CHICAGO --- Accumulation of neurofibrillary tau tangles not only causes the memory loss that occurs in Alzheimer's disease but also may be responsible for the memory deficits seen in normal aging and in some cases of mild cognitive impairment, a study from Northwestern University and the University of Miami has found. Mild cognitive impairment is isolated memory loss more severe than what is associated with "normal aging," but without the additional cognitive difficulties or disruptions of daily living activities characteristic of Alzheimer's disease. Individuals with mild cognitive impairment have been shown to develop Alzheimer's at a higher rate than those without cognitive impairment, suggesting that mild cognitive impairment may represent an intermediate stage between aging-related memory loss and Alzheimer's disease.

Keyword: Alzheimers
Link ID: 3820 - Posted: 05.20.2003

By Rossella Lorenzi, Discovery News — Baby seals can recognize their mother's voice in the hubbub of large dense breeding colonies as early as two days after birth, according to a study published in the current issue of the journal Animal Behavior. One of the few investigations of voice recognition in mammals, the study focuses on subantarctic fur seals (Arctocephalus tropicalis) living on the remote Amsterdam Island in the Indian Ocean. "By conducting playback experiments with both natural and synthetic signals, I identified the acoustic parameters effectively used in these recognition processes. I also studied the ontogeny of mother's voice in pup: we demonstrated that pups need to be 2 to 5 days old to be able to recognize their mother's voice," lead author Isabelle Charrier, from University of Alberta, told Discovery News. Copyright © 2003 Discovery Communications Inc.

Keyword: Development of the Brain; Hearing
Link ID: 3819 - Posted: 06.24.2010

Anti-anti-smoking study provokes furore among researchers. HELEN PEARSON Public-health experts are up in arms over a controversial new study claiming that passive smoking may not be a killer. The 39-year analysis, involving some 118,000 subjects, finds that smokers' spouses were no more likely than those in smoke-free households to die from lung cancer and heart disease1. It is co-authored by James Enstrom of the University of California, Los Angeles, and Geoffrey Kabat of the State University of New York, Stony Brook. Based on the findings, Enstrom questions whether banning smoking in public spaces really saves lives. "I feel that the question about whether it protects people from dying is overblown," he says. © Nature News Service / Macmillan Magazines Ltd 2003

Keyword: Drug Abuse
Link ID: 3818 - Posted: 06.24.2010

3-dimensional pictures of ALS mutant proteins support two major theories about how the disease is caused A new study reveals for the first time how gene mutations lead to the inherited form of amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. The study suggests that the two most prominent theories of how familial ALS (FALS) and other related diseases develop are both right in part. "No one has ever demonstrated at the molecular level how ALS mutations might lead to disease," says study author John Hart, Ph.D., director of the University of Texas Health Science Center X-ray Crystallographic Core Laboratory in San Antonio. "Using a technique commonly used in structural biology, we could see the intimate details of how toxic familial ALS proteins interact. And we found out that the proteins are interacting in a way they shouldn't be." The study was funded by the National Institute of Neurological Disorders and Stroke and appears in the June 2003 issue of Nature Structural Biology. ALS is a progressive, fatal neurological disease that usually strikes in mid-life. It causes muscle weakness, leads to paralysis, and usually ends in death within 2 to 5 years of diagnosis. Affecting as many as 20,000 Americans, ALS occurs when specific nerve cells in the brain and spinal cord that control voluntary movement gradually degenerate.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 3817 - Posted: 05.19.2003

Was Orton right? Washington, DC – Using functional magnetic resonance imaging (fMRI) to study brain activity in children, researchers today confirmed part of an eighty-year-old theory on the neurobiological basis of reading disability, and shed new light on brain regions that change as children become accomplished readers. Their findings were reported in the May 18 online publication of the journal Nature Neuroscience. In 1925 Dr. Samuel Orton, a clinician and prominent dyslexia researcher, hypothesized that normally developing readers suppress the visual images reported by the right hemisphere of the brain because these images could potentially interfere with input from the left. Advanced technology allowed researchers at Georgetown University Medical Center to discover that children do in fact "turn off" the right side of the visual parts of the brain as they become accomplished readers. This confirms an aspect of Orton's theory--born out of observations of individuals with reading disability--is correct. For the first time, they also were able to demonstrate that different phonological skills relate to activity in different parts of the brain when children read. Phonological skills allow readers to sound out words by correctly associating sounds with written symbols. They are critical for children learning to read and are often found to be impaired in children with developmental dyslexia.

Keyword: Dyslexia
Link ID: 3816 - Posted: 06.24.2010

Overextended polyglutamine in huntingtin protein has eclectic effects on the cell By Ricki Lewis In the late 1800s, Long Island physician George Huntington lent his name to this disorder, which is characterized by uncontrollable, dancelike movements and personality changes.6 After a long illness, individuals with HD die from complications such as choking or infection. The genetic marker discovered in 1983 had the uninspiring name G8 and the gene discovered 10 years later had the equally ineloquent IT15, for "interesting transcript 15." HD was one of the first expanded triplet repeat disorders identified, caused by extra glutamines at huntingtin's amino end. Normal huntingtin has 34 glutamine repeats and is likely antiapoptotic. Mutant proteins with more than 40 repeats cause HD. Wild-type huntingtin is cleaved and stays in the cytoplasm. Elongated, it invades the nucleus, where its effects are dual. "Mutant huntingtin enters the nucleus through pores, losing its antiapoptotic function and generating toxic products. So HD is both a gain of function through the generation of polyglutamine fragments, and a loss of antiapoptotic function," explains Michael Hayden, a professor of medical genetics at the University of British Columbia. Abnormally extended huntingtin may disable transcription factors as well as clog proteasomes. "It is becoming increasingly challenging to make sense of it all, to see all the effects of polyglutamine and to identify those important to the disease mechanism, as opposed to the so-called epiphenomena that just happen," says Kenneth Fischbeck, director of the neurogenetics division at the National Institute of Neurological Disorders and Stroke. HD may reflect an unfortunate pairing: polyglutamine is more likely to aggregate than other amino acids, and neurons are more likely to feel the effects than other cells.7,8 "Neurons appear to be exquisitely sensitive to expanded stretches of polyglutamines. This may be because they no longer divide, they have different sets of proteins expressed, and as they age, their ability to deal with cellular insults decreases," explains Larry Marsh, professor of developmental and cell biology at the University of California, Irvine.4 Adds co-author and colleague Joan Steffan, associate professor of psychiatry and human behavior, "Neurons have a different set of transcription factors expressed than other cells, and these transcription factors are more sensitive to interference by polyglutamine-containing proteins." ©2003, The Scientist Inc.

Keyword: Huntingtons
Link ID: 3815 - Posted: 06.24.2010

When Tessa found out she was pregnant after fertility treatment, she felt a mix of delight and doubt. .... Estimates suggest that 5% of the population may have a different father to the one they think they are related to, says Professor John Burn, of the Institute of Human Genetics in Newcastle. He runs one of the UK's few paternity testing services, which carries out about 300 DNA tests a year - a third of results surprise those involved. But men should be cautious about trying to prove their suspicions, he says, for the truth is often unkind.

Keyword: Sexual Behavior
Link ID: 3814 - Posted: 05.19.2003

A friendly approach works best when a male hyena wants a mate - while bullying or aggressive courting gets him nowhere, researchers have found. The study, of hyenas in the Serengeti, Tanzania, turns on its head the assumption that socially dominant males would have more reproductive success. It also shows that females have clear tactics to keep over-enthusiastic suitors at bay. The researchers used genetic testing to establish which pups had been sired by which males within groups of hyenas. They found that males which had attempted to use harassment or "monopolisation" to mate with females rarely ended up fathering offspring. Males that took their time to "befriend" females had far more success. Friendly tactics included grooming, greeting and making "amicable" gestures. (C) BBC

Keyword: Sexual Behavior
Link ID: 3813 - Posted: 05.19.2003

Chronic wasting disease, a cousin of mad cow disease, is spreading among wild deer in parts of the U.S. Left unchecked, the fatal sickness could threaten North American deer populations--and maybe livestock and humans By Philip Yam A place called the eradication zone, lying about 40 miles west of Madison, Wis., covers some 411 square miles. There thousands of white-tailed deer live--or rather, used to live. Last year the Wisconsin Department of Natural Resources instituted special hunting periods to try to wipe out upward of 18,000 deer. During the fall, dead deer were taken to registration areas, where state employees in protective suits and gloves dragged carcasses from pickup trucks and lifted them onto plastic-covered picnic tables. With hacksaws, they severed the heads, double-bagged them and sent them for testing; the bodies themselves were incinerated. © 1996-2003 Scientific American, Inc.

Keyword: Prions
Link ID: 3812 - Posted: 06.24.2010

Although thought of as a psychological problem, the eating disorder anorexia nervosa often runs in families, suggesting that it has a genetic component. Now researchers have found two genes that help determine the risk of acquiring the disease. The results suggest that variations in genes involved in mood and appetite can put women at risk for anorexia. People with anorexia, usually women, have a distorted body image, starve themselves, and tend to be perfectionists. Studies over the last decade have suggested that genes play a role. The risk of becoming anorexic is about half a percent in the general population, but in 2000, researchers found that the risk jumped 11-fold in people with anorexic family members. Family dynamics don't appear to explain the link: Psychiatrist Walter Kaye at the University of Pittsburgh and colleagues found a variation of a region on chromosome 1 that was common in people with the disease. Copyright © 2003 by the American Association for the Advancement of Science.

Keyword: Anorexia & Bulimia
Link ID: 3811 - Posted: 06.24.2010

Work published in Journal of Medical Genetics indicates break may lead to an understanding of an important piece of the puzzle Researchers at the University of Alberta have discovered a genetic flaw in a family suffering with schizophrenia that may help to explain an important biochemical process implicated in the onset of the disease. Studying a British mother and daughter, the researchers discovered that both were found to have a "break" in a large gene on human chromosome 14, due to a rearranged chromosome. The broken gene is a member of a family of similar genes affecting brain development and function. The genes in this group are involved in behaviour, memory and regulating day/night cycles.

Keyword: Genes & Behavior; Schizophrenia
Link ID: 3810 - Posted: 05.19.2003

* Mecamylamine is a drug that blocks the effects of nicotine in the brain. * Mecamylamine is believed to reduce the rewarding effects of cigarette smoking. * A new study has found that mecamylamine also reduces self-reported stimulant and euphoric effects of alcohol in humans, as well as their desire to drink more. Mecamylamine is a central nicotinic receptor antagonist that is believed to reduce the rewarding effects of cigarette smoking. Scientists have suspected for some time that common mechanisms may be involved in both nicotine and alcohol reward. Furthermore, prior research has suggested that mecamylamine blocks the reinforcing effects of alcohol in animals. A new study, published in the May issue of Alcoholism: Clinical & Experimental Research , has found that mecamylamine reduces the self-reported stimulant and euphoric effects of alcohol in humans, and also decreases their desire to drink more. "Of all the drugs that act in the brain to produce their rewarding effects," said Harriet de Wit, associate professor in the department of psychiatry at the University of Chicago and corresponding author for the study, "alcohol has some of the most complex and varied effects on neurotransmitter receptor systems. One of the receptor systems where alcohol may act is the nicotinic acetylcholine (NACh) receptor system, the same system where nicotine acts. By acting at these NACh receptors, alcohol also increases the activity of another neurotransmitter system, the dopamine system, which is where most drugs are thought to produce their rewarding effects. We hypothesized that mecamylamine would block the effects of alcohol on the NACh receptors which would, in turn, reduce the activity of the dopamine system, resulting in a dampening of the rewarding effects of the alcohol."

Keyword: Drug Abuse
Link ID: 3809 - Posted: 05.19.2003

Robin McKie, science editor The Observer Autism, the devastating mental illness that affects thousands of UK children every year, is not a single psychological condition, scientists have discovered. Researchers have found the ailment is really a combination of two separate illnesses, each controlled by different sets of genes. The discovery, outlined yesterday at the British Psychological Society conference, is expected to cause intense interest among psychologists. Many believe prospects of uncovering the condition's genetic causes and finding new treatments have been significantly boosted. © Guardian Newspapers Limited 2003

Keyword: Autism; Genes & Behavior
Link ID: 3808 - Posted: 06.24.2010

By ANNE EISENBERG THE nerve center of a conventional robot is a microprocessor of silicon and metal. But for a robot under development at Georgia Tech, commands are relayed by 2,000 or so cells from a rat's brain. A group led by a university researcher has created a part mechanical, part biological robot that operates on the basis of the neural activity of rat brain cells grown in a dish. The neural signals are analyzed by a computer that looks for patterns emitted by the brain cells and then translates those patterns into robotic movement. If the neurons fire a certain way, for example, the robot's right wheel rotates once. The leader of the group, Steve M. Potter, a professor in the Laboratory for Neuroengineering at Georgia Tech, calls his creation a Hybrot, short for hybrid robot. Copyright 2003 The New York Times Company

Keyword: Robotics
Link ID: 3807 - Posted: 05.19.2003

By ERICA GOODE It was just one voice at first, loud and male, coming from the ceiling, saying, "Hi, John," calling him by name as if they were buddies. But after a while, the voice, which he came to know as the "evil genius," urged him to steal other people's brain cells and told him that he had a cancerous tumor in his head. Eventually, other voices joined in, maybe 50 of them, male and female, yelling "as loud as humans with megaphones," John recalled, from the moment he awoke in the morning until he fell asleep at night, cursing or ordering him to kill himself or, once, when he picked up a ringing telephone, screaming in chorus, "You're guilty! You're guilty!" "It was utter despair," John said. "I felt scared. They were always around." Copyright 2003 The New York Times Company

Keyword: Schizophrenia; Hearing
Link ID: 3806 - Posted: 05.19.2003

By JAMES GORMAN The study of consciousness has always fascinated me. I love all the impossible arguments about the self and the nature of experience. I also love fishing, but I never expected the two interests to coincide or, more precisely, collide. I heard the crash when I read the word "nociception" in the current issue of that esteemed scientific journal Field and Stream, which I often read, but not usually for news of neurobiology. The word was in a news item about the research of Dr. James D. Rose at the University of Wyoming. Dr. Rose published a paper last year in The Review of Fisheries Science. In it, he argued that fish do not have the brains to produce a level of consciousness capable of feeling pain. Copyright 2003 The New York Times Company

Keyword: Animal Rights; Pain & Touch
Link ID: 3805 - Posted: 05.19.2003

Of all the addictions, some scientists say addiction to alcohol is one of the most powerful. As this ScienCentral News video reports, they may have identified what actually regulates the craving for alcohol in the brain, which could lead to new therapies for alcoholics. Why is it that some of us can stop after a few drinks, but others struggle hard to control the craving? Some neuroscientists say it may be because of a specific brain protein called urocortin. © ScienCentral, 2000-2003

Keyword: Drug Abuse
Link ID: 3804 - Posted: 06.24.2010

The sex hormone estrogen plays a part in many brain processes, including memory. As women age, their bodies make estrogen. Neuroscientists are studying just what effect this has on the brain. “When there’s more estrogen,” explains Teresa Milner, professor of neuroscience at Weill Cornell Medical College, “the nerve cells can form more connections between each other and make the memories stronger. Then, the better you’re able to learn certain things.” Nerve cells in the brain form connections when their branches, called dendrites, sprout twig-like protrusions called spines. Writing in the March 15, 2003 issue of the journal Neuroscience, Milner and her team explained how they used a powerful electron microscope to study nerve cells associated with learning and memory in female rats. They found that as estrogen levels increase in the female rats during their estrous cycle, there is an increase in the formation of new spines. © ScienCentral, 2000-2003.

Keyword: Learning & Memory; Hormones & Behavior
Link ID: 3803 - Posted: 06.24.2010

by Jan Volavka, M.D., Ph.D., and Leslie Citrome, M.D., M.P.H. Psychiatric Times Vol. XX Issue 5 The development of new atypical antipsychotics and their introduction to the U.S. market has been proceeding at a fast pace. The Table provides an overview of their indications, formulations available, dosing, efficacy and safety in typical adult patients. More detailed information on dosing, as well as on treatment-resistant schizophrenia, can be found elsewhere (Citrome et al., 2002; Citrome and Volavka, 2002). The most recent additions to the antipsychotic armamentarium, ziprasidone (Geodon) and aripiprazole (Abilify), differ from the previously available products in their mechanisms of action and side-effect profiles. Antipsychotic efficacy of these two agents appears similar to older agents, but definitive head-to-head, randomized clinical trials will be required to answer questions about relative efficacy. Also reviewed is information about a new intramuscular (IM) formulation of olanzapine (Zyprexa) and an indication for clozapine (Clozaril) recently approved by the U.S. Food and Drug Administration. Ziprasidone acts as a D2, 5-HT2A, 5-HT1D and H1 antagonist, and as a 5-HT1A agonist. This combination of activities, somewhat different from those of other antipsychotics, may be responsible for ziprasidone's pattern of side effects. Unlike most other antipsychotics, it does not have significant effects on weight, lipid profile or glucose metabolism. Furthermore, it shows low rate of persistent prolactin elevation and low incidence of extrapyramidal symptoms (EPS). Ziprasidone increases the QTC , however, and this particular side effect has raised concerns about its cardiac safety. Such prolongation increases the risk of torsade de pointes, a ventricular tachycardia-fibrillation with a characteristic electrocardiogram (ECG) presentation. Episodes of torsade de pointes may be brief and self-limiting. They may also be manifested by syncope. Torsade de pointes rarely progresses to typical ventricular fibrillation and death. This risk must be evaluated in the context of the fact that no cases of mortality from ziprasidone overdoses or torsade de pointes and no excess in sudden and unexpected deaths have so far been reported, even though by mid-2002 more than 150,000 patients received long-term treatment (Glassman and Bigger, 2002), and an overdose of 4020 mg of ziprasidone elicited only minor ECG changes (House, 2002).

Keyword: Schizophrenia
Link ID: 3802 - Posted: 05.19.2003

by Sherie Novotny, M.D., and Eric Hollander, M.D. Psychiatric Times Vol. XX Issue 5 Autism and related spectrum disorders such as Asperger's syndrome and pervasive developmental disorder have been estimated to affect as many as 62.6 children per 10,000, with prevalence for autism affecting as many as 16.8 children per 10,000 and milder variants possibly affecting as many as 45 per 10,000 (Chakrabarti and Fombonne, 2001). Symptoms include deficits in social and communication abilities, as well as compulsive and repetitive behaviors such as stereotypic complex hand and body movements, rigidity, and narrow repetitive interests. Currently, there are no pharmacological treatments approved by the U.S. Food and Drug Administration for autism. Although many pharmacological treatment studies have been published, most are inconclusive and suffer from methodological shortcomings in study design, including subject selection, outcome measures utilized and open-label design. The few controlled studies suggest efficacy rates of approximately 40% to 70% for the various pharmacological agents studied (Hollander et al., 1998; McDougle et al., 1996; Posey and McDougle, 2000). No one medication has yet emerged as a primary treatment, most likely due to the inherent heterogeneity in the neurobiology of these disorders. However, treatments for the core and associated symptom domains of the autism spectrum disorders show promise. The most promising treatments include the use of atypical antipsychotics such as risperidone (Risperdal) for the treatment of disruptive behaviors (McCracken et al., 2002) and the selective serotonin reuptake inhibitors such as fluvoxamine (Luvox) and fluoxetine (Prozac) for the treatment of repetitive behaviors (Buchsbaum et al., 2001; Hollander et al., 1998; McDougle et al., 1996). Studies are attempting to determine the neurobiology of the symptom domains of autism spectrum disorders and predict treatment response to a variety of psychopharmacological agents. © 2003 Psychiatric Times. All rights reserved.

Keyword: Autism
Link ID: 3801 - Posted: 06.24.2010