When cats smell catnip they exhibit several behaviors common to queens in season (females in heat): They may rub their heads and body on the herb or jump, roll around, vocalize and salivate. This response lasts for about 10 minutes, after which the cat becomes temporarily immune to catnip's effects for roughly 30 minutes. Response to catnip is hereditary; about 70 to 80 percent of cats exhibit this behavior in the plant's presence. In addition, catnip does not affect kittens until they are about six months old and begin to reach sexual maturity. Catnip plants (Nepeta cataria and other Nepeta species) are members of the mint family and contain volatile oils, sterols, acids and tannins. Native to Europe, Asia and Africa, the plant was brought to North America by settlers; nowadays, the plant is popular in herb gardens and grows widely as a weed. Catnip is considered to be nonaddictive and completely harmless to cats. So, how does catnip work? Nepetalactone, one of catnip's volatile oils, enters the cat's nasal tissue, where it is believed to bind to protein receptors that stimulate sensory neurons. These cells, in turn, provoke a response in neurons in the olfactory bulb, which project to several brain regions including the amygdala (two neuronal clusters* in the midbrain that mediate emotional responses to stimuli) and the hypothalamus, the brain's "master gland" that plays a role in regulating everything from hunger to emotions. The amygdala integrates the information flow from the olfactory bulb cells and projects to areas governing behavior responses. The hypothalamus regulates neuroendocrine responses through the pituitary gland, creating a "sexual response." That is, the cat essentially reacts to an artificial cat pheromone. © 1996-2007 Scientific American, Inc.

Keyword: Drug Abuse; Sexual Behavior
Link ID: 10398 - Posted: 06.24.2010

Alzheimer’s disease researchers may be able to reduce the time and expense associated with clinical trials, according to early results from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), a public-private research partnership organized by the National Institutes of Health. Preliminary results from ADNI show how it might yield improved methods and uniform standards for imaging and biomarker analysis, so these techniques can be employed in the fight against Alzheimer’s disease. These first findings will be presented at the Alzheimer’s Association International Conference on the Prevention of Dementia being held in Washington, D.C., June 9-12. The ADNI study observes and tracks changes in normal individuals, in people with mild cognitive impairment — a condition which often precedes Alzheimer’s — and in people with Alzheimer’s. Researchers will use PET (positron emission tomography) and MRI (magnetic resonance imaging) scans to track changes in the brain, laboratory analyses of cerebrospinal fluid and blood to study biomarkers, and clinical interviews to track cognitive performance over time. ADNI is expected to improve neuroimaging and biomarker measures and consequently allow faster and more efficient evaluation of potential therapies for Alzheimer’s. The $60 million, five-year study began recruiting in early 2006, and today about 800 older people at 58 sites in the United States and Canada participate in the effort.

Keyword: Alzheimers; Brain imaging
Link ID: 10397 - Posted: 06.24.2010

Researcher James Bibb and his team were on a mission to learn more about the role of the gene Cdk5 in brain function. When they turned off this gene in mice, they expected deficiencies to appear. Instead, the mice showed increased flexibility in learning. Can you explain more about what you mean by flexibility with the water maze experiments? The animals that no longer had the CDK5 gene were able to find this platform faster, but even more interestingly was how flexible they were. We did an experiment called "reversal," in which we moved the platform to a different position underneath the water. So that meant they had to reestablish where it was with regard to the spatial cues, and then they would swim to the new position. What was amazing, is the knockouts were very, very quickly, after the first trial, able to understand that the platform had been moved and began to adjust so they always went to the new position. Whereas the normal animals continued to kind of look for the platform and were not sure if it moved or was at the old location on subsequent trials. So that was a really clear indication that these animals were much more flexible and adaptable in the way they were able to perceive and learn and remember things. © ScienCentral, 2000-2007.

Keyword: Learning & Memory
Link ID: 10396 - Posted: 06.24.2010

Human trials of isradipine (or DynaCirc) – which is prescribed for hypertension and stroke – are now planned. Over time, Parkinson's patients lose a set of brain cells that produce the crucial signalling chemical dopamine – and these cells do not regenerate. Without enough dopamine, people cannot control their body movements and ultimately develop severe neurological problems, including dementia. Scientists have struggled to understand why the dopamine-producing brain cells start dying, but ageing plays a strong role. James Surmeier at Northwestern University in Illinois, US, and colleagues found that in young mice these cells use sodium channels to send signals, but in older mice they rely more on a certain kind of calcium channel. This can prove deadly for a neuron because calcium accumulates inside the cell, eventually triggering a complete breakdown. Surmeier wondered whether he could reverse the switch to calcium channels: "The cells had put their old childhood tools in the closet. The question was, if we stopped them from behaving like adults, would they go into the closet and get them out again?" © Copyright Reed Business Information Ltd

Keyword: Parkinsons
Link ID: 10395 - Posted: 06.24.2010

Helen Pilcher Human stem cell transplants have eased the symptoms of Parkinson's disease in a monkey model of the brain disorder. The study, which brings the prospect of human trials one step closer, hints that stem cells do more than just replace cells — they may help persuade the brain to heal itself. Parkinson's disease, which affects around 1 in 500 people, destroys nerve cells that produce the chemical dopamine, leading to movement and balance problems. Most treatments attempt to boost dopamine levels through drugs, but the results can be patchy and short-lived. So the hope is that stem cells — primitive cells that can produce many other cell types — may offer a more permanent solution. In the current study, published in Proceedings of the National Academy of Sciences1, researchers isolated stem cells from the brains of aborted fetuses and grew them into large numbers in the laboratory. The cells were then injected into the brains of monkeys with a severe form of chemically induced Parkinson's disease. Before the treatment, the animals couldn't walk unaided, struggled to use their hands and were sometimes unable to move at all. But two months afterwards, they could walk, feed themselves and move more normally. "They're not as good as normal monkeys, but the improvement is still dramatic," says team-member and neuroscientist Richard Sidman from the Harvard Institutes of Medicine, Boston, Massachusetts. ©2007 Nature Publishing Group

Keyword: Parkinsons; Stem Cells
Link ID: 10394 - Posted: 06.24.2010

Urgent safety studies are needed for newer anti-epilepsy drugs that are being increasingly prescribed for children, say UK researchers. The British Journal of Clinical Pharmacology report says prescriptions have risen five-fold in 13 years. Yet the drugs' long-term safety has not been established, say the researchers. Many medicines are not fully tested on children before licensing, meaning consultants have no official guidance on doses to refer to when prescribing. Instead they often have to estimate a safe and effective dose based on the age and the size of the child. Lead author Professor Ian Wong, from the Centre for Paediatric Pharmacy Research in London, studied antiepileptic drugs given to nearly 8,000 children over a 13-year period. The centre is a collaborative project run by the School of Pharmacy at the University of London, the UCL Institute of Child Health and Great Ormond Street Hospital. Professor Wong and his colleagues found three drugs in particular - lamotrigine, topiramate and levetiracetam - had seen a "massive" rise in prescribing. Professor Wong said this was concerning. "The uptake of these drugs has been rapid, yet their long-term safety has not been established and further research must now be seen as a priority." (C)BBC

Keyword: Epilepsy
Link ID: 10393 - Posted: 06.11.2007

US scientists have unveiled what they say could be the next generation of implants designed to offer hearing to the profoundly deaf. The new device described by the University of Michigan team fits directly to the auditory nerve. The researchers claim it works better than cochlear implants, currently the leading technology. But the device has been tested only in animals, the Journal of the Association for Research in Otolaryngology reports. A UK researcher hailed the project as "potentially a brilliant idea". Cochlear implants have been in use since the mid-1980s, and are placed near to the nerve that carries sound impulses to the brain. However, they are still separated from the nerve by a bony wall and fluid, and users often find it hard to hear low-pitched sounds, which can make conversation difficult, especially in noisy environments. The Michigan team have managed to place their tiny device inside the nerve itself in cats. Lead researcher Professor John Middlebrooks said testing showed the new device performed better over a wider range of frequencies, suggesting that users might be able to enjoy a far wider range of hearing. They measured the cats' brain responses to sounds, and compared the results with those in cats given cochlear implants. Professor Middlebrooks said: "The intimate contact of the array with the nerve fibres achieves more precise activation of fibres signalling specific frequencies, reduced electrical current requirements and dramatically reduced interference among electrodes when they are stimulated simultaneously." (C)BBC

Keyword: Hearing; Robotics
Link ID: 10392 - Posted: 06.11.2007

The progression of Parkinson's disease could be slowed or even stopped by a drug commonly used to treat high blood pressure, a study in Nature suggests. Tests on mice at Northwestern University in Chicago showed isradipine can rejuvenate the brain neurons which are dying in Parkinson's patients. The disease, which mainly affects those aged over 40, leads to tremors and ultimately the inability to walk. Parkinson's charities welcomed the study but said they were early results. "It is too early to state with confidence that this drug will be appropriate for the treatment for Parkinson's disease," said Kieran Breen, director of research and development at the Parkinson's Disease Society. "A significant amount of further research will be required before any definite conclusions can be drawn." Isradipine is a calcium-blocker which is usually used to tackle high blood pressure, angina and stroke. But researchers at Northwestern University found mice, who had been engineered to develop a progressive Parkinson's-type disease, did not become ill when their condition was treated with the drug. Their dopamine neurons - cells which start to die in Parkinson's patients - appeared to revert back to their original, youthful form. Dopamine is a critical substance which affects the control of movement. When it is lacking, that movement becomes increasingly difficult and unco-ordinated. The team found that when people become older, calcium ions start to enter the dopamine neurons and change how they behave. It is thought that isradipine's ability to stop calcium entering the cells is key to the effectiveness of the treatment. (C)BBC

Keyword: Parkinsons
Link ID: 10391 - Posted: 06.11.2007

By STEPHANIE SAUL IN the book “Mrs. Frisby and the Rats of NIMH,” a group of lab rats acquire human intelligence through a genetic experiment. Every child recognizes the charming tale as pure fantasy, yet something similar is occurring at a major pharmaceuticals company, Wyeth, where rodents tested in its labs have, indeed, taken on some features of the human brain. Unlike the fictional rats that learned to read, write and operate machinery, Wyeth’s animals are slow-witted, confused and forgetful because they suffer from the crippling dementia of Alzheimer’s disease, which they acquired from a transplanted human gene. Something else extraordinary is going on at Wyeth. The company’s scientists not only can give rodents Alzheimer’s — they have also figured out how to take it away. Curing mice is a lot simpler than curing people, but the results are a tantalizing development that offers hope to humans suffering from the disease. The work also advances what Wyeth executives describe as their war on Alzheimer’s. Wyeth’s team faces a formidable foe. In an industry often criticized as making pricey “me too” drugs that involve minor tweaks to competitors’ products, as well as promoting medicines of marginal value, Wyeth has decided to go full bore against Alzheimer’s, a disease that has defied effective treatment since it was first identified a century ago. The company has dedicated more than 350 scientists exclusively to Alzheimer’s research, and they are working on 23 separate projects for medicines to possibly treat the disease. Copyright 2007 The New York Times Company

Keyword: Alzheimers
Link ID: 10390 - Posted: 06.24.2010

By Maggie Fox WASHINGTON (Reuters) - New tests involving blood and brain scans can detect symptoms of Alzheimer's disease, and brief appraisals of real-life functioning can predict who is likely to develop it, researchers saidSunday. The tests will be critical, experts told a meeting on Alzheimer's disease, because more than 26 million people now have the brain-wasting disease and this number will quadruple, to 106 million, by 2050. "By 2050, 1 in 85 persons worldwide will have Alzheimer's disease," said Ron Brookmeyer of Johns Hopkins University, who led the study on how many people have the disease. No drugs can significantly affect Alzheimer's disease, although four have a very modest impact if given early on. The disease is very difficult to detect until it has progressed from mild memory loss to clear impairment. Patients eventually lose all ability to care for themselves. Detecting the disease early can help patients and their families plan better for the future but can also help researchers develop drugs to treat and perhaps even prevent the disease. © 2007 Reuters

Keyword: Alzheimers
Link ID: 10389 - Posted: 06.24.2010

By Shankar Vedantam For more than a decade, families across the country have been warring with the medical establishment over their claims that routine childhood vaccines are responsible for the nation's apparent epidemic of autism. In an extraordinary proceeding that begins tomorrow, the battle will move from the ivory tower to the courts. Nearly 5,000 families will seek to convince a special "vaccine court" in Washington that the vaccines can cause healthy and outgoing children to withdraw into uncommunicative, autistic shells -- even though a large body of evidence and expert opinion has found no link. The court has never heard a case of such magnitude. The shift from laboratory to courtroom means the outcome will hinge not on scientific standards of evidence but on a legal standard of plausibility -- what one lawyer for the families called "50 percent and a feather." That may make it easier for the plaintiffs to sway the panel of three "special masters," which is why the decision could not only change the lives of thousands of American families but also have a profound effect on the decisions of parents around the world about whether to vaccinate their children. A victory by the plaintiffs, public health officials say, could increase the number of children who are not given vaccines and fall sick or die from the diseases they prevent. © 2007 The Washington Post Company

Keyword: Autism; Neurotoxins
Link ID: 10388 - Posted: 06.24.2010

Launch footage for the London 2012 logo sparked seizures, but how is television checked for footage that could harm people with epilepsy? For the organisers of the 2012 Olympics vilification over its logo has taken a turn for the worse with reports that people with epilepsy suffered seizures as a result of watching an animation in the launch video. One section, featuring a diver causing ripples in a pool, has led to 18 people reporting ill effects. It is believed to be the biggest episode of triggering of photosensitive epilepsy in British broadcasting history. Episodes like this are now rare in the UK because of a gadget called the Harding Flash and Pattern Analyser, used by broadcasters and advertising agencies to avoid triggering seizures. Only 5% of people with epilepsy suffer from photosensitivity, but this still amounts to 23,000 people in the UK, Epilepsy Action says. For them flashes, strobing and flickers, typically at rates of 16 to 25 times a second but as low as three and as high as 60, are a danger. Two incidents in the 1990s intensified research into the way television triggers photosensitive epilepsy. A Pot Noodle advert in 1993 sparked three reports of seizures and prompted concern and a ban on the advert. But nothing in Britain has come near the episode sparked by a Pokemon cartoon in Japan in 1997 when more than 600 children were admitted to hospital after suffering epileptic seizures. Three-quarters of those had never suffered from symptoms of epilepsy before. (C)BBC

Keyword: Epilepsy
Link ID: 10387 - Posted: 06.09.2007

Scientists say they have discovered a new gene linked with late-onset Alzheimer's disease. People with a damaged copy of the gene, GAB2, may be at four times increased risk of developing dementia, Neuron journal reports. Experts said the latest findings were some of the most significant to emerge since the discovery of the ApoE4 Alzheimer's gene. Late-onset Alzheimer's affects one in 10 people over 65 and half of over 85s. The researchers, from 15 institutions including the Institute of Neurology in London, analysed the DNA of 1,411 people and found GAB2 influenced the risk of dementia among those with APOE4. GAB2 appears to modify the effects of this better known Alzheimer's gene. In turn, this leads to the formation of the characteristic protein "tangles" found in the brains of people with Alzheimer's, the researchers told Neuron. (C)BBC

Keyword: Alzheimers; Genes & Behavior
Link ID: 10386 - Posted: 06.09.2007

By Charles Q. Choi Chimpanzees readily learn and share techniques on how to fiddle with gadgets, new research shows, the best evidence yet that our closest living relatives pass on customs and culture just as humans do. The new findings help shed light on the capabilities of last common ancestor of humans and chimps. And the research could also help develop better robots and artificial intelligences, the researchers say In the wild, chimpanzee troops often are distinct from one another, possessing collections of up to 20 traditions or customary behaviors that altogether seem to form unique cultures. Such practices include various forms of tool use, including hammers and pestles; courtship rituals such as leaf-clipping, where leaves are clipped noisily with the teeth; social behaviors such as overhead hand-clasping during mutual grooming; and methods for eradicating parasites by either stabbing or squashing them. While observing chimpanzees, evolutionary psychologist Antoine Spiteri at the University of St. Andrews in Scotland wanted to help settle the question of whether or not the apes learned such practices by watching others like humans do, as opposed to simply knowing how to perform such behaviors innately. © 2007 MSNBC.com © 2007 Microsoft

Keyword: Evolution
Link ID: 10385 - Posted: 06.24.2010

By NICHOLAS WADE Applying a new genomic technique to a large group of patients, researchers in Britain have detected DNA variations that underlie seven common diseases, discovering unexpected links between them. The variations pinpoint biological pathways underlying each of the diseases, and researchers hope that as the pathways are analyzed, new drugs and treatments will emerge. The seven common diseases are bipolar disorder, coronary artery disease, Crohn’s disease, hypertension, rheumatoid arthritis, and Type 1 and Type 2 diabetes. Unveiling the complex genetics of common diseases was the promised payoff of the $3 billion human genome project, completed in 2003, but progress was slow until the recent development of devices that in a single operation can read the DNA sequence at up to 500,000 points across an individual’s genome. With the devices, called chips, researchers can compare large numbers of patients with healthy individuals, looking for points of differences in their genomes that may be associated with disease. The approach is known as whole genome association, and studies on Type 2 diabetes, heart disease and breast cancer have been reported within the last few weeks. Those and the new study, which was financed by the Wellcome Trust of London, demonstrate the power and reliability of the whole genome association method, which stands in contrast to the many uncorroborated claims of disease genes made previously. Copyright 2007 The New York Times Company

Keyword: Schizophrenia; Genes & Behavior
Link ID: 10384 - Posted: 06.24.2010

In a laboratory at the University of Texas Southwestern Medical Center in Dallas, researchers study a mouse swimming in a pool of milky water. While it looks like any other mouse, something is quite different about this mouse's genetically-modified brain. It finds a hidden platform in the water much faster than the other mice. This smart mouse is giving brain researchers new insights into intelligence. "Most people think of intelligence, they think learning and remembering," brain researcher James Bibb says. "However, flexibility in the face of changing situations may be a more important feat of intelligence." By turning off a certain gene, James Bibb (left) and his team found that the mice became smarter. James Bibb and his team didn't set out to make mice smarter. They simply wanted to study the function of a gene nobody knew much about. "We wanted to understand features of the brain's function and we didn't expect the animals to end up showing improved or enhanced performance in anything," he says. "We expected deficiencies to appear and for that to tell us what the role of this gene for Cdk5 was." Bibb wanted to study the Cdk5 gene because it is suspected to be involved in Alzheimer's disease as well as in drug addictions. © ScienCentral, 2000-2007

Keyword: Learning & Memory; Genes & Behavior
Link ID: 10383 - Posted: 06.24.2010

NEW YORK (Reuters Health) - A pre-existing defect in body temperature regulation may be a factor underlying some fatal reactions to the illegal "club drug" ecstasy (3,4-methylenedioxymethamphetamine, MDMA), researchers from Canada propose. "Fatal MDMA intoxication is idiosyncratic and the reasons why some ecstasy users are especially susceptible to the toxic effects of the drug are still unknown," Dr. Stephen J. Kish of the University of Toronto and the Centre for Addiction and Mental Health and colleagues point out. They also note that deaths attributed to MDMA intoxication, which are fairly infrequent compared with the estimated number of recreational users, are often associated with a sharp increase of body temperature, also referred to as hyperthermia. In the current issue of the Journal of Forensic Sciences, Kish's team describes a 24-year-old woman who developed fatal hyperthermia with complications affecting multiple organs after taking ecstasy. An autopsy showed that the woman had diffuse thyroid hyperplasia (also called Graves' disease), a thyroid disorder that could have made her less tolerant to heat. Comprehensive drug screening showed only MDMA and traces of methamphetamine in a blood sample collected 3 to 4 hours after the woman took the drugs. © 1996-2007 Scientific American, Inc.

Keyword: Drug Abuse; Hormones & Behavior
Link ID: 10382 - Posted: 06.24.2010

By Lucas Laursen Heavy snacking after exercise may have little to do with hunger or appetite hormones. In a new study, people who rode a bike for an hour ate more for lunch than those who just sat around ate, despite similar levels of hunger and short-term appetite-suppressing hormones. The urge to gobble after exercise, it turns out, may be a more complicated mixture of psychology and body chemistry. Hoping to get a better sense of why many people chow down after an hour at the gym, graduate student Cátia Martins of the University of Surrey, U.K., and colleagues recruited 12 adult volunteers with normal weight and eating habits, half of them male and half female. The team then divided the volunteers into two groups. Both groups drank a cup of hot chocolate for breakfast, but 1 hour later, volunteers from one group took a moderate 60-minute spin on a stationary bike, while volunteers in the other group sat around reading or writing. At the end of either activity, the researchers provided both groups with identical buffet lunches of unlimited sandwiches, fruit, cake, cookies, and yogurt. At various points throughout the experiment, Martins and her colleagues collected blood samples from the subjects and had them fill out a questionnaire about their hunger. During their workout, the exercisers reported less hunger than the inactive volunteers and had elevated levels of PYY, GLP-1, and PP, hormones that suppress appetite in the short term. By lunchtime, both groups reported similar amounts of hunger, and both had indistinguishable levels of the three hormones. Yet the exercisers out-ate the slackers, consuming nearly 20% more calories at lunch. © 2007 American Association for the Advancement of Science.

Keyword: Obesity
Link ID: 10381 - Posted: 06.24.2010

Jennifer Viegas, Discovery News — Neanderthals likely did not possess the cognitive complexities of modern humans and, as a result, probably did not suffer from schizophrenia and certain other mental disorders, according to a new theory. The theory proposes that language, creativity and many mental diseases are linked, due to the fact that they may originate in the neocortex, as well as the densely cell-packed cortex, located towards the top of the brain. These brain regions appear to mature and develop more slowly than other areas. Although there are conflicting claims about possible Neanderthal creative abilities, no direct evidence supports that this extinct human species or subspecies possessed full-fledged grammatical language. Neanderthals had large brains, but researchers believe their mental skills matured rapidly, closing the door to disorders associated with the cortex. Modern humans, on the other hand, must take the bad with the good. "In a nutshell, I feel that the extremely long maturation time of our brains — greater than 20 years — allows them to develop many and various capabilities, such as language and schizophrenia," H. Lee Seldon, the theory’s author, told Discovery News. © 2007 Discovery Communications Inc.

Keyword: Evolution
Link ID: 10380 - Posted: 06.24.2010

Researchers have identified a master hormone that allows the body to fuel itself with stored fat during times of fasting. The hormone mobilizes lipids from fat cells, and then directs the liver to transform those lipids into energy-rich molecules that circulate throughout the body. The researchers said their findings reveal a more complete picture of the far-reaching role of the hormone, fibroblast growth factor 21 (FGF21), which is already in development as a treatment for type 2 diabetes. In addition to switching the body to a fat-burning mode, the team found FGF21 induces the hibernation-like state of torpor that conserves energy in fasting animals. FGF21's unexpectedly broad role in fat-burning was reported in two papers published in the June, 2007, issue of the journal Cell Metabolism. One paper was from the laboratory of Steven Kliewer and Howard Hughes Medical Institute investigator David Mangelsdorf at the University of Texas Southwestern Medical Center. Coauthors on the paper are Kliewer and Mangelsdorf's colleagues at UT Southwestern and scientists from Van Andel Research Institute and New York University School of Medicine. The other Cell Metabolism paper was by Eleftheria Maratos-Flier of Harvard University and colleagues. © 2007 Howard Hughes Medical Institute

Keyword: Obesity
Link ID: 10379 - Posted: 06.24.2010