Eye movement provides insight on mechanisms of aerial maneuvering By Laura DeFrancesco Insects rule, says Michael Dickinson , professor of integrative biology at the University of California, Berkeley, and one of this year's MacArthur fellowship genius award winners. Insects, he contends, have reigned for half a billion years and are likely to do so for a billion more, considering their biomass, the sheer number of species, and their ecological impact. What really moves Dickinson is the insects' flying proficiency. The first organisms to evolve flight, insects still represent the most sophisticated aerial machine on the planet, he says. Flies, in particular, have unique specializations that lead to extraordinary behaviors: they can take off backwards, fly sideways, and land upside down. These singular behaviors, Dickinson says, "push the envelope of useful design, presenting a clearer picture of the structure/function of relationships than do more mundane behaviors." But understanding insect flight requires more than studying the nervous system, Dickinson told neuroscientists at their annual meeting last November. "From the mechanics of the muscle, to the biomechanics of the skeleton, and the aerodynamics of the wing, [all this] is important for understanding what was originally a neurobiological question," he said. The Scientist 16[2]:27, Jan. 21, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Vision
Link ID: 1363 - Posted: 06.24.2010

Scientists' focus on the secretases holds promise for Alzheimer's patients By Brendan A. Maher The all-out assault to impede production of b-amyloid (Ab ), the plaque-forming peptide believed by many to cause neurodegenerative Alzheimer's disease (AD), entails a war on two fronts. For those aiming to prevent plaques at their cellular source, the two clear targets are b-secretase and g-secretase, which sequentially cleave amyloid precursor protein (APP) to generate Ab. Some victories are emerging: Small molecules designed to inhibit g-secretase activity are being clinically tested, and the 1999 identification and cloning of b-secretase led researchers to design small molecule inhibitors. g-secretase, which has made it farthest as a drug target, still has an identity problem. One camp of researchers, including physician Dennis J. Selkoe, professor of neurologic diseases at Harvard Medical School, has put its money on presenilin1 (PS1),1 a molecule long associated with g -secretase activity. It is mutated in one form of early onset familial AD, which accounts for 5% to 10% of Alzheimer's cases. Selkoe says an upcoming paper, scheduled for publication in the Proceedings of the National Academy of Sciences, moves closer to showing that Presenilin-1 is indeed g-secretase. But not everyone is completely convinced. Raphael Kopan , associate professor of medicine, molecular biology and pharmacology at Washington University in St. Louis, explains, "The absolute proof will, of course, require demonstration that you can isolate presenilin1 with the substrate, play some mood music ... and eventually cleavage will occur." Sangram Sisodia , director for the center of neurobiology at the University of Chicago, is even less convinced. "My guess," says Sisodia, "is that [g -secretase] is going to be several different proteases that require presenilin and nicastrin for their function." Yet, in vitro demonstration continues to elude researchers. N.S. Halim, "Elusive b-secretase identified," The Scientist 14[13]:6, June 26, 2000. The Scientist 16[2]:25, Jan. 21, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Alzheimers
Link ID: 1362 - Posted: 06.24.2010

Researchers seek to turn antibodies against the amyloid-forming peptide in both mice and humans By Douglas Steinberg In 1999, scientists at Elan Corp.'s South San Francisco, Calif. facility stunned the Alzheimer Disease (AD) research community: vaccination, they announced, reduces AD-like pathology in transgenic mice.1 Since then, dozens of labs have been working on vaccines to prevent, retard, or reverse AD's devastating symptoms. One clinical trial is finished, a second is under way, and others appear imminent. In animal studies, researchers are testing different types of vaccines and examining how the immune system might foil the disease. After soliciting applications for AD vaccine projects, the National Institutes of Health last fall began distributing $22.5 million (US) to 13 studies, according to D. Stephen Snyder, a program director at the National Institute on Aging. Before Elan's study, "there were a lot of reasons to think not only that [vaccines] shouldn't be done but that they would make things worse," says Dale B. Schenk, the company's vice president of discovery research. The prevailing wisdom was that disease-fighting antibodies, which vaccines stimulate, couldn't penetrate the blood-brain barrier. If antibodies did sneak into the brain, the fear was that they would trigger a massive, unhealthy immune response. Schenk recalls that the vaccine study consequently had a "very low priority" at Dublin-based Elan. But he eventually mustered a large team that discovered the benefits to vaccinating an AD mouse model with b-amyloid (Ab ), the peptide that aggregates into amyloid plaques in Alzheimer brains. Mice that started receiving intramuscular injections when six weeks old didn't develop plaques and other neuropathology. Vaccinations begun at 11 months of age sharply reduced pathology, with plaques in the frontal cortex plunging 84% compared to controls. D. Schenk et al., "Immunization with amyloid-b attenuates Alzheimer-disease-like pathology in the PDAPP mouse," Nature, 400:173-7, 1999. The Scientist 16[2]:23, Jan. 21, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Animal Communication
Link ID: 1361 - Posted: 06.24.2010

Researchers say glutamate is more essential to addiction than dopamine By Tom Hollon In cocaine research, dopamine and glutamate make a brilliant star and supporting player, respectively. One takes center stage, the anointed crowd-pleaser; the other, though a leading actor in other productions, is so overshadowed that admiration of its performance is relegated to an acquired taste. A quick PubMed search recently disclosed their perceived importance: 3,628 abstracts on cocaine and dopamine, 178 for cocaine and glutamate. Now, however, perceptions may shift—not that dopamine descends from the firmament, but that glutamate will sparkle as brightly. Recent knockout mouse evidence1 from researchers led by François Conquet , CEO of Addex Pharmaceuticals in Geneva, Switzerland, reveals that glutamate's role in cocaine dependence is even more central than dopamine's. The case for dopamine's centrality remains airtight. Cocaine binds the dopamine transporter, blocking reuptake of dopamine into presynaptic neurons. Blockade increases dopamine concentration in synapses, an event responsible for cocaine's pleasurable effects and suggested as key to developing drug dependence. But although loss of the transporter and dopamine receptors in knockout mice may alter behavior toward cocaine, always the drug remains addictive. When the dopamine transporter is lost, for instance, mice may still become cocaine dependent through cocaine's ability to bind the serotonin transporter. This is not necessarily surprising, observes Peter Kalivas , of the Medical University of South Carolina in Charleston, who is a leading investigator of the glutamate-cocaine relationship. "The ability of an organism to predict rewarding stimuli in the environment is absolutely critical to survival," says Kalivas, "so there probably is some redundancy." 1. C. Chiamulera et al., "Reinforcing and locomotor stimulant effects of cocaine are absent in mGluR5 null mutant mice," Nature Neuroscience, 4:873-4, September 2001. The Scientist 16[2]:16, Jan. 21, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Drug Abuse
Link ID: 1360 - Posted: 06.24.2010

As funding increases, more investigators look for causes By Christine Bahls In 1977, Alzheimer Disease researcher Peter Davies spoke with some neurologists about his work, which he began a year earlier. "One [neurologist] said, 'This is lovely..., but why don't you work on something that is more common?'" he remembers. Davies says the comment epitomized scientists' then-dismissive attitude about Alzheimer Disease (AD). When Alois Alzheimer first identified this memory-destroying disorder in 1907, his patient was a 50-year-old woman; a very early age, as researchers now know, for most Alzheimer cases to appear. "The disease was largely ignored because it was considered to be presenile dementia," says Davies, the Resnick professor of AD research at Albert Einstein College of Medicine, New York. "Nobody paid attention to rarer patients." Today, with some 80 AD-related papers published weekly, the research is no longer rare. Says Zaven S. Khachaturian , who launched the Dementias of Aging and Neuroscience and Neuropsychology programs at the National Institute on Aging in the late 1970s, "I don't think any of us envisioned how large [the field] was going to get." Two reasons for this growth are the work of people such as Davies, whose research on acetylcholine provided a scientific basis to support further investigations, and the amount of funding that AD has since attracted. Says Marcelle Morrison-Bogorad , associate director, neuroscience and neuropsychology of the NIA's aging program, "if there hadn't been money going into Alzheimer's research for the last 25 years, it wouldn't have gone where it has." 1. G.G. Glenner, C.W. Wong, "Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein," Biochemical and Biophysical Research Communications, 120:885-90, 1984. The Scientist 16[2]:14, Jan. 21, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Alzheimers
Link ID: 1359 - Posted: 06.24.2010

Several diseases once thought to have very little in common now appear to share a key feature. Cell pores, known as ion channels, normally either directly or indirectly affect cell communication. But following a decade of research, scientists have found evidence that defects in the channels can give rise to a range of seemingly diverse diseases that intermittently attack patients who are otherwise healthy. The discovery may lead to new therapies that specifically target the channel defects and prevent the eruption of a variety of at tacks, including the seizures that are characteristic of epilepsy and migraine headaches. A man suffers bouts of muscle weakness. A young child shakes and convulses during a seizure. A woman's nemesis is blinding headaches. On the surface these afflictions, known as periodic paralysis, epilepsy and migraine, seem to share about as much in common as Britney Spears, Mozart and The Blue Man Group. A closer look, however, reveals that they all create intermittent, or episodic, attacks in otherwise healthy individuals. Copyright © 2002 Society for Neuroscience. All rights reserved.

Keyword: Epilepsy
Link ID: 1356 - Posted: 06.24.2010

Yesterday on top of the world, down in the dumps today: manic-depressives suffer from extreme fluctuations of mood. Many such people take their own lives during the phase of depression. An interdisciplinary team headed by the University of Bonn's Institute of Human Genetics has succeeded in localising a gene which contributes towards the manic depressive disease. The results were recently published in the journal Human Molecular Genetics. Charles Burgess Fry has the reputation of being one of the greatest sportsmen Britain has ever produced. The captain of the England cricket team, who also played football and rugby as well as writing several books about cricket, was an outstanding classical philologist whose hobby was translating English hymns into Greek. The popular partygoer, who was a notorious rake, turned down the Albanian throne in 1919; allegedly because the position was not salaried. Yet up to his death in 1956 he was prone to phases of unusual hyperactivity alternating with episodes of deep despondency: Fry showed many of the features of manic depression. About one per cent of all humans suffer, in the course of their lives, from this bipolar emotional disorder and this occurs in all the cultures which have hitherto been investigated. The causes are as yet unknown; therapy is therefore correspondingly difficult. Many of those affected commit suicide during the course of the disease. Hum. Mol. Genet. 2001 10: 2933-2944 © AlphaGalileo 2001

Keyword: Depression; Genes & Behavior
Link ID: 1355 - Posted: 06.24.2010

Washington, D.C. — Georgetown University Medical Center is conducting a clinical trial to assess the effectiveness of venlafaxine HCI, marketed as Effexor XR, on post traumatic stress disorder (PTSD). The drug is currently approved by the Food and Drug Administration for treatment of generalized anxiety disorder and depression, but not PTSD. Symptoms of PTSD include disturbed sleep, flashbacks, an increased heart rate, heavy sweating, and avoidance of activities that remind the person of the traumatic event. "Many people suffered shock and grief following the events of September 11," said David M. Goldstein, MD, professor of psychiatry and principal investigator of this project. "People who are still suffering from the aftereffects of this tragedy may have PTSD and could benefit from treatment." Effexor, whose manufacturer, Wyeth Ayerst, is funding the Georgetown study, works by increasing levels of two brain chemicals, serotonin and norepinephrine; Zoloft and many other antidepressants raise levels of serotonin alone. A deficiency of these two chemicals is believed to be a possible cause of PTSD (as well as depression and anxiety).

Keyword: Stress
Link ID: 1353 - Posted: 06.24.2010

James Meek, science correspondent The Guardian One of the last frontiers of the unexplored left on earth, the living human brain, is yielding up its secrets to a new tool developed in Britain. The revolutionary development allows researchers to see with extraordinary clarity the networks of nerve fibres - "white matter" - which link the different, thinking units of the brain, or "grey matter." Known as Vivid, for virtual in-vivo interactive dissection, the system harmlessly picks out patterns of nerve connections inside the brains of living people. The pathways are uncannily similar to those which previously could only be pictured by a draughtsman, laboriously sketching the bisected brains of the dead. Guardian Unlimited © Guardian Newspapers Limited 2002

Keyword: Brain imaging
Link ID: 1352 - Posted: 06.24.2010

Stress Hormones Change Brain Chemicals in Mice for Weeks. By Lauran Neergaard The Associated Press Jan. 17 — Even relatively short periods of stress may cause changes that leave brain cells hypersensitive for weeks, report Israeli scientists trying to uncover the molecular root of post-traumatic stress disorder. The experiments were with mice, and it's far from clear if human brain cells react the same way. But the research is generating interest among scientists struggling anew to unravel traumatic stress in the aftermath of terrorism. "It's a tantalizing new lead," said Rockefeller University professor Bruce McEwen, who researches stress effects on the brain. Copyright © 2002 ABCNEWS Internet Ventures.

Keyword: Stress
Link ID: 1351 - Posted: 06.24.2010

By SIMON COLLINS A classic "nature or nurture" debate has been reignited by research claiming that childhood sexual abuse is often a factor in causing schizophrenia. The research, led by Auckland University clinical psychologist Dr John Read, concludes that treatment of schizophrenia should include helping patients to talk about the traumas that may have helped bring on the disease. But an emeritus professor of psychiatry at the university, Dr John Werry, insisted yesterday that the illness was genetic and needed medication. ©Copyright 2002, New Zealand Herald

Keyword: Schizophrenia; Sexual Behavior
Link ID: 1350 - Posted: 06.24.2010

By Eric Haseltine Regions of the brain-such as left prefrontal cortex- believed to be involved in maintaining mood are often abnormally small and under-active in patients who have suffered episodes of major depression. The relationship between these abnormalities and depressive symptoms is not clear, but one intriguing possibility is that prolonged or acute stress and associated over-secretion of stress hormones -such as cortisol -might impair mood centers in the brain, increasing the chances that individuals under stress will become depressed. This simulation shows one kind of complex interaction that could connect stress and depression. © Copyright 2001 The Walt Disney Company.

Keyword: Depression; Stress
Link ID: 1349 - Posted: 06.24.2010

By Eric Haseltine It's hard to be a productive member of the human race unless you can recognize faces and facial expressions, so our brains have evolved special circuits for processing facial information. These facial image processors are so aggressive that they often report the presence of faces where none are present. Examine these slabs of marble for a moment and you'll probably perceive several visages in both front and side views. Click on the "Play" button to see an area where a face suggested itself to me, then click on the button again to see the exact facial contours my brain perceived. You might see a different face. Usually, the people we are looking at are rightside up; when they're not, our face processing neurons struggle to do their job. © Copyright 2002 The Walt Disney Company.

Keyword: Miscellaneous
Link ID: 1348 - Posted: 06.24.2010

By Jennifer Viegas, Discovery News — Neanderthal tools were built to last, according to a recent analysis of artifacts that revealed Neanderthals made a strong, relatively high-tech adhesive to affix wooden handles to flint stone knives. The discovery suggests that, despite their bumbling reputation, Neanderthals were perhaps as intelligent and industrious as early modern humans. Neanderthals appeared approximately 230,000-300,000 years ago and are believed to have gone extinct 30,000 years ago. Copyright © 2001 Discovery Communications Inc.

Keyword: Evolution
Link ID: 1347 - Posted: 06.24.2010

DALLAS – In one of the most ambitious medical experiments ever conducted aboard a space shuttle, UT Southwestern Medical Center at Dallas space researchers have pinpointed the mechanism responsible for the brief loss of consciousness and lightheadedness that many astronauts experience in the upright posture after space flight. The findings have broad application to medicine, both in space and on earth. Two-thirds of astronauts experience orthostatic intolerance after space flight. Symptoms include lightheadedness, dizziness, palpitations and difficulty concentrating upon standing. The same condition also affects 500,000 people in the United States. Using data collected during the 1998 Neurolab space shuttle mission, UT Southwestern researchers reported in one of three papers in a series of studies published in the January issue of The Journal of Physiology, that orthostatic intolerance is due to the heart shrinking and becoming stiff.

Keyword: Miscellaneous
Link ID: 1346 - Posted: 06.24.2010

Researchers studying learning disabilities associated with neurofibromatosis type 1, or NF1, have traced the problem to excessive activity of a crucial signaling molecule and have successfully reversed the disabilities in mice by giving them an experimental drug. The findings provide hope that these learning problems may one day be treatable in humans. This study provides the first clear picture of what causes learning impairments in NF1, says study author Alcino J. Silva, Ph.D., of the University of California, Los Angeles (UCLA). NF1 is a genetic disorder that affects about one in every 4000 people. Patients with the disorder have an array of symptoms, including benign tumors called neurofibromas and light brown spots on the skin called café-au-lait spots. About half of the affected individuals have cognitive disabilities, which typically include problems with spatial learning (which affects organization and other abilities) and reading. The study appears in the January 16, 2002, electronic edition of Nature* and was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS).

Keyword: Trophic Factors; Miscellaneous
Link ID: 1345 - Posted: 01.17.2002

Neural Plasticity Rather than a General Measure Better Defines the Potentials and Limitations of Intelligence WASHINGTON - According to neuro and cognitive scientists, different intellectual abilities are based on neural circuits that require environmental stimulation for development and are open to change. However, intelligence researchers' argue that there is a general factor of intelligence or g, that is highly heritable and defines intelligence as an overall innate ability to perform well on different measures of intelligence, which are not open to change. This debate is reviewed in an analysis of 124 studies of the underlying basis of intelligence in the January issue of Psychological Review published by the American Psychological Association. Psychologist Dennis Garlick, Ph.D., of the University of Sydney in Australia, submits that the neural plasticity model of intelligence better explains how intelligence is developed. This model suggests that intelligence is created when neural connections in the brain are changed in response to environmental cues. According to Garlick, recent advances in neuroscience and cognitive science have suggested that different intellectual abilities require different neural connections in the brain and that the only mechanism that allows the brain to grow such connections would be an adaptation mechanism that responds to environmental input. © PsycNET 2001 American Psychological Association

Keyword: Intelligence
Link ID: 1344 - Posted: 06.24.2010

Copyright © 2002 AP Online By JOANN LOVIGLIO, Associated Press PHILADELPHIA - A new study of mice suggests repeated head injuries may accelerate Alzheimer's disease. Researchers found mice that received repetitive knocks to the head - similar in severity to what a professional boxer or football player would experience - developed deposits of a plaque-like protein faster than mice who did not suffer head trauma. The protein, called amyloid beta, seemed to appear in mice in response to the injuries and can be found in brains of Alzheimer patients, the University of Pennsylvania researchers said. Copyright © 2001 Nando Media

Keyword: Alzheimers; Brain Injury/Concussion
Link ID: 1343 - Posted: 06.24.2010

Copyright © 2002 AP Online By LINDSEY TANNER, Associated Press CHICAGO- A new study shows at least 47 million American adults - or more than one in five - have metabolic syndrome, a disorder that often includes a beer belly, high blood pressure, poor cholesterol readings and high blood sugar. Metabolic syndrome has been recognized since at least the 1920s, though it has been called different things over the years. It is not a single disease but a cluster of health problems, and despite its name, does not necessarily mean a person's metabolism is defective. Though experts say the syndrome may be caused by a combination of genes and lifestyle factors, lifestyle - including overeating and a lack of exercise - are probably the most important factors, said Dr. Earl Ford of the Centers for Disease Control and Prevention, who led the study. Copyright © 2001 Nando Media

Keyword: Obesity
Link ID: 1342 - Posted: 06.24.2010

(Philadelphia, PA) - The posthumous gift of eyes from a patient with a rare retinal disease, enhanced S cone syndrome (ESCS), has taught researchers more about the role of NR2E3, the gene that causes this form of blindness. ESCS is an inherited condition that gradually causes night blindness, loss of peripheral vision, and sensitivity to blue light. Researchers at the Scheie Eye Institute at the University of Pennsylvania Medical Center led the study, which was presented in the January 8 edition of the Proceedings of the National Academy of Sciences. "This is one of those occasions where a generous eye donor has helped scientists to understand a rare disease," said Ann H. Milam, PhD, lead author and a researcher at the F. M. Kirby Center for Molecular Opthalmology within the Scheie Eye Institute. The donated retinas came from a person with two copies of the mutated gene, one from each parent. "Here, we can learn what the NR2E3 gene does by seeing what physically happens when it fails to work correctly."

Keyword: Vision; Genes & Behavior
Link ID: 1341 - Posted: 01.17.2002