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

New painkiller may be 10,000 times stronger than morphine. INGRID HOLMES A sea-snail toxin could relieve chronic pain1 . Tests on rats hint the chemical could be 10,000 times more potent than morphine, non-addictive and not cause side-effects. A team from the University of Melbourne led by Bruce Livett extracted the 'conotoxin' from a cone-shell snail. They will announce their patented discovery, called ACV1, this week at the Venoms to Drugs 2002 conference on Heron Island, Australia. More than 60% of us will suffer long-term pain at some time. Despite the addictive nature of morphine, many patients suffering from chronic pain eventually receive it, as there are few effective alternatives. © Nature News Service / Macmillan Magazines Ltd 2002

Keyword: Pain & Touch
Link ID: 2338 - Posted: 06.24.2010

St. Louis, -- Researchers at Washington University School of Medicine in St. Louis have developed a mouse model of the genetic disorder tuberous sclerosis complex (TSC). The mice develop epilepsy within the first few months of life, mimicking one of the most devastating complications of TSC in children. This research represents one of the first animal models of epilepsy that does not require toxic injections or injury and results from a single gene defect. It appears online July 18 in the Annals of Neurology and will be published in the September issue of the journal. "What's enormously exciting about this study is the potential to employ this mouse model as a pre-clinical model for TSC-related epilepsy," says David H. Gutmann, M.D., Ph.D., the Donald O. Schnuck Family Professor of Neurology. "In addition, we disrupted a gene for TSC in one of the brain's support cells, called astrocytes, instead of in the brain's main communication cells, neurons. Our results therefore shed light on the contribution of cells other than neurons to the development of seizures and epilepsy."

Keyword: Epilepsy
Link ID: 2337 - Posted: 07.19.2002

Copyright © 2002 AP Online By EMMA ROSS, AP Medical Writer LONDON - You've heard it before: If you want to remain healthy, eat more fruit and vegetables and less red meat. But scientists now say such a diet also may help prevent Alzheimer's disease. In fact, mounting evidence indicates the risk factors for heart disease - high blood pressure, diabetes, excess weight, high cholesterol and lack of exercise - may play a role in Alzheimer's. New studies to be presented next week at an international Alzheimer's conference in Stockholm establish the big picture for the first time, giving scientists a better understanding of how to reduce the likelihood of the disease. Copyright © 2001 Nando Media

Keyword: Alzheimers
Link ID: 2336 - Posted: 06.24.2010

The amygdala, the brain structure known as the hub of fear, responds differently to pictures of scary faces, depending on which version of a gene one has inherited, report National Institute of Mental Health scientists. Functional Magnetic Resonance Imaging (fMRI) scans revealed that subjects who inherited one or two copies of the short variant of the human serotonin transporter gene experienced greater activation of the amygdala when shown the pictures than those with two copies of the long variant of the gene. The gene's effect on the amygdala's response to emotional stimuli may help shape a dimension of temperament, suggest Drs. Ahmad Hariri and Daniel Weinberger, NIMH, and colleagues, in the July 19, 2002 Science. "How biologically reactive we are to a signal of danger, which is partly heritable, can place us at risk for an anxiety disorder or it may be an adaptive, positive attribute, such as increased vigilance, depending on the circumstances," explained Weinberger. "Anxiety is a complex experience not caused by any one gene or environmental factor. By showing how a variation in a gene exerts its influence on the brain's center for fear processing, this finding may lend credence to earlier reports linking the short gene variant to slightly higher levels of anxiety. It provides potential insight into one factor that contributes to the way people experience emotion." Each of us inherits two copies of the transporter gene for the chemical messenger serotonin , one from each parent. It codes for the protein in neurons that recycles secreted serotonin from the synapse. Serotonin reuptake inhibitors (SSRIs), the most widely prescribed medications for anxiety and depression, act by blocking the transporter. The two common genetic variations occur in a region of the gene that acts like a dimmer switch, controlling the level of the gene's turning on and off.

Keyword: Emotions; Genes & Behavior
Link ID: 2335 - Posted: 07.19.2002

— A protein that escalates the rate of growth of the cerebral cortex in young mice may help scientists explain how changes in a relatively small number of genes that regulate neural development may have contributed to increases in the size of the brains of higher mammals. In an article published in the July 19, 2002, issue of the journal Science , HHMI physician postdoctoral fellow Anjen Chenn and Christopher A. Walsh at Beth Israel Deaconess Medical Center and Harvard Medical School reported that the cerebral cortex of transgenic mice bearing an altered form of the protein ?-catenin expanded horizontally in area but not in thickness. These changes produced characteristic crests and grooves, called gyri and sulci, which anatomically distinguish human brains from those of lower animals. The cerebral cortex is the region of the brain responsible for higher intellectual functioning. “It has long been known that during evolution, the size of the cerebral cortex expanded disproportionately relative to the rest of the brain,” said Chenn. “But not very much was known about the developmental mechanism underlying that expansion. One theory is that the number of progenitor cells increased during evolution, and these cells gave rise to neurons that made up a greater number of repeating functional units called cortical columns.” According to this theory, said Chenn, the greater number of progenitor cells might result from immature cells that continue to divide to produce even more progenitor cells, before ultimately “committing” to develop into neurons. ©2002 Howard Hughes Medical Institute

Keyword: Development of the Brain; Cerebral Cortex
Link ID: 2334 - Posted: 06.24.2010

— Beginning with cultured mouse embryonic stem cells, researchers have administered a precise mix of chemical signals to coax the cells to differentiate into functioning motor neurons. The achievement was made possible by a decade of work in deciphering the signals that trigger differentiation of motor neurons, which are responsible for controlling the movement of muscles. The experiments represent an important step in applying that knowledge to grow functioning neurons from stem cells — undifferentiated cells that have the potential to become many different types of adult cells. According to the researchers, the success of the experiments with mouse cells suggests that the same type of approach might be used to grow human motor neurons from stem cells. Such neurons could enable regeneration of nerve tissue lost to disease or trauma. ©2002 Howard Hughes Medical Institute

Keyword: Development of the Brain
Link ID: 2333 - Posted: 06.24.2010

— By studying gene mutations in patients with the complex set of behavioral and neurological symptoms that accompany Rett syndrome, Howard Hughes Medical Institute investigator Huda Zoghbi and her colleagues at Baylor College of Medicine have designed a mouse model that faithfully recapitulates the disease down to its distinctive hand-wringing behavior. The development of the mouse, reported in the July 18, 2002 issue of the journal Neuron, provides a springboard into the study of Rett syndrome, the leading cause of mental retardation in girls. First recognized as a syndrome in the 1980s, the disorder affects one in 10,000-15,000 girls. It is particularly devastating for families with affected children because infants are seemingly normal at birth and achieve the usual developmental milestones for the first few months of life. Then, as the infant reaches toddlerhood, a sudden and dramatic decline in physical and mental capabilities takes hold, accompanied by onset of seizures, irregular breathing, awkward gait, and hand-wringing. “I know of no other neurological disease that gives this distinctive stereotypic behavior — this hand-wringing these girls do basically all the time they are awake,” said Zoghbi. “With this mouse model we can now ask, ‘Why is that?’” ©2002 Howard Hughes Medical Institute

Keyword: Genes & Behavior; Intelligence
Link ID: 2332 - Posted: 06.24.2010

Elephants may be listening to and communicating with each other through their feet. Recent research by US scientists supports previous claims that elephants can interpret slight vibrations they pick up in the ground. Speaking to BBC World Service, Stanford University biologist Caitlin O'Connell-Rodwell, said: "For people who have spent time studying elephants, this is a relief. "They finally understand some strange things that were happening with elephants and they really are excited about it." (C) BBC

Keyword: Animal Communication; Hearing
Link ID: 2331 - Posted: 07.18.2002

How to distinguish a phony grin from the real thing By Eric Haseltine and Andrew Epstein You've probably seen driver's license photos in which the subjects looked anything but happy, even though they were smiling. Apparently, a smile by itself is not enough to convey genuine joy. But what distinguishes a real grin from a fake one? And what goes on in the brain to produce genuine versus ersatz expressions in the first place? To find out, click on the camera on the left, then the box on the right. When a photographer asks you to name an aged, fermented dairy product, the part of your cerebral cortex that controls voluntary movements in your lower face gets busy, instructing the muscles around your mouth to contract into a forced smile. © Copyright 2002 The Walt Disney Company.

Keyword: Vision
Link ID: 2330 - Posted: 06.24.2010

Functional MRI scans have revealed a "biologically embedded" basis for altruistic behavior, with several characteristic regions of the brain being activated when players of a game called "Prisoner's Dilemma" decide to trust each other and cooperate, rather than betray each other for immediate gain, say researchers from Emory University. They report on their study in the July 18 issue of the journal Neuron, published by Cell Press. For many years, evolutionary biologists, behaviorists, economists and political scientists have attempted to understand why cooperation exists between human beings, even though that cooperation may not result in a direct or immediate reward. This unselfish behavior called "altruism" is almost uniquely a human trait. Up until now, almost all brain imaging experiments that have studied the social brain have done so by exposing subjects to static 2-D images inside the scanner. "This study represents an attempt to learn about the social brain by scanning people as they are engaged in a true social interaction," said James K. Rilling, Ph.D., principal investigator in the Emory study, who is currently serving a postdoctoral fellowship at Princeton University.

Keyword: Brain imaging
Link ID: 2329 - Posted: 07.18.2002

Copyright © 2002 AP Online By PAUL RECER, AP Science Writer WASHINGTON - Cancer patients often suffer needlessly because the nation's medical system does a poor job of treating pain that is a common part of the disease, according to experts who produced a study for the National Institutes of Health. "Cancer-related pain, depression and fatigue are undertreated and this situation is simply unacceptable," said Dr. Donald Patrick, a medical professor at the University of Washington, Seattle, and chairman of the committee. "We have to move to the point that patient comfort and care are a part of the cancer treatment agenda," said Dr. Andrew T. Turrisi III, a radiation oncologist at the Medical University of South Carolina, Charleston. "Some patients are more fearful of pain than they are of death itself." Copyright © 2001 Nando Media

Keyword: Pain & Touch
Link ID: 2328 - Posted: 06.24.2010

Copyright © 2002 AP Online By LAURAN NEERGAARD, AP Medical Writer WASHINGTON - The notorious date-rape drug GHB won government approval Wednesday to treat a rare but dangerous complication of the sleep disorder narcolepsy - but it will be sold under some of the most severe restrictions ever imposed on a medicine. The Food and Drug Administration approval puts the chemical in a peculiar position. Throughout the 1990s, the government cracked down on illegal use of GHB - abused as a party drug, sex and athletic enhancer and - because it can knock people out - a date-rape drug. Several dozen deaths are blamed on the chemical's abuse. Now the maker of the only FDA-approved version, Orphan Medical Inc., will have to balance how to get GHB to the relatively few patients who qualify while keeping it from falling into the wrong hands. Copyright © 2001 Nando Media

Keyword: Narcolepsy; Drug Abuse
Link ID: 2327 - Posted: 06.24.2010