Results Hold Possibilities For Treating Parkinson’s and Lou Gehrig’s Disease HOUSTON, Jan. 18, 2002 – New research from University of Houston scientists may lead to techniques for jump-starting the faulty "wiring" in damaged nerve cells, and suggests possible avenues for treating spinal cord injuries, Parkinson’s disease and amyotrophic lateral sclerosis, or ALS, also known as Lou Gehrig’s disease. University of Houston scientists studying how spinal nerve cells in chicken embryos develop and function have found that chemicals called growth factors play a key role in regulating how embryonic nerve cells acquire the ability to start processing information. "In some cases, when nerves are damaged or succumb to neurodegenerative diseases such as ALS and Parkinson’s, they don’t die, but they quit working and may actually revert to an immature embryonic-like state," says Stuart Dryer, a neuroscientist in the department of biology and biochemistry at UH. Embryonic nerve cells are able to fire electrical impulses shortly after the cells have divided for the last time – after they are "born." But these impulses are extremely generic, and not necessarily specialized for the kind of information the cell is going to eventually process, Dryer says.

Keyword: ALS-Lou Gehrig's Disease ; Parkinsons
Link ID: 1368 - Posted: 06.24.2010

Researchers discover that our perception of diagnostic features is controlled by single neurones. Perception is something that must be learned. As we recognize things in our environment we gather experience and this experience in turn colours our perception. This is nothing new, of course. But brain researchers are going one step further to ask how different kinds of information are integrated in the brain and what principles govern how perceived objects are represented there. Scientists at Tuebingen's Max Planck Institute for Biological Cybernetics have carried out experiments that prove that single nerve cells in the brain are responsible for controlling our perception by drawing on prior experience. They report their findings in the January 17, 2002 issue of the journal Nature. Our perception of objects depends on our prior experience with them. What most people would call a bird is "obviously" a sparrow, sandpiper, or cockatiel for a birdwatcher. Expertise sharpens our ability to notice details. The more we learn about objects and the more familiar they become, the more details we recognize. Thus, we continue to make generalizations, but these generalizations get better and more accurate all the time. A research group at the Max Planck Institute for Biological Cybernetics has studied what happens in the brain when we familiarize ourselves with objects. To do this they first taught rhesus monkeys to categorize objects according to specific features. Monkeys are ideal subjects for such experiments, for they are able to master a variety of visual categorization tasks and the organization of their visual system is strikingly similar to that of humans.

Keyword: Vision; Learning & Memory
Link ID: 1367 - Posted: 01.19.2002

Nathan Seppa A comparison of Latino, white, and Chinese-American smokers suggests that people of East Asian descent are apt to clear nicotine from their blood more gradually than the other smokers do, thereby staving off a craving for the next cigarette. Researchers recruited 131 smokers—37 Chinese-Americans, 40 Latinos, and 54 whites—for the analysis. Each volunteer gave a blood sample before receiving an intravenous infusion of nicotine. The substance was labeled with deuterium atoms, a heavy form of hydrogen, to make it detectable in the blood. After the injection, the participants provided 10 blood samples at specific intervals over the next 8 hours, then one per day for 4 days. Nicotine is cleared from the blood by liver enzymes that convert it to its metabolite cotinine. Blood analysis showed that it took an average of 152 minutes for half the injected nicotine to degrade in the blood of the Chinese-Americans in this study. Nicotine's half-life in whites and Latinos was 134 and 122 minutes, respectively. Slow metabolism of nicotine draws out its effects, says Neal L. Benowitz, a clinical pharmacologist at the University of California, San Francisco. He and his colleagues report their work in the Jan. 16 Journal of the National Cancer Institute. From Science News, Vol. 161, No. 3, Jan. 19, 2002, p. 38. Copyright ©2002 Science Service. All rights reserved.

Keyword: Drug Abuse
Link ID: 1366 - Posted: 06.24.2010

The acetylation state of nuclear proteins could be one key to pathology and treatment By Douglas Steinberg For the first time, a study is suggesting a viable treatment to stop and even reverse Huntington's disease (HD), a lethal disorder afflicting about one of every 15,000 people. This treatment involves a class of drugs already being tested on cancer patients. Typically striking around age 40, HD causes uncontrolled movements, cognitive deficits, and emotional disturbances. Neurons degenerate in certain brain regions. The disease is inevitable if a person inherits a mutant copy of the HD gene in which the first exon contains 40 or more consecutive CAG repeats, each encoding the amino acid glutamine. According to one prominent theory, the gene product, mutant huntingtin (mHTT), folds differently than its wild-type counterpart (the function of which is unknown). As a result, mHTT is cleaved and migrates from the cell's cytoplasm to its nucleus. What happens next has become the focus of intense scrutiny because it is apparently a key to HD pathology. A recent Nature paper reported that mHTT's polyglutamine-containing region binds to the acetyltransferase domains of several transcriptional co-activator proteins and inhibits enzymatic activity.1 Ranked ninth on the Faculty of 1000's December 10th Neuroscience Top 10 list, the paper also disclosed that mHTT reduces acetylation of histones H3 and H4 in a rat cell line. Histone deacetylase inhibitors reversed that process, and when administered to Drosophila models of polyglutamine disease, these inhibitors stopped neuronal degeneration and prevented flies from dying. T S. Steffan et al., "Histone deacetylase inhibitors arrest poly-glutamine-dependent neurodegeneration in Drosophila," Nature, 413:739-43, Oct. 18, 2001. The Scientist 16[2]:34, Jan. 21, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Huntingtons
Link ID: 1365 - Posted: 06.24.2010

It's not necessarily about who is better at what, but why the sexes process some stimuli in dissimilar ways By Karen Young Kreeger Stereotypes aside, women and men do process information in singular ways. In the past, tests that tried to pinpoint those variations were fraught with inconsistencies and irregularities. But now, by studying the brain itself, researchers are learning that the sexes use different parts of the brain to handle the same input. A growing number of imaging studies reveal that women and men do not process certain cognitive information in the same way. For instance, researchers have found that women, when trying to exit a virtual 3-D maze, activated the right parietal cortex and right prefrontal cortex; men triggered the left hippocampus alone.1 When viewing emotionally disturbing images, women showed an increase in activity on the amygdala's left side; in men, it was the right side.2 The amygdala is a small brain region associated with mood and feelings. Fertile research ground exists for researchers who want to figure out why and how this processing differs, and more specifically, how hormones are involved. And even bigger questions lie ahead in terms of assigning any adaptive significance to these differences. "I think that it's appropriate that we should expect a fair number of proximate processing differences because the ecology of being male and the ecology of being female has been, through our evolutionary history, so different," says evolutionary biologist and behavioral ecologist Bobbi S. Low, University of Michigan, Ann Arbor. G. Gron et al., "Brain activation during human navigation: gender-different neural networks as substrate of performance," Nature Neuroscience, 3:404-8, 2000. The Scientist 16[2]:28, Jan. 21, 2002 © Copyright 2002, The Scientist, Inc. All rights reserved.

Keyword: Sexual Behavior
Link ID: 1364 - Posted: 06.24.2010

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