The only known adults in the world who possess a rare genetic mutation that prevents their bodies from producing leptin may open the door to a new way of fighting fat. After injections with leptin -- a human hormone linked to appetite control -- the adults' dramatic weight loss suggests that leptin offers significant promise for treating obesity. Dr. Julio Licinio, professor of medicine at the David Geffen School of Medicine at UCLA, flew three cousins -- two women and one man -- from a tiny village in Turkey to UCLA Medical Center last September for clinical research treatment with leptin. Ranging in age from the late 20s to 40, all of the cousins were severely obese and one was still prepubescent. "We hypothesized that leptin deficiency may lead to obesity and, in some cases, delay sexual and psychological maturity," explained Licinio, also a professor of psychiatry and biobehavioral sciences at the UCLA Neuropsychiatric Institute. "Although this is a small study, it produced striking results."

Keyword: Obesity
Link ID: 2360 - Posted: 07.24.2002

Identifying factors that increase the reserve capacity of the brain and enable people to tolerate the pathological changes that occur in the brains of people with Alzheimer's disease offers a new and potentially powerful approach to delaying the clinical signs of the Alzheimer's and other neurodegenerative diseases, according to researchers at Rush-Presbyterian-St. Luke's Medical Center, Chicago. Research is underway at Rush to identify the factors that increase or maintain the reserve capacity of the human brain. Researchers have known for some time that education and related lifestyle experiences affect cognitive function across the lifespan. There is also evidence that these educational experiences can reduce one's risk of developing Alzheimer's disease. "How these lifestyle experiences actually affect the brain is unknown," according to Dr. David A. Bennett, director of the Rush Alzheimer's Disease Center. "We think that education and factors related to education may affect the way the brain responds to the abnormal proteins that accumulate in the brains of people with Alzheimer's disease. In other words, in people with similar amounts of these abnormal Alzheimer's disease protein deposits, those with more educational experiences will be less likely to have memory loss than those with less education," he explained.

Keyword: Alzheimers
Link ID: 2359 - Posted: 07.24.2002

Emotional recall better than men's, study says Paul Recer ASSOCIATED PRESS WASHINGTON — Matrimonial lore says husbands never remember marital spats and wives never forget. A new study suggests a reason: Women's brains are wired both to feel and to recall emotions more keenly than the brains of men. A team of psychologists tested groups of women and men for their ability to recall or recognize highly evocative photographs three weeks after first seeing them and found that the women's recollections were 10 per cent to 15 per cent more accurate. The study, appearing in the Proceedings of the National Academy of Sciences , also used MRIs to image the subjects' brains as they were exposed to the pictures. It found that the women's neural responses to emotional scenes were much more active than the men's. Copyright 1996-2002. Toronto Star Newspapers Limited.

Keyword: Learning & Memory; Brain imaging
Link ID: 2358 - Posted: 06.24.2010

Copyright © 2002 AP Online The Associated Press - Scientists have found new evidence linking the reading problem called dyslexia to glitches in a particular region of the brain. The evidence comes from brain scans of 70 dyslexic and 74 non-impaired children, ages 7 to 18. It follows a 1998 brain scan study that reported the link in adults. The new work, by including children as young as 7, shows the brain problem is present at the beginning of reading ability, said researcher Sally Shaywitz of Yale University. Copyright © 2001 Nando Media

Keyword: Dyslexia
Link ID: 2357 - Posted: 06.24.2010

Copyright © 2002 AP Online By EMMA ROSS, AP Medical Writer - The number of Americans with Alzheimer's disease could more than triple to 16 million by 2050, new research indicates. The projections, presented Monday at an international Alzheimer's conference in Stockholm, Sweden, are slightly higher than those conducted 10 years ago, mostly because more people are expected to live beyond the age of 85 than were predicted a decade ago. Some 4.6 million Americans currently suffer from Alzheimer's. Copyright © 2001 Nando Media

Keyword: Alzheimers
Link ID: 2356 - Posted: 06.24.2010

Traditional allies split on EPA animal tests Glen Martin, Chronicle Staff Writer A fight has erupted between environmental groups and the nation's leading animal rights organization over the issue of laboratory animal testing. The dispute is the result of a media campaign by People for the Ethical Treatment of Animals against three mainstream environmental groups: the World Wildlife Fund, the Natural Resources Defense Council and Environmental Defense. PETA has denounced the three organizations for their support of the U.S. Environmental Protection Agency's use of laboratory animals to test toxic compounds. Such tests are unnecessary, PETA claims, and could be replaced with toxicology evaluations that don't use animals. ©2002 San Francisco Chronicle.

Keyword: Miscellaneous
Link ID: 2355 - Posted: 06.24.2010

Activity in brain's fear center affects response, study finds Los Angeles Times Scientists have identified a specific gene variation that sparks heightened activity in the brain's "fear center" -- the first gene identified to affect a function of the brain related to human emotion, according to researchers at the National Institutes of Health. The gene activates the amygdala, a portion of the brain that controls its response to frightening situations, and has been weakly linked to increased anxiety. David Weinberger, chief of the Clinical Brain Disorders Branch at the National Institutes of Health, said the research is a key step in understanding the complex biological puzzle of human temperament. ©2002 San Francisco Chronicle.

Keyword: Emotions; Genes & Behavior
Link ID: 2354 - Posted: 06.24.2010

By Peggy Peck UPI Science News STOCKHOLM, Sweden, (UPI) -- Brain researchers report that by using high-tech brain scans and computer simulations, they are now able to detect subtle, almost invisible changes in brain function 40 years before those changes cause the memory lapses, confusion and dementia associated with Alzheimer's disease. Such early detection may be the key to devising effective treatments to prevent the onset of symptoms. The findings were reported at the eighth International Conference on Alzheimer's Disease and Related Disorders. Dr. Eric Reiman said he discovered the changes in brain metabolism in 12 healthy volunteers, average age 30, who carry a single copy of the so-called Alzheimer's gene, apoliprotein E (APOE) e4 allele. Worldwide about one in four people carry a single copy of the Alzheimer's gene, which is associated with late onset Alzheimer's disease -- meaning the disease is diagnosed at age 70 or older. Copyright © 2002 United Press International

Keyword: Alzheimers; Brain imaging
Link ID: 2352 - Posted: 06.24.2010

A severe kind of bacteria which causes stomach ulcers could play a role in certain kinds of stroke, researchers suggest. Specific strains of Helicobacter pylori (H. pylori) were found to be much more prevalent in the blood of patients who had suffered an atherosclerotic stroke. Atherosclerosis refers to the narrowing and hardening of the arteries because of the build up of fatty deposits. H. pylori causes ulcers in the stomach. Researchers from Tor Vergata University in Rome found that strains of the bacteria which produce poisonous cytotoxins can aggravate the risk of arteriosclerosis in large arteries leading to the brain. If cytotoxins attack the artery wall, they can cause inflammation and swelling, restricting blood flow and increasing the chance of stroke. (C) BBC

Keyword: Stroke
Link ID: 2351 - Posted: 07.22.2002

Scientists have succeeded in making brainier mice. Whether the animals were actually smarter remains unknown, but their cerebral cortex surface area was significantly larger than that of normal mice. The findings, published today in the journal Science, may help explain how human brains came to be disproportionately large compared to those of other species. As the largest structure in the brain, the cerebral cortex harbors two-thirds of the brain's neurons in a thin layer. In humans the cortex folds in on itself in order to fit inside the skull, giving the brain a unique, wrinkled topography. To investigate what controls the surface area of the cerebral cortex, Anjen Chenn, now at Northwestern University School of Medicine, and Christopher A. Walsh of Beth Israel Deaconess Medical Center developed a line of transgenic mice. The animals carried a variant of a gene that makes a protein thought to play a role in regulating cell growth in the developing brain. "We found that in mice that overproduced the beta-catenin protein the mouse's cerebral cortex grew dramatically so that instead of a flat sheet, it folded in on itself and appeared 'wrinkled' much like it is in humans," Walsh explains. (The image to the right shows the brains of a control mouse (top) and a transgenic mouse (bottom).) © 1996-2002 Scientific American, Inc. All rights reserved.

Keyword: Cerebral Cortex; Development of the Brain
Link ID: 2350 - Posted: 06.24.2010

By ADAM LIPTAK Hey, Mom," Michael Grinsted, 16, said as he opened his mail recently, "they sent me Prozac." His mother, Sue Grinsted, of West Palm Beach, Fla., said she had worried about people offering illegal drugs to her son but had not thought about unsolicited mailings of prescription drugs like Prozac, an antidepressant. Eli Lilly, the manufacturer of Prozac, has apologized for earlier mailings of unsolicited drugs to adults with histories of depression. A spokesman for Lilly, Austin Blair, said the company was unaware of the new incident. Copyright 2002 The New York Times Company

Keyword: Depression; Miscellaneous
Link ID: 2349 - Posted: 07.21.2002

THE father of murdered mum Jane Thurgood-Dove says revolutionary technology that provides a window into a criminal's mind will solve her killing. The Niddrie mother was shot execution-style in her driveway in 1997 as her three children - then aged three, five and 10 - looked on. Now her shattered father, John Magill, believes "brain fingerprinting" - developed by a Harvard University scientist and the CIA and used in the War on Terror - will trap the killer. © News Limited

Keyword: Miscellaneous; Vision
Link ID: 2348 - Posted: 06.24.2010

Elevated levels of cholesterol may play an even greater role in the development of Alzheimer's disease than was first thought. Researchers from Georgetown University Medical Center examined the link between cholesterol and a protein called APP. APP is found in several major organs including the brain and heart. Nobody knows what role it plays in normal circumstances, but in people with Alzheimer's APP is processed in an abnormal way and is converted to beta amyloid protein. When fragments of this protein break off, they form the plaques that are one of the characteristic structural abnormalities found in the brains of people suffering from Alzheimer's. Past research has shown that high cholesterol levels appear to increase APP levels. However, the latest study has found that high cholesterol also increases the rate at which the amyloid beta peptides break off and form plaques. (C) BBC

Keyword: Alzheimers
Link ID: 2347 - Posted: 07.21.2002

NewScientist.com news service New evidence suggests that some drugs might prolong the notoriously lengthy incubation period of vCJD, the human form of mad cow disease - perhaps extending it sufficiently for the sickness to never take hold in a human lifetime. Millions of Europeans who have eaten BSE-infected meat could be harbouring vCJD. A key reason scientists do not know is the very fact that vCJD takes so long to develop. Hans Kretzschmar and colleagues at the Ludwig-Maximillians University in Munich infected mice with scrapie, a disease related to BSE. Some were also injected with a string of six nucleotide bases called CpG oligodeoxynucleotide 1826. © Copyright Reed Business Information Ltd.

Keyword: Prions
Link ID: 2345 - Posted: 06.24.2010

By Ania Lichtarowicz Having a healthy diet, exercising and not being overweight can not only reduce the risk of developing heart disease, but may also protect against Alzheimer's, new research claims. The research is being presented to 4,000 scientists at the six-day Alzheimer's Association conference in Stockholm from Saturday, the largest meeting dedicated to the disease. So far doctors have been unsure about what causes Alzheimer's disease; however, both genetic and environmental influences are thought to play a part. Now researchers believe they may have linked certain risk factors which are known to cause heart disease to the neurological condition. (C) BBC

Keyword: Alzheimers
Link ID: 2344 - Posted: 07.20.2002

Humans can read, write, and solve problems thanks to a huge cerebral cortex. To fit this sheet of brain tissue into a reasonably sized skull, the cortex of primates is wrinkled and creased, like a carpet that's much too large for its room. No one knows what prompted the cortex's expansion during primate evolution, but experiments described in the 19 July issue of Science point to one gene that might have played a role. Developmental neuroscientists Anjen Chenn and Christopher Walsh of Brigham and Women’s Hospital and Beth Israel Deaconess Medical Center in Boston created transgenic mice that made an engineered form of ß-catenin--a ubiquitous protein that has a hand in a dizzying array of developmental processes--in developing cells of the central nervous system. Because the designer protein resisted the cellular process that normally breaks it down, it accumulated in these cells. The resulting embryos had dramatically enlarged brains and a whopping cerebral cortex. The thickness of cortex was normal, but it had increased surface area--and folds and cavities similar to those seen in monkeys or humans. The mice died soon after birth, so the researchers do not know how the bigger brains would affect their behavior, but they suggest that increased ß-catenin expression in the brain might have been one of the evolutionary changes that led to bigger brains. Copyright © 2002 by the American Association for the Advancement of Science.

Keyword: Development of the Brain; Cerebral Cortex
Link ID: 2343 - Posted: 06.24.2010

By Laura DeFrancesco It's a dieters' dream: Eat what you want and never gain weight. But shedding pounds is an unwanted health issue for those who have cachexia--uncontrollable weight loss unaffected by eating. Cachexia adds significantly to the morbidity of cancer and chronic infectious diseases such as AIDS. The condition also compromises the health of the elderly, who lose muscle mass by the same process. Two papers recently reviewed by the Faculty of 1000 have added to the understanding of cachexia by approaching the subject from entirely different angles.1,2 According to David Sassoon , associate professor of biochemistry and molecular biology, Mount Sinai School of Medicine, NY, the field now is "moving quickly towards understanding the devastating collateral effect of infection and cancer." Many cachexia researchers focus on the preferential loss of muscle mass, which is cachexia's hallmark. In the first paper, however, the authors concentrated on changes in energy metabolism that accompany the condition. In fact, energy imbalance lies at the very heart of the process, says senior author Bruce Spiegelman , professor of cell biology, Dana-Farber Cancer Center, Boston. In Spiegelman's view, cachexia is widely misunderstood. "It's not just a problem of muscle differentiation. It starts with the energy balance issue." The key finding that propelled Spiegelman's work was his group's discovery of a master regulator of oxidative metabolism, the transcriptional activator PPAR*, and the coactivator PGC-1. PGC-1 has pleiotropic effects on respiration in response to various physiological signals that mediate energetic processes such as thermogenesis or gluconeogenesis. Spiegelman has linked this regulatory pathway to the cytokine TNF*, which was shown to induce cachexia in experimental models more than 20 years ago.3 This observation had tied certain diseases to cachexia, but it has provided no insight into the mechanism. The Scientist 16[15]:27, Jul. 22, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Obesity; Muscles
Link ID: 2342 - Posted: 06.24.2010

Latest discoveries by Rockefeller group show, among other things, what the channel looks like when it is open By Nicole Johnston Underlying every thought, heartbeat and movement are ion channels, busily conducting high-speed streams of ions into cells, like subway trains coursing through tunnels. Ion channels span the cellular membrane, forming passageways, or pores, through which ions flow down electrochemical gradients. Despite extensive studies of ion channels dating back more than 50 years, crucial structural pieces of the puzzle were still missing that would explain how the high-throughput transmission of ions is achieved, how channels discriminate between ions, and how they open and close in a fraction of a millisecond. One team is helping put those pieces together. Since 1998, Roderick MacKinnon , head of molecular neurobiology and biophysics, Rockefeller University, and Howard Hughes Medical Institute (HHMI) investigator, and colleagues have published papers revealing the potassium and chloride channel structures.1,2 In May the group published its latest findings, which show what the potassium channel looks like when it is open and how the calcium-mediated gating mechanism works like an on-off switch, controlling potassium ion flow through the channel.3,4 The Scientist 16[15]:23, Jul. 22, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Miscellaneous
Link ID: 2341 - Posted: 06.24.2010

Last summer, The Cellular Biology of Addiction Course at Cold Spring Harbor Laboratory was held from August 7-13, 2002. The lectures were videotaped and now can be seen online. The lecturers in the course were Terry Robinson, University of Michigan Jonathan D. Pollock, National Institute on Drug Abuse Roger Tsien, UCSD David Self, UT Southwestern Medical Center Robert Edwards, UCSF Gary Rudnick, Yale University Nora Volkow, Brookhaven National Laboratory Bertha Madras, Harvard Medical School Mark Von Zastrow, UCSF Paul Worley, Johns Hopkins University John Crabbe, Oregon Health Sciences University Henry Lester, Caltech Kent Vrana, Wake Forrest University Medical School Chris Evans, UCLA Mary Jean Kreek, Rockefeller University Dean Wong, John Hopkins Unversity

Keyword: Drug Abuse
Link ID: 2340 - Posted: 07.20.2002

Scientists have developed a treatment which may eventually help produce drugs to protect humans from vCJD incubating in their bodies. Mice with scrapie - a disease with causes and symptoms broadly similar to CJD - on average lived 38% longer if given the treatment after being exposed to the molecule that causes the illness. A group given daily injections for 20 days managed to stay completely disease free. Experts are hopeful that a treatment can be developed in case thousands of people worldwide are incubating the illness. Variant CJD is a brain disease in which the progressive death of brain cells gives the organ a spongy appearance. It is invariably fatal, and has been blamed on consumption of meat from cattle with BSE, or "mad cow disease". (C) BBC

Keyword: Prions
Link ID: 2339 - Posted: 07.19.2002