Brain implants have been used to "read the minds" of monkeys to predict what they are about to do and even how enthusiastic they are about doing it. It is the first time such high level cognitive brain signals have been decoded and could ultimately lead to more natural thought-activated prosthetic devices for people with paralysis, says Richard Andersen project leader at the California Institute of Technology, in Pasadena, US. By decoding the signals from 96 electrodes in a region of the brain just above the ear – called the parietal cortex - the researchers were able to predict 67 per cent of the time where in their visual field trained monkeys were planning to reach. They also found that this accuracy could be improved to about 88 per cent when the monkeys expected a reward for carrying out the task. The team were even able to predict what sort of reward the monkeys were expecting - whether it was juice or just plain water – from their brain signals. "In the future you could apply this cognitive approach to language areas of the brain," says Andersen. By doing so it may be possible to decode the words someone was thinking, he says. © Copyright Reed Business Information Ltd.

Keyword: Vision
Link ID: 5779 - Posted: 06.24.2010

Contrary to popular belief, people in east Asia are no more genetically susceptible to short-sightedness than any other population group, according to researchers who have analysed past studies of the problem. The epidemics of myopia in countries such as Singapore and Japan are due solely to changes in lifestyle, they say, and similar levels could soon be seen in many western countries as lifestyles there continue to change. "As kids spend more time indoors, on computers or watching telly, we are going to become just as myopic," says Ian Morgan of the Australian National University in Canberra. Myopia is on the increase in most places, but in countries such as Singapore it has reached extraordinary levels. There, 80 per cent of 18-year-old male army recruits are myopic, up from 25 per cent just 30 years ago. Employers such as the police are having problems finding people who meet their requirements. There is also an increasing incidence of extreme myopia, which can lead to blindness. © Copyright Reed Business Information Ltd.

Keyword: Vision
Link ID: 5778 - Posted: 06.24.2010

DURHAM, N.C. -- Researchers at Duke University Medical Center have provided the first direct evidence in mice for the role of an enzyme that specifically controls the production of serotonin in the brain. Different versions of that serotonin enzyme have a major effect on brain levels of the chemical messenger, which has been linked to many basic behavioral and physiological functions including mood, emotion, sleep and appetite, the researchers reported in the July 9, 2004, issue of Science. The finding has major implications for understanding psychiatric disorders and their treatment, the researchers said. Serotonin is a "neurotransmitter," a chemical that one neuron uses to trigger a nerve impulse in its neighbors. Thus, serotonin levels can profoundly affect brain function, and therefore behavior. "For the first time, we've identified a naturally occurring genetic difference that controls the production of serotonin in the brain," said Howard Hughes Medical Institute investigator Marc Caron, Ph.D., James B. Duke professor of cell biology at Duke and senior author of the study. The finding in mice sets the stage for new insights into the role the serotonin enzyme and the gene that encodes it might play in animal behavior and human psychiatric disorders, said the researchers. Low levels of serotonin have been implicated in many disorders such as depression, anxiety, post-traumatic stress disorder and attention deficit hyperactivity disorder. © 2001-2004 Duke University Medical Center.

Keyword: ADHD; Depression
Link ID: 5777 - Posted: 06.24.2010

Mpdz gene's discovery could someday lead to addiction-reducing therapy PORTLAND, Ore. -- One of the genes that influences drug physical dependence and associated withdrawal has been identified at Oregon Health & Science University. The gene, Mpdz, is involved in physical dependence on a class of drugs known as sedative-hypnotics, which are widely used for their euphoric and sedative effects. Drugs in this class include alcohol, inhalants, barbiturates, benzodiazepines, like Rohypnol or "roofies," and some other "club drugs." Scientists in the Portland Alcohol Research Center (PARC) and the Department of Behavioral Neuroscience, OHSU School of Medicine, found Mpdz using mice bred to possess a region of a chromosome known to be associated with a predisposition to physical dependence and withdrawal from sedative-hypnotics like alcohol and barbiturates. During the four-year search, the scientists narrowed the initial field of more than 1,000 candidate genes to only five genes, and finally to one. "We know that a host of biological and environmental factors interact in a complex manner throughout the addictive process to influence drug use or abuse. We think that physical dependence on sedative-hypnotic drugs and associated withdrawal episodes constitutes a motivational force that perpetuates drug use or abuse and contributes to relapse," said Nikki Walter, research associate in behavioral neuroscience and a study co-author.

Keyword: Drug Abuse; Genes & Behavior
Link ID: 5776 - Posted: 07.09.2004

FALMOUTH, Maine - Just before summer vacation began last month, the playground at Plummer-Motz Elementary School was filled with hordes of children swinging on tires, running one another ragged around a large dirt field, and darting in and out of a wooden castle called the "maze craze." Jan Rankowski was not among them. The 9-year-old, diagnosed five years ago with Asperger Syndrome, a neurological disorder similar to autism that causes him to misunderstand the social world, was climbing on a jungle gym in his front yard. In November, after a string of complaints about what school officials said was aggressive and rude behavior, they banned Jan, who is home-schooled but spent recess with the other children, from the playground. The officials told the third-grader's parents not to bring him back until they allowed Jan to undergo an extensive evaluation known in educational parlance as a Functional Behavioral Assessment. Jan's parents, Charles Rankowski and Gayle Fitzpatrick, sued the school, charging discrimination. School officials say prohibiting Jan from going to the playground was necessary to Copyright 2004, azcentral.com.

Keyword: Autism
Link ID: 5775 - Posted: 07.09.2004

By RICK CALLAHAN, ASSOCIATED PRESS WRITER INDIANAPOLIS -- Rats fed artificial sweeteners ate three times the calories of rats given sugar, a finding the study's authors said suggests sugar-free foods may play a role in the nation's obesity epidemic. Other scientists, however, dismissed that conclusion, saying studies on people don't indicate that. One researcher called the rat study nonsense. The experiment by Purdue University researchers appears in the July issue of the International Journal of Obesity. The scientists said their rodent findings could help explain why Americans have grown fatter over the past two decades even as the nation's consumption of artificially sweetened sodas and snack foods has soared. They contend that artificial sweeteners could be interfering with people's natural ability to regulate how much they eat by distinguishing between high- and low- calorie sweets. As part of their study, they fed two groups of rats sweet-flavored liquids for 10 days. One group got only sugar-sweetened liquids, while the other was fed liquids sweetened by both sugar and saccharin. ©1996-2004 Seattle Post-Intelligencer

Keyword: Obesity
Link ID: 5774 - Posted: 06.24.2010

Researchers are to examine whether vaccinations play a part in the development of autism. A Bristol University team will also examine the possible impact of problems with birth, diet, infections and exposure to toxins. They will also test the theory that other conditions, such as coeliac disease, may increase the risk. More than 500,000 people in the UK are estimated to be affected by autism spectrum disorders. The condition affects the way people communicate and relate to people around them and sufferers have problems with everyday social interaction. They have a limited ability to develop friendships and find it hard to understand other people's emotional feelings. The incidence of the condition appears to have risen sharply over the last 30 years. However, nobody knows why this is, and it is possible that more cases are simply being diagnosed than in the past. Some scientists have suggested the MMR jab may be linked to autism. However, no research has ever proved a link, and the overwhelming majority of experts believe the vaccine is safe. The new research will be based on data generated from 14,000 children already taking part in the Children of the 90s study - a long-term project to examine the role of environment and genes on children's health. Lead researcher Professor Jean Golding said: "Because of the number of children we'll be looking at, and the quality and type of data available, our study should help find the answers to a number of currently unanswered questions about the environmental risks for developing autism spectrum disorders. (C)BBC

Keyword: Autism
Link ID: 5773 - Posted: 07.08.2004

Watching too much television and spending too long in front of a computer is behind rising rates of short-sightedness, say scientists. Australian researchers examined rising rates of short-sightedness in Asia. Countries like Japan and Singapore have seen a sharp increase in cases in recent years. Some experts say genes are behind the rise. But the researchers found people's lifestyle was to blame, according to a report in New Scientist magazine. They said the findings may also explain rising rates of short-sightedness in other parts of the world. East Asia has much higher rates of short-sightedness or myopia than other parts of the world. In Singapore, 80% of 18-year-old men recruited to the army are short-sighted. This compares with 25% just 30 years ago. There has also been an increase in the number of people with extreme myopia, which can lead to blindness. (C)BBC

Keyword: Vision; Development of the Brain
Link ID: 5772 - Posted: 07.08.2004

By ROBERT PEAR WASHINGTON, - Congressional investigators said Wednesday that 15,000 children with psychiatric disorders were improperly incarcerated last year because no mental health services were available. The figures were compiled by the Democratic staff of the House Committee on Government Reform in the first such nationwide survey of juvenile detention centers. "The use of juvenile detention facilities to warehouse children with mental disorders is a serious national problem,'' said Senator Susan Collins, Republican of Maine, who sought the survey with Representative Henry A. Waxman, Democrat of California. The study, presented at a hearing of the Senate Committee on Governmental Affairs, found that children as young as 7 were incarcerated because of a lack of access to mental health care. More than 340 detention centers, two-thirds of those that responded to the survey, said youths with mental disorders were being locked up because there was no place else for them to go while awaiting treatment. Seventy-one centers in 33 states said they were holding mentally ill youngsters with no charges. Copyright 2004 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 5771 - Posted: 07.08.2004

Two years ago, Stephen Bloom and his group at Imperial College London touched off a scramble in labs around the world with the latest discovery of how the body regulates appetite. The investigators reported in Nature that a molecule called peptide YY3-36 (PYY3-36), when injected into rodents, dampens appetite for 12 hours or more. But in an unusual joint letter published online today by Nature, more than 40 scientists announced that they cannot reproduce Bloom's central findings. Endocrinologist Bloom and his colleagues reported that PYY3-36 is formed in the digestive tract after eating and travels to the brain, where the peptide controls short-term appetite. Subsequently, other teams tried to reproduce the findings--without success. As word spread that several labs were experiencing similar troubles, the investigators decided to collaborate. They bought rodents from the same vendor as Bloom, purchased food from the same supplier, and injected animals at exactly the same time of day with the same kind of syringes filled with PYY3-36 manufactured by the same chemical supply house. "And still we weren't able to reproduce the results," says Mattias Tschöp of the University of Cincinnati in Ohio. Copyright © 2004 by the American Association for the Advancement of Science.

Keyword: Obesity
Link ID: 5770 - Posted: 06.24.2010

University of Chicago researchers may have found a crucial clue to understanding and ultimately eliminating sudden infant death syndrome, the leading cause of post-neonatal mortality in the United States. Approximately 3,000 infants die each year from the disorder, according to the Centers for Disease Control and Prevention. In the July 8, 2004, issue of the journal Neuron, the researchers describe the specific group of neurons that are responsible for gasping and what happens to these cells when they are deprived of oxygen. Since gasping resets the normal breathing pattern for babies, the scientists suspect that a malfunction in these respiratory pacemakers is the cellular mechanism that leads to SIDS. "This paper sets the groundwork for everything that has to do with breathing," says lead author Jan-Marino Ramirez, an associate professor of organismal biology and anatomy. "We've now defined the players in the system." The study follows a paper published in Nature four years ago in which Ramirez and colleagues showed that the same network of respiratory cells in the brainstem controls different forms of breathing: the sigh, the gasp and normal rhythm.

Keyword: Sleep
Link ID: 5769 - Posted: 07.08.2004

The selective killing of spinal cord neurons in amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, occurs when tiny cellular components called mitochondria actively recruit a mutant disease-causing protein into specific neuron cells, according to new research by University of California, San Diego (UCSD) School of Medicine investigators. Published in the July 8, 2004 issue of the journal Neuron, the findings identify mitochondria as the focus of ALS toxicity and provide the first explanation of how a mutant protein called SOD1 that occurs in all cells in the body is damaging only to specific neuron cells. The result is ALS, a progressive degeneration of motor nerve cells in the spinal cord that leads to wasted muscles and premature death in middle-aged adults. Found in all cells, mitochondria provide cellular energy in their role as the body's power generators. In addition, mitochondria are intricately involved in a process called apoptosis, or programmed cell death, which is the body's normal method of disposing of damaged, unwanted or unneeded cells. "We believe that when the mutant SOD1 binds to mitochondria, it affects the ability of these components to generate cell energy," said the study's senior author, Don Cleveland, Ph.D., a UCSD professor of medicine, neurosciences, and cellular and molecular medicine, and a faculty member of the Ludwig Institute for Cancer Research.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 5768 - Posted: 07.08.2004

Heavy drinking during the teenage years begins taking a serious health toll by the time people are 24 years old. A University of Washington study has found that people who began binge drinking at age 13 and continued throughout adolescence were nearly four times as likely to be overweight or obese and almost 3½ times as likely to have high blood pressure when they were 24 years old than were people who never or rarely drank heavily during adolescence. It also found four distinct patterns or trajectories of binge drinking among teenagers. The study looked at young adult health consequences of adolescent binge drinking – consuming five or more drinks on a single occasion – between the ages of 13 and 18. Previous research has shown that adolescent binge drinking results in a number of immediate negative consequences, including involvement in fatal or injurious automobile accidents and engaging in risky sexual behavior. But little had been known about the effects of adolescent heavy drinking into young adulthood. "In our analysis, we did look at whether people were currently binge drinking at age 24. We controlled for it, along with other factors, such as adolescent drug use, ethnicity, gender and family poverty, and we still saw different patterns of health outcomes depending on which trajectory of binge drinking teenagers followed," said Karl Hill, a co-author of the study and director of the Seattle Social Development Project. "It is the pattern of early and on-going drinking that is the key."

Keyword: Drug Abuse; Obesity
Link ID: 5767 - Posted: 06.24.2010

People who have so-called mini-strokes should be assessed by specialists within days rather than weeks, say doctors. The Royal College of Physicians said this could prevent many people going on to have full strokes. At present, people who have mini-strokes can wait weeks to be assessed by specialist doctors in NHS hospitals. New guidelines from the college suggest they should now be seen within a maximum of seven days. The college also recommends that people who have more than one mini-stroke in a week should be seen by specialists immediately. Mini-strokes, or transient ischaemic attacks (TIAs), occur when bloodflow to the brain is blocked. This can cause eyesight or brain problems. However, unlike full strokes, these symptoms disappear within 24 hours. Overall, 130,000 people in England and Wales have a stroke each year. One in three will die within a month. Another third will never fully recover. (C)BBC

Keyword: Stroke
Link ID: 5766 - Posted: 07.07.2004

The most common form of Alzheimer's disease isn't inherited, and little is known about its causes. Now, researchers have found a handful of DNA mutations that arise more frequently in patients with the disorder. The results bolster earlier suggestions that Alzheimer's is caused partly by deficits in cells' energy plants. Researchers have found some of the genes involved in the familial form of Alzheimer's, which accounts for about 10% of cases and typically strikes people in their 60s, but they've had little success finding genetic glitches associated with the more common, late-onset form. Some evidence has pointed to a lifelong buildup of mutations in the DNA inside mitochondria, the energy-producing organelles inside cells. For example, Douglas Wallace, now at the University of California, Irvine, and colleagues found that a small percentage of Alzheimer's patients carried a specific mutation in their mitochondrial DNA. But that simply couldn't account for the large number of late-onset victims. So they kept up the search. After examining every mitochondrial gene that codes for a protein, to no avail, Wallace's team decided to check for mutations in a short DNA region that regulates expression of mitochondrial genes and helps copy mitochondrial DNA when cells divide. Comparing DNA from the brains of 23 Alzheimer's patients against 40 healthy brains matched for age, the team found one mutation that occurred exclusively in Alzheimer's brains--65% of diseased brains contained this mutation, the team reports online this week in the Proceedings of the National Academy of Sciences. Other mutations were also more prevalent in Alzheimer's patients. In addition, the team noticed that brains of people who died of Alzheimer's before age 80 harbored a few mutations in many cells, whereas those who died later carried a greater variety of mutations in fewer cells. That suggests that mutations that occur early in life and accumulate in brain cells may heighten the risk of disease. Copyright © 2004 by the American Association for the Advancement of Science

Keyword: Alzheimers; Genes & Behavior
Link ID: 5765 - Posted: 06.24.2010

by Garry Walter, M.D., and Andrew McDonald, M.D. Hollywood has had a long-standing love affair with psychiatry (Gabbard and Gabbard, 1999; Schneider, 1987, 1977). Dating from the first psychiatric film, Dr. Dippy's Sanitarium (1906), almost 500 movies dealing with the specialty have been made. While the film industry has demonstrated a particular fascination for depicting psychotherapy, physical treatments including electroconvulsive therapy have also been featured (McDonald and Walter, 2001; Walter, 1998). Indeed, some of the major psychiatric films--The Snake Pit (1948), One Flew Over the Cuckoo's Nest (1975), Frances (1982) and Shine (1996)--have prominent convulsive therapy scenes. (See the Table for a selected chronology of films depicting ECT.) Portrayals of ECT reflect and influence public attitudes toward the treatment. For example, in a survey of lay attitudes toward convulsive therapy, the majority of respondents who had seen One Flew Over the Cuckoo's Nest were "put off ECT" by the film (O'Shea and McGennis, 1983). In another study, one-third of medical students decreased their support for the treatment after being shown ECT scenes from movies, and the proportion of students who would dissuade a family member or friend from having ECT rose from less than 10% prior to viewing to almost 25% afterward (Walter et al., 2002). So what is the legacy of portrayals that have been so abhorrent, and are there any exceptions to the rule? Electroconvulsive therapy made its film debut in 1948 in Anatole Litvak's Academy Award-winning The Snake Pit, a movie set at Juniper Hill State Hospital. The film follows the path to recovery of Virginia Cunningham (Olivia de Havilland), a young writer who develops a psychosis shortly after marriage. © 2004 Psychiatric Times. All rights reserved.

Keyword: Depression
Link ID: 5764 - Posted: 06.24.2010

by William Kanapaux The underdiagnosis and undertreatment of depression in older adults has been well documented in recent years, and while certain gains have been made over the last decade, researchers say there is much room for improvement. A study appearing in the Journal of the American Geriatrics Society (2003;51[12]:1718-1728) found that while rates of diagnosis for depression for patients aged 65 and older increased dramatically during the 1990s, "significant disparities by age, ethnicity, and supplemental insurance coverage persist in treatment of those diagnosed." The researchers, led by Stephen Crystal, Ph.D., examined Medicare claims and interview data from 1992 through 1998 for nearly 21,000 recipients aged 65 and older who lived in community settings. They found that depression diagnoses more than doubled by 1998, to 5.8%. However, certain groups were significantly less likely to receive treatment: people aged 75 and older, people of "Hispanic or other" ethnicity, and people without supplemental insurance coverage. Hispanic beneficiaries who were diagnosed with depression received no treatment 43% of the time, compared with 31.9% of elderly white Medicare beneficiaries. People without supplemental insurance received no treatment 50.8% of the time, compared with 31.5% of beneficiaries with extra coverage. And 40.9% of diagnosed beneficiaries who were 80 and older received no treatment, compared with 24.4% of beneficiaries aged 65 to 69. Even in the best of conditions, mental health treatment for late-life depression remains largely inadequate, as indicated by the disproportionate rate of suicide among the elderly. © 2004 Psychiatric Times. All rights reserved.

Keyword: Depression
Link ID: 5763 - Posted: 06.24.2010

by Stephen I. Deutsch, M.D., Ph.D., Richard B. Rosse, M.D., Lynn H. Deutsch, D.O., and Judy Eller The majority of the pharmacological mechanisms of action of the current medications for the treatment of Alzheimer's disease (AD) are based on the assumption of a cholinergic deficiency. Indeed, the intactness of cholinergic projections, particularly those arising in the basal forebrain, is crucial for learning and memory. Elderly patients with advanced AD consistently show histopathological evidence of degeneration of cholinergic projection pathways and reduced levels and activity of choline acetyltransferase (ChAT), a biochemical marker of cholinergic neurons. Lesions of cholinergic nuclei (i.e., nucleus basalis magnocellularis and medial septum/diagonal band) that project to the neocortex and hippocampus and administration of centrally acting muscarinic and nicotinic acetylcholine receptor antagonists have been shown to disrupt memory performance in a variety of paradigms in animals (Terry and Buccafusco, 2003). However, biochemical markers of cholinergic neurons, such as the activity of ChAT and acetylcholinesterase (AChE) and levels of vesicular acetylcholine transporter protein, were not reduced in autopsy studies of patients with recently diagnosed mild AD or mild cognitive impairment (Davis et al., 1999; DeKosky et al., 2002). On the surface, these data seem to challenge long-held assumptions about cholinergic dysfunction in AD--especially its early role in AD pathogenesis. © 2004 Psychiatric Times. All rights reserved.

Keyword: Alzheimers
Link ID: 5762 - Posted: 06.24.2010

Senior citizens played an important role in the dramatic spread of human civilisation some 30,000 years ago, a study of the human fossil record has shown. Rachel Caspari at the University of Michigan and Sang-Hee Lee at the University of California at Riverside studied dental fossils belonging to early humans and pre-human species dating back 3 million years. They judged the age of specimens by examining wear to teeth and classified "old" as twice the age of sexual maturity - roughly 30 years. The fossils examined included Australopithecines, who lived up to three million years ago, Homo erectus, a more human-like ancestor that emerged 1 million years ago, as along with Neanderthals and early modern humans, which co-existed some 50,000 years ago. Caspari and Lee found a five-fold increase the number of individuals surviving into old age in the Early Upper Palaeolithic period - around 30,000 years ago. This coincides with an explosive population growth of modern humans and the spread of archaeological artefacts that suggest the development of more complex social organisation. "In the Upper Paleolithic the proportion just skyrocketed," Caspari said. "It was just unbelievable. We didn't expect that." © Copyright Reed Business Information Ltd.

Keyword: Evolution
Link ID: 5761 - Posted: 06.24.2010

By LOUIS B. PARKS Copyright 2004 Houston Chronicle Write this down so you won't forget it later. Eating certain berries and vegetables on a regular basis now may keep you from age-related memory problems down the road. Granted, it has not been proved in human studies, but it certainly works for lab rats, which have similar brain components and suffer from age-related memory loss for reasons similar to humans. Now, a study coordinated by University of Houston-Clear Lake researchers shows it might also work in people. And since we are talking about readily available foods such as blueberries, strawberries and spinach, what have we got to lose by hitting the produce aisle? "We have an opportunity to ensure a better and healthier aging," said Pilar Goyarzu of the National Autonomous University of Mexico. Goyarzu participated in the research project coordinated by Dr. David Malin of the University of Houston-Clear Lake. Findings are published in an upcoming issue of Nutritional Neuroscience. The researchers used blueberries because their antioxidant properties are believed to counter the damaging effects of free radicals. Free radicals are compounds that are destructively reactive with other compounds, so they can damage important cellular components and contribute to aging.

Keyword: Learning & Memory
Link ID: 5760 - Posted: 07.07.2004