The identity of the protein which is key to developing long-term memory has been confirmed. say US scientists. The discovery may lead to advancements in treatment for Alzheimer's disease and other people with memory loss. Scientists have suspected for a long time that the mBDNF protein plays a role in memory development. But the Institutes of Health team claims in the journal Science to have proved the protein is the key, using experiments on mouse brains. Protein mBDNF, which stands for mature brain-derived neurotrophic factor, is produced by a chemical reaction involving the enzyme plasmin and proBDNF. The team carried out a series of experiments on mice brains, which are easy to mutate, to see how the protein affected long-term memory and what was needed to create the protein. In tests where the mouse brain was incapable of producing mBDNF, long-term memory formation was not possible. But when the conditions were right to produce mBDNF, the researchers, including teams from Cornell University in New York and the Chinese University of Hong Kong, found long-term memory development was possible. Dr Bai Lu, of the National Institute of Child Health and Human Development, part of the National Institutes of Health, said the findings had the potential to treat people with Alzheimer's disease. "The fundamental problem is the part of the brain associated with memory is dying. If you can stop it from dying or improve the functions of memory you can help patients with Alzheimer's disease." But he admitted doctors were not yet at the stage where they could alleviate memory deficits - as the substance which creates plasmin, which it is thought people with Alzheimer's disease lack, can affect the blood. The possibility that mBDNF could play a key role in long-term memory was first raised in 1996 and since then doctors have established how the protein is formed during chemical reactions involving plasmin and other proteins (C)BBC

Keyword: Learning & Memory; Trophic Factors
Link ID: 6385 - Posted: 11.08.2004

By CLIFFORD KRAUSS VANCOUVER, British Columbia - Beverley Sharpe wondered what was wrong when her 2-year-old daughter, Allison, did not talk. Something seemed askew when her child would not respond to a rolling ball but would find great pleasure from running her hands repetitively through a bowl of soaking beans. A diagnosis of autism resolved the mystery. But the Sharpes' marriage broke up and Ms. Sharpe was left to pay for Allison's intensive therapy on her own. Ms. Sharpe dug in her heels. She refurbished and rented out her garage and rented out several more rooms of her West Vancouver house to pay for the 36 hours of therapy Allison needed every week from four therapists, costing more than $1,400 a month. She also joined a group of parents with autistic children in filing a suit in 1998 seeking public financial aid to meet the children's needs. The case has since wound its way through the British Columbia provincial courts and has reached the Supreme Court of Canada to become one of the most important cases touching social policy to come before the high court in years. Provincial governments are now paying for some services for autistic children, but overall Canadian autistic children currently have fewer legal rights than American children with the same neurological disorder. The American children are entitled by federal legislation to receive educational therapy in their public schools, although services are spotty, depending on how well the local district complies. Copyright 2004 The New York Times Company

Keyword: Autism
Link ID: 6384 - Posted: 11.08.2004

By JOHN SCHWARTZ and JAMES ESTRIN Dr. Jules Lodish welcomes visitors to the downstairs bedroom of his Bethesda, Md., home with a robotic greeting that bursts from his computer's speaker. Ten years of living with amyotrophic lateral sclerosis, or A.L.S., a progressive, paralyzing disease, have stilled nearly every muscle; he types with twitches of his cheek, detected by a sensor clipped to his glasses. But ask him how he feels about his life, and Dr. Lodish, his eyes expressing the intensity denied to his body, responds: "I still look forward to every day." A.L.S., or Lou Gehrig's disease, is often described as a kind of living death in which the body goes flaccid while the mind remains intact and acutely aware. The prospect of being trapped in an inert body and being totally dependent on others drives many sufferers to suicide. When Attorney General John Ashcroft attacked an Oregon law allowing doctor-assisted suicide in 2001 - a case that is still working its ways through the legal system - patients with the disease were among those who supported the law in court. But while the legal case and much of the national attention has focused on the issue of the right to die, less is known about those patients who want to live, and, like Dr. Lodish, will go to extraordinary lengths to do so. Copyright 2004 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 6383 - Posted: 11.08.2004

Ron G. Weisman, Laurene Ratcliffe More than 2,000 years ago, the acerbic philosopher Marcus Tullius Cicero observed that Roman songbirds compose more excellent melodies than any musician. He certainly doesn't stand alone in history on that count; it is a nearly universal human experience to find joy and wonder in birdsong—and to compare the songs to human music. People have been transcribing melodies of birds into the notation of music since at least the 18th century; Vivaldi's Goldfinch concerto and Handel's Cuckoo and the Nightingale organ concerto include musical notation for birdsongs. In the early 1900s, the New England naturalist and composer F. Schuyler Mathews presented the songs of many North American birds in musical notation in his Field Book of Wild Birds and Their Music in order to help readers identify species common in the eastern United States. Later biologists did not share Mathews's enthusiasm for musical descriptions of birdsongs. Donald Borror, a master bioacoustician and field biologist, found many of the song descriptions inadequate by modern standards, as he wrote in his foreword to the 1967 reprinting of Mathews's book. Borror acknowledged that Mathews lacked modern electronic equipment and that his primary interest was in the musical content of birdsongs. Today, however, Mathews's approach seems dated and quaint. Musical notation is simply unable to provide the detailed, accurate and reproducible descriptions required in modern bioacoustical analyses of vocal communication among songbirds. Mathews's approach helps musically trained people recognize birdsongs, but it fails to objectively describe birdsongs and calls. For bioacousticians, accurate observations are a crucial first step in analyzing the role of songs in the life of a species. © Sigma Xi, The Scientific Research Society

Keyword: Hearing; Evolution
Link ID: 6382 - Posted: 06.24.2010

The identification of brain receptors in mice that seem to control nicotine addiction may lead to new drugs to help smokers quit, researchers hope. It is thought nicotinic acetylcholine receptors found on the surface of brain cells are key. The team from the California Institute of Technology found that carrying a particular variant of the receptor increases vulnerability to nicotine. The findings are published in the journal Science. The receptors can be composed of different combinations of subunits. The California team discovered that mice with a mutation in the "alpha4" subunit were unusually sensitive to the effects of nicotine. Compared to normal neurons, the mutant neurons responded to lower concentrations of nicotine and, after this exposure, they also responded more robustly to larger doses. Behavioral tests showed that mutant mice exhibited signs of addiction at lower doses than normal mice. Professor Robert West, of the Cancer Research UK Health Behaviour Unit at University College London, said: "This study is useful in helping with development of medications that target the receptors involved in nicotine dependence but not others and so minimising unwanted side effects." (C)BBC

Keyword: Drug Abuse
Link ID: 6381 - Posted: 11.06.2004

Research on nicotine's molecular targets in the brain has provided new insight into the mechanism of nicotine addiction. The researchers hope that their work, published in the 5 November issue of Science, may one day lead to more effective ways to wean people off tobacco. Nicotine's addictive power comes from its ability to elicit pleasure by mimicking chemicals that stimulate the brain's "reward" circuits. One of these chemicals is acetylcholine. Once in the brain, nicotine hijacks neurons' receptors for acetylcholine, causing them to fire even in the absence of the real thing. Acetylcholine receptors are made up of several subunits. Scientists have identified 12 such subunits that can be mixed and matched to form receptors with different physiological properties. But they haven't been able to nail down which subunits are the most important for addiction. To narrow down the list, a team of researchers led by Henry Lester, a neuroscientist at the California Institute of Technology in Pasadena, designed a mouse with a mutant version of the a4* acetylcholine receptor subunit. Acetylcholine receptors containing the mutant subunit were about 50 times more sensitive than usual. That meant that the scientists could activate the a4*-containing receptors with doses of nicotine too small to affect other types of acetylcholine receptors. Even on these low doses of nicotine, the genetically engineered mice still exhibited the classic symptoms of addiction. The results provide strong evidence that the a4* receptors are sufficient to create nicotine addiction. Copyright © 2004 by the American Association for the Advancement of Science.

Keyword: Drug Abuse
Link ID: 6380 - Posted: 06.24.2010

Diana Parsell Small doses of nicotine can halt the progression of the often-fatal condition called sepsis, according to experiments in mice. The finding, coupled with tests of nicotine on cultured human cells, suggests a pathway to more-effective therapies for the infection-triggered problem. Twice as many mice injected with nicotine survived at least 3 weeks after sepsis set in than did mice receiving inert injections. Luis Ulloa of the Institute for Medical Research at North Shore-Long Island Jewish Health System in Manhasset, N.Y., and his coinvestigators conclude that the treatment works by inhibiting overproduction of an immune system molecule that promotes inflammation. Other studies have suggested that nicotine may be effective against inflammatory diseases such as ulcerative colitis, which is chronic inflammation of the large intestine. When Ulloa and his colleagues began experimenting in lab dishes with human macrophages, a type of immune system cell, they discovered that the biochemical acetylcholine put the brakes on the cells' production of the protein called high mobility group box 1 (HMBG1). This protein is one of the family of immune chemicals called cytokines, which play a role in infection-fighting inflammation. In sepsis, however, HMBG1 overstimulates inflammation. Copyright ©2004 Science Service

Keyword: Drug Abuse
Link ID: 6379 - Posted: 06.24.2010

New York, NY, - Researchers at Columbia University Medical Center have found two locations in the human genome that may harbor genes that increase the risk of Alzheimer’s disease. If confirmed, they will be the first genes linked to Alzheimer’s disease since ApoE4 was discovered in 1993. The findings are published in the November issue of Molecular Psychiatry, a journal of the Nature Publishing Group. “We feel confident that we may be closing in on new Alzheimer’s genes,” says the study’s senior author, Richard Mayeux, M.D., co-director of the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain at Columbia University Medical Center. “This is a major collection of families, and family studies really give you more confidence that the region you’re looking at is significant.” Researchers think that Alzheimer’s is caused by the interaction of several different genes, but so far only one gene, ApoE4, has been linked conclusively to the disease. Finding the other genes will be a huge step toward understanding how Alzheimer’s begins and how it can be treated. It will also allow clinicians to predict who will develop Alzheimer’s later in life and who will benefit from drugs that prevent the disease. The new study found strong evidence for new Alzheimer’s genes on chromosomes 18 and 10. The region on 18 had never been strongly linked to the disease before, while the link to chromosome 10 confirms previous findings by other Alzheimer’s researchers.

Keyword: Alzheimers
Link ID: 6378 - Posted: 06.24.2010

Helen Pearson An immense database of Parkinson's disease patients is being launched in California. Medical researchers say the database will be essential for tracking down the causes of the disease. Once established, the state-wide registry will be the biggest for the disease in the world. It gained formal approval in late September when Governor Arnold Schwarzenegger signed a bill requiring doctors to register every new patient diagnosed with the movement disorder in a central database. Researchers say the new registry will be crucial for pinning down which environmental factors, such as pesticides or diet, are important in triggering the disease. This has become a priority with the growing realisation that genes alone cannot explain people's risk. Parkinson's is caused when dopamine-producing cells in the brain die or are damaged, causing symptoms such as tremors, stiff or slow movement and problems with balance. Although the disease is thought to affect as many as 2% of people, researchers have struggled to build up an accurate picture of the types of people it strikes. Unlike cancer, for example, the disease is rarely recorded as a cause of death because patients succumb to other conditions. ©2004 Nature Publishing Group

Keyword: Parkinsons
Link ID: 6377 - Posted: 06.24.2010

CHAPEL HILL -- University of North Carolina at Chapel Hill scientists have reported - for the first time - a burst in new brain cell development during abstinence from chronic alcohol consumption. The UNC findings, from research at UNC's Bowles Center for Alcohol Studies, were based on an animal model of chronic alcohol dependence, in which adult rats were given alcohol over four days in amounts that produced alcohol dependency. The study is in the Nov. 3 issue of the Journal of Neuroscience. In 2002, Dr. Fulton T. Crews, Bowles Center director, and Bowles Center research associate Dr. Kim Nixon were the first to report that alcohol, during intoxication, has a detrimental effect on the formation of new neurons in the adult rat hippocampus. This brain region is important for learning and memory - in animals and humans - and is linked to psychiatric disorders, particularly depression. "When used in excess, alcohol damages brain structure and function. Alcoholics have impairments in the ability to reason, plan or remember," said Crews, also professor of pharmacology and psychiatry in UNC's School of Medicine. "A variety of psychological tests show alcoholics have a difficulty in ability to understand negative consequences."

Keyword: Drug Abuse; Neurogenesis
Link ID: 6376 - Posted: 11.06.2004

William Cocke Something fishy is happening in the headwaters of the Potomac River. Scientists have discovered that some male bass are producing eggs—a decidedly female reproductive function. In June 2002 reports appeared of fish die-offs in the South Branch of the Potomac River. The West Virginia Division of Natural Resources asked U.S. Geological Survey (USGS) scientists to examine fish health in the watershed near the town of Moorefield, about three hours' drive from Washington, D.C. Anglers were also reporting fish with lesions. USGS scientists determined that some of the lesions indicated exposure to bacteria and other contaminants. The following year, the USGS conducted a more intensive assessment with a statistically significant number of fish, this time looking for internal damage. That's when they discovered a so-called intersex condition—where one sex exhibits both testicular and ovarian tissue. "It was not something we were really looking for," said Vicki Blazer, a fish pathologist with the USGS's Leetown Science Center in Kearneysville, West Virginia. Some 42 percent of male smallmouth bass surveyed showed signs of intersex development. A second sampling this spring produced an even higher rate—79 percent showed sexual abnormalities. © 2004 National Geographic Society.

Keyword: Sexual Behavior
Link ID: 6375 - Posted: 06.24.2010

LOCAL hospitals are not allowed to do brain surgery on drug addicts as a means of curing them of their bad habit, according to sources in the Ministry of Health, the Shanghai Morning Post reported. Previously some Chinese clinics had launched experimental projects using such methods. The paper released by the health ministry said such brain surgery is still in the experimental stage, and clinical research on its safety and effectiveness has not been concluded. So far no conclusions can be made about the exact point in the brain the surgery should target, nor the most successful techniques to use. Until now this surgery has not been widely popularized by clinics as a means of curing drug addicts. Prior to the new policy, two Shanghai hospitals, Renji and Huashan, had begun to offer such services, and a total of 29 patients had undergone the operation. Sources with the two hospitals said they had not received any such paper from the health ministry. However, they insisted that if they did receive such instructions they would of course stop providing the operations as soon as possible. Copyright by Shanghai Star.

Keyword: Drug Abuse
Link ID: 6374 - Posted: 11.06.2004

More than four million people die from smoking-related causes each year, making nicotine addition a leading cause of preventable mortality worldwide. But nicotine's highly addictive nature makes kicking the smoking habit very difficult. A report published today in the journal Science identifies brain receptors in mice that may help explain why it's so hard to quit, and help scientists develop new drugs to help smokers butt out. Receptors embedded in the surface of neurons allow compounds such as nicotine to act on brain cells. Researchers had previously identified so-called nicotinic acetylcholine receptors as important in cigarette addiction. Henry A. Lester of the California Institute of Technology and his colleagues created genetically engineered mice that had alterations in these receptors. They found that animals with a mutation in the “alpha4” subsection were particularly sensitive to nicotine's effects. Mice with the alpha4 mutation showed signs of addiction at lower doses than did normal mice and, once exposed to the chemical, the altered neurons responded more strongly to large doses of it than regular neurons did. © 1996-2004 Scientific American, Inc

Keyword: Drug Abuse
Link ID: 6373 - Posted: 06.24.2010

For those who have wondered why they like or dislike certain things, or how they decide what to order from a menu, a team of researchers at the University of Colorado at Boulder says it's dopamine. A CU-Boulder team studying Parkinson's disease patients found strong evidence that dopamine in the brain plays a key role in how people implicitly learn to make choices that lead to good outcomes, while avoiding bad ones. The finding could help researchers understand more about how the brain works and could lead to a better understanding and treatment of brain disorders like schizophrenia, according to CU-Boulder psychology graduate student Michael Frank, who led the study. A paper on the subject by Frank, CU-Boulder psychology Associate Professor Randall O'Reilly and Lauren Seeberger of the Colorado Neurological Institute's Movement Disorders Center appears in the Nov. 5 issue of Science Express, an online version of Science magazine. Often people will get a "gut feeling" that allows them to make a choice depending on how often it was associated with positive outcomes in the past. But people with Parkinson's disease often have difficulty making these kinds of choices, Frank said. To understand why, they developed a computer model of the effects of Parkinson's disease and the medications used to treat it in the brain. From this model they predicted that Parkinson's patients would differ in their decision making depending on whether or not they were taking their medication, which they confirmed in a subsequent study.

Keyword: Parkinsons; Learning & Memory
Link ID: 6372 - Posted: 11.06.2004

Researchers at the Monell Chemical Senses Center and the University of Pennsylvania School of Medicine used functional magnetic resonance imaging (fMRI) to reveal that food cravings activate brain areas related to emotion, memory and reward – areas also activated during drug-craving studies. Study lead author Marcia Levin Pelchat, PhD, a Monell Center sensory psychologist, comments, "This is consistent with the idea that cravings of all kinds, whether for food, drugs, or designer shoes, have common mechanisms." Studies of food craving, possibly the evolutionary basis of all craving behavior, may provide insight into drug craving and how it contributes to maintenance and relapse of drug addiction. Pelchat notes, "Identifying the brain regions involved can tell us a great deal about the normal and pathological neurochemistry of craving, and in turn, lead us to better pharmacological treatments for obesity and drug addiction." During food craving episodes, craving-specific activation was seen in three regions of the brain: the hippocampus, insula, and caudate. These same three areas have also been reported to be involved in drug craving. In the study, to be published in the December 2004 issue of NeuroImage, 10 healthy volunteers were not permitted to consume anything other than a vanilla nutritional supplement beverage for the one-and-a-half days before the imaging session. The researchers used the monotonous diet to increase the probability of cravings during fMRI sessions. Previous findings had shown that consuming a monotonous diet leads to large increases in the number of food cravings.

Keyword: Obesity; Drug Abuse
Link ID: 6371 - Posted: 06.24.2010

Gulf war syndrome may have been caused by exposure to the nerve gas sarin, according to reports. The New Scientist journal has reported a leak of a US inquiry into the ill-health of veterans of the 1991 war. The US Department of Veterans Affairs' Research Advisory Committee on Gulf War Veterans' Illnesses is due to publish its findings next week. But the magazine said researchers have found neural damage consistent with the nerve agent used by Saddam Hussein. The link is said to have been "crucial" to a change of heart by the US authorities over Gulf war syndrome. The New York Times newspaper reported last month that US scientists believed the syndrome did exist and was caused by "toxic exposure" but it was not clear whether this was from drugs or nerve agents. The UK government has always insisted a unique Gulf war syndrome does not exist. But campaigners say 6,000 British war veterans are suffering from the syndrome, with symptoms ranging from mood swings, memory loss, lack of concentration, night sweats, general fatigue and sexual problems since the war. According to the New Scientist report "a substantial proportion of Gulf war veterans are ill with multi-system conditions not explained by wartime stress or psychiatric illness". Instead, the magazine reported the ill-health could have been caused by low level exposure to sarin. Three research groups had independently found specific kinds of neural damage that could explain some of the veterans' symptoms. (C)BBC

Keyword: Neurotoxins
Link ID: 6370 - Posted: 11.04.2004

During a football game early last season, Virginia Tech Hokie linebacker Brandon Manning took a hard hit that shook him up a little bit. But he shook it off and stayed in the game. "It wasn't necessarily a matter of me not wanting to tell them," says Manning. "I just maybe didn't realize it. I'm worked up, I'm in the game, and I'm maybe able to put some things behind me and continue to play like I hope I can. It wasn't really till the next day when I came in to watch film that I found I didn't really remember half the plays that I was in [in] the game. I started to see myself but I didn't really remember what I was doing, and that's when I really sort of realized that I had had a concussion." Micky Collins, a concussion specialist at the University of Pittsburgh Medical Center Sports Medicine Concussion Program, says Manning's continued play put him in great danger, especially if he had gotten hit again. "The worst that can happen is second impact syndrome, when you have two concussions in relatively short duration," says Collins. "That can cause death in an athlete." Now the Hokies are participating in a study that might help team trainers spot these dangerous collisions right away. The team's helmets are rigged with tiny sensors—like the ones that deploy airbags in cars—called accelerometers, which measure the impacts to the helmets. During play, a transmitter immediately sends real-time information about the force of a collision to a laptop computer on the sideline. The system is called HITS—Head Impact Telemetry System—and is manufactured by Simbex. © ScienCentral, 2000- 2004.

Keyword: Brain Injury/Concussion
Link ID: 6369 - Posted: 06.24.2010

Jonathan Knight George W. Bush has won the presidential election. But Republicans are not the only ones celebrating the poll results: biologists who wish to pursue human embryonic stem-cell research have also had good news. All they have to do is move to California, if they aren't already there, and apply for a share of the $3 billion that voters have just approved for their field. By 59% to 41% of votes, Californians said "yes" to Proposition 71, the California Stem Cell Research and Cures Initiative, which will raise around $300 million a year for a decade through bond sales. The money will pay for research that has not been eligible for government money since 9 August 2001, when President George W. Bush limited federal spending on human embryonic stem-cell research to cell lines in existence as of that date. The creation of new cell lines involves the destruction of a days-old human embryo. Most biomedical researchers believe that the number of lines available under the 2001 rule will be inadequate to realize the potential of stem-cell research, which might give insight into the causes of degenerative diseases such as muscular dystrophy and Parkinson's. Such discoveries may to lead to new treatments, and therapies that use embryonic stem cells themselves to replace damaged tissues could also emerge. ©2004 Nature Publishing Group

Keyword: Stem Cells
Link ID: 6368 - Posted: 06.24.2010

East Hills, NY (- - There is increasing evidence that infectious prions that can cause variant Creutzfeldt-Jakob Disease (vCJD), the human form of "mad cow" disease, can be transmitted through blood transfusion, according to Roger Eglin, Ph.D., Head of National Transfusion Microbiology Laboratories for the English National Blood Service. He spoke at a symposium on Transmissible Spongiform Encephalopathies (TSEs) where he was joined by prominent government, public health and blood safety experts from around the globe, including the U.S. and Canada, who raised concerns about a second wave of the disease brought about by human-to-human transmission via blood transfusions. The panelists convened to discuss the adequacy of safeguards and precautionary measures to prevent human-to-human transmission of this fatal, neurodegenerative prion disease at a symposium held last night at the annual AABB blood banking conference in Baltimore, Maryland. The symposium was sponsored by Pall Corporation (NYSE: PLL), the global leader in filtration technology. Citing two confirmed cases in the UK, where vCJD was transmitted via blood transfusions from donors who were young and apparently healthy at the time of donation, Dr. Eglin said the current decline in reported cases could be followed by a new wave of vCJD infections around the world of unknown magnitude. These concerns were echoed by the panelists, who noted the increase of vCJD in France from six to eight cases in just the past few months and the news that blood from a vCJD-infected donor was transfused to 10 people and used to manufacture medicines.

Keyword: Prions
Link ID: 6367 - Posted: 11.04.2004

Babies who continue to cry excessively for no obvious reason can go on to have difficulties in childhood, according to a new study. Excessive, uncontrolled crying that persisted beyond three months of age was linked with behavioural problems and lower IQ at the age of five. The US National Institutes of Health study, in Archives of Disease in Childhood, supports prior UK findings. Experts said most crying was normal and parents should not be unduly concerned. The NIH team, working with researchers at the Norwegian University of Science and Technology, looked at 327 babies and their parents. They assessed the babies' crying patterns at six and 13 weeks of age and whether or not the crying could be explained by simple colic. When the children were five years old, the researchers assessed their intelligence, motor abilities and behaviour. The children who had continued to cry beyond three months of age as infants, which was not due to colic, had intelligence scores (IQs) nine points lower than the other children studied. Prolonged crying was also linked with poorer fine motor abilities, hyperactivity and discipline problems in childhood. In 2002, a team of UK researchers, led by Professor Dieter Wolke at Bristol University, found children who had cried excessively as babies, beyond three months, were 14 times more likely to develop attention deficit hyperactivity disorder (ADHD) and do worse at school as eight year olds. Professor Wolke said: "This confirms what we found. "Now there really is more certainty there is really something going on." He believes the core of the problem is one of under-regulation. "With ADHD you can't regulate your attention. You can't concentrate, for example. The same thing is happening with crying. (C)BBC

Keyword: Development of the Brain; ADHD
Link ID: 6366 - Posted: 11.04.2004