that develop into brand-new nerve cells later in life. Doctors are tantalized by this because many ailments associated with aging, such as Parkinson's or Alzheimer's disease, are caused by degeneration of neurons in the brain. If doctors could stimulate neuron development at will, it might be possible to slow or even reverse the damage caused by such diseases. Until now, however, researchers have made little progress in understanding what turns on adult neuron development. So New York neuroscientists Grigori Enikolopov of the Cold Spring Harbor Laboratory and Steven Goldman of Cornell University decided to look instead for the off switch. They focused on an enzyme called neuronal nitric oxide synthase (nNOS), suspected to put the brakes on cell proliferation by producing NO. Using rats, the team injected a nNOS inhibitor into areas of the brain where new stem cells are known to divide. To their surprise, the number of stem cells that developed into neurons increased by 70%. "It was like we released the parking brake," said Enikolopov. A neuron-specific dye proved that the new stem cells had indeed become neurons. Copyright © 2003 by the American Association for the Advancement of Science.
Keyword: Neurogenesis
Link ID: 4108 - Posted: 06.24.2010
By TINA HESMAN Post-Dispatch New research by neuroscientists at Washington University suggests that anti-depressant drugs may have additional benefits beyond helping patients feel better now. In a study published today in the American Journal of Psychiatry, Dr. Yvette I. Sheline and her colleagues found that women who had taken drugs to fight depression had less shrinkage in a region of the brain known as the hippocampus than women whose depression was left untreated. The hippocampus is a part of the brain involved in learning and memory. People with smaller hippocampus volumes tend to perform poorly on verbal memory tests, Sheline said. And depression has been linked to an increased risk of Alzheimer's disease. Anti-depressant drugs may help stave off those complications by keeping the hippocampus pumped up. St. Louis Post-Dispatch COPYRIGHT 2003
Keyword: Depression
Link ID: 4107 - Posted: 08.02.2003
New Study Sharpens Debate on Men, Sex and Gender Roles By Shankar Vedantam Washington Post Staff Writer A fierce debate about whether jealousy, lust and sexual attraction are hardwired in the brain or are the products of culture and upbringing has recently been ignited by the growing influence of a school of psychology that sees the hidden hand of evolution in everyday life. Fresh sparks flew last month when a study of more than 16,000 people from every inhabited continent found that men everywhere -- whether single, married or gay -- want more sexual partners than women do. "This study provides the largest and most comprehensive test yet conducted on whether the sexes differ in the desire for sexual variety," wrote lead researcher David P. Schmitt, an evolutionary psychologist at Bradley University in Peoria, Ill. "The results are strong and conclusive -- the sexes differ, and these differences appear to be universal." © 2003 The Washington Post Company
Keyword: Sexual Behavior; Evolution
Link ID: 4106 - Posted: 06.24.2010
Sylvia Pagán Westphal Breathing problems are to blame for many cases of bed-wetting in children, and perhaps even in some adults too. And a simple treatment might solve the problem within weeks. That, at least, is the claim of a few researchers. If you find it implausible, you are not the only one. "When I speak to professionals, they shake their heads in disbelief," says Derek Mahony, an orthodontist in Sydney, Australia, who is about to start a trial of a potential treatment. Very few doctors and parents are even aware there may be a link, he says. Much of the evidence comes from follow-up studies of children who have enlarged adenoids or tonsils removed. For instance, a 2001 study of 321 children found that over a third of them wet their beds prior to surgery. Of these, 63 per cent stopped completely three months after surgery (International Journal of Pediatric Otorhinolaryngology, vol 59, p 115). Other studies have produced similar results. © Copyright Reed Business Information Ltd.
Keyword: Sleep
Link ID: 4105 - Posted: 06.24.2010
By DAVID TULLER They are called smart pills or brain boosters or, to use the preferred pharmaceutical term, cognitive enhancers. But whatever the name given to compounds created to prevent or treat memory loss, drug companies and supplement producers — eager to meet the demands of a rapidly growing market — are scrambling to exploit what they view as an enormous medical and economic opportunity. Three drugs being prescribed for Alzheimer's disease — donepezil (Aricept), galantamine (Reminyl) and rivastigmine (Exelon ) — have been shown to delay somewhat the loss of mental abilities in people with the illness. So has the drug memantine, which has been used for years in Europe but has not been approved in the United States. Some experts also say that performing mental exercises and adding fish oil to the diet can delay memory decline. Copyright 2003 The New York Times Company
Keyword: Alzheimers; Learning & Memory
Link ID: 4104 - Posted: 06.24.2010
Age-dependent learning deficit can be overcome by the reduced production of a potassium channel in the mouse model All of us experience a successive decline in learning and memory capacities with ageing. In the course of their investigations of the neurophysiological basis of this decline, Thomas Blank, Ingrid Nijholt, Min-Jeong Kye, Jelena Radulovic, and Joachim Spiess from the Max Planck Institute for Experimental Medicine in Göttingen have obtained new insight into the mechanisms of age-related learning deficits in the mouse model. In experiments with mice, the Max Planck researchers were able to revert the observed age-related learning and memory deficits by down-regulation of calcium-activated potassium channels (SK3) located in the hippocampus, a brain region recognized to be important for learning and memory. The researchers published their results as a Brief Communication in the journal Nature Neuroscience. In the study, young (4-6 months) and aged mice (22-24 months) had to learn that a defined tone was associated with a mild electric footshock serving as an aversive stimulus. If the tone was immediately followed by a footshock, young and aged mice remembered easily the association on the following day. They showed their memory by a so-called "freezing response" when exposed to the same tone used for training, but without application of a foot shock. This freezing, a naturally occurring defense behavior, is characterized by complete immobility of the mouse. The scientists then generated a more complex learning task by separating the tone from the shock by several seconds. As result of this change, the task now required specifically the hippocampus. Under these conditions, the aged mice were strongly impaired in comparison to the young mice. In agreement with the behavioral differences between aged and young mice, the scientists observed that "long-term potentiation" (LTP), an electrophysiological phenomenon indicating neuronal plasticity was lower in hippocampal brain tissue of aged mice when compared to LTP in hippocampus of young mice.
Keyword: Intelligence; Alzheimers
Link ID: 4103 - Posted: 06.24.2010
Rodent 'g' might reveal genes for intellect. HELEN PEARSON Some mice are cleverer than others, say US neuroscientists. Their rodent equivalent of an IQ test might fuel the controversial pursuit for genes linked to human intelligence. Scientists have long used a factor called general intelligence or 'g' to rate people's brainpower. The measure spans verbal, logical and mathematical tasks - so a person with a big 'g' tends to score highly in all intelligence quotient (IQ) tests, and do well in school and work. Mice have a version of 'g', according to a team led by Louis Matzel of Rutgers University in Piscataway, New Jersey1. Animals that come top in one learning test often score better on others, they found: a maze champion might be a sniffing sensation too. "Once in a while you come across one that's absolutely stunning," says Matzel. © Nature News Service / Macmillan Magazines Ltd 2003
Keyword: Intelligence; Genes & Behavior
Link ID: 4102 - Posted: 06.24.2010
Mouse dementia model hints that protein prevents brain degeneration. HELEN R. PILCHER A protein called Pin1 may prevent degenerative brain disorders from developing. When it is removed, ageing mice develop symptoms similar to those of Alzheimer's disease, a new study reveals1. Future human therapies may seek to boost Pin1 levels. Pin1 is an enzyme. In the test tube, it hastens the untangling of clumps of a spaghetti-like protein called tau that build up inside sickly, ageing nerve cells. "By increasing Pin1 function in degenerating neurons, we might be able to protect the brain from Alzheimer's disease," says Kun Ping Lu of Harvard Medical School in Boston, who led the study. © Nature News Service / Macmillan Magazines Ltd 2003
Keyword: Alzheimers
Link ID: 4101 - Posted: 06.24.2010
Self-awareness makes some yawn-susceptible. HELEN PEARSON Self-aware or empathetic people are more likely to catch the yawns, say US researchers1. Contagious yawning is known to be more than coincidence. Studies have shown that 40-60% of people who watch videos or hear talk about yawning end up joining in. But psychologists have wondered what causes it. "It seems like such a hokey phenomenon," says psychologist Steven Platek at Drexel University in Philadelphia. Platek and his colleagues at the State University of New York in Albany sat subjects in front of videos of others yawning and tallied their responses to find out why people are susceptible or immune to contracting yawns. © Nature News Service / Macmillan Magazines Ltd 2003
Keyword: Emotions
Link ID: 4100 - Posted: 06.24.2010
St. Louis, –- Studying women with histories of clinical depression, investigators at Washington University School of Medicine in St. Louis found that the use of antidepressant drugs appears to protect a key brain structure often damaged by depression. Previous research has shown that a region of the brain involved in learning and memory, called the hippocampus, is smaller in people who have been clinically depressed than in those who never have suffered a depressive episode. Now, researchers have found that this region is not quite as small in depressed patients who have taken antidepressant drugs. The study, led by Yvette I. Sheline, M.D., associate professor of psychiatry, radiology and neurology, appears in the August issue of the American Journal of Psychiatry. The hippocampus is a part of the brain's limbic system, a group of structures important to emotion and motivation. Using high-resolution magnetic resonance imaging (MRI), Sheline's team measured hippocampal volumes in 38 women who had experienced an average of five episodes of major depression in their lifetimes. Only some of those episodes had been treated with antidepressant drugs.
Keyword: Depression
Link ID: 4099 - Posted: 06.24.2010
By ABRAHAM VERGHESE In the early mornings, when I head out to work, I often see the same middle-aged jogger go by, fussing with his stopwatch. Though his pace is rapid, it is also shuddering, like a cart with a wobbly wheel. I picture bone grinding on bone with no cartilage left to intervene. And yet it is not pain that shows on his face but pleasure. I speculate about this man even as I envy him. Exercise for him is its own reward. It is life affirming and it is his addiction. My addiction is tennis. In summer I may hobble around home and office, but on the court, once I hear the opening pop of a new can of balls, pain is forgotten, and I lunge and sprint with abandon. My game peaked 10 years ago and then came down to a steady club level. Since then, the biggest change is in the time it takes to recover from my on-court exertions. There was a week not long ago, for example, when I dreaded shaking hands because my elbow hurt, I limped from Achilles tendinitis, lying flat was preferable to sitting because my back ached and the Advil was taking its toll on my stomach. And yet, when my partner called to see if I would play, I couldn't get out the door fast enough. I felt comforted that even President Bush, a committed exerciser, had complained just that month of aching knees. Last month, it was revealed he had torn his calf muscle in April. He is no exception. On the courts, I see players his age, or mine (upper 40's), wearing strange patellar bands or air-filled forearm straps or thigh wraps or wrist braces, not to mention magnets parked over various body sites. No doubt at home they have gel packs cooling in the freezer and supersize bottles of Motrin. All for good health! Copyright 2003 The New York Times Company
Keyword: Pain & Touch
Link ID: 4098 - Posted: 07.27.2003
By RICHARD PÉREZ-PEÑA For several years, new drugs have offered powerful hope for people who suffer strokes, cutting the risk of death or disability. But the vast majority of stroke patients never get that medicine, because they are not treated quickly enough. New York City, New York State and several hospitals in Brooklyn and Queens have set out to change that, accelerating treatment in the precious first hours when a stroke patient's brain is being damaged beyond repair. That makes New York one of the few cities around the country to adopt practices that neurologists have spent years pushing for. The State Department of Health, which is overseeing the project, hopes to take it citywide and even statewide in the near future. Copyright 2003 The New York Times Company
Keyword: Stroke
Link ID: 4097 - Posted: 07.27.2003
By NICHOLAS WADE When Julius Caesar was touring the Spanish city of Cadiz in his early 30's, the ancient Roman biographer Suetonius reports, he came across a statue of Alexander the Great and wept beside it. Alexander at the same age had conquered the known world, while Caesar was just a minor Roman official, a source of severe chagrin to the ambitious future autocrat. It must be almost equally discouraging for scientists to see the graph that plots the age at which eminent male scientists make their big discoveries. It peaks at age 30 and then plummets, giving precious little time after one's hard-earned Ph.D. to get that invitation from the Nobel prize committee. The productivity of jazz musicians and painters is also highest in their mid-30's. And it's not just creativity that attains its zenith early in the male career. Crime, too, follows just the same parabolic curve. Dr. Satoshi Kanazawa, an evolutionary psychologist at the London School of Economics who has studied these patterns of male achievement, believes he has the explanation. Young men in any profession are driven to seek wealth and prestige because these attributes are attractive to women. Once men's urges to start a family have been satisfied, the wellsprings of productivity, whether in science, art or crime, run dry, Dr. Kanazawa suggests. Copyright 2003 The New York Times Company
Keyword: Sexual Behavior; Evolution
Link ID: 4096 - Posted: 07.27.2003


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