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January 26, 2006, 11:52 AM CT

Link Between Cat Faeces And Schizophrenia

Link Between Cat Faeces And Schizophrenia
Research published recently in Procedings of the Royal Society B, shows how the invasion or replication of the parasite Toxoplasma gondii in rats may be inhibited by using anti-psychotic or mood stabilising drugs.

The scientists tested anti-psychotic and mood stabilising medications used for the therapy of schizophrenia on rats infected with T. gondii and found they were as, or more, effective at preventing behaviourial alterations as anti-T. gondii drugs. This led them to think that T. gondii may have a role in the development of some cases of schizophrenia.

Dr Joanne Webster from Imperial College London, and lead researcher said: "Eventhough we are certainly not saying that exposure to this parasite does definitely lead to the development of schizophrenia, this and prior studies do show there may be a link in a few individuals, providing new clues for how we treat toxoplasmosis and schizophrenia".

Prior epidemiological and neuropathological studies have indicated some cases of schizophrenia may be associated with environmental factors, such as exposure to the parasite T. gondii. At the same time several of the medications used to treat schizophrenia have been shown to posess anti-parasitic and in particular anti-T.gondii properties. This led the authors to suspect that the anti-psychotic activity of these medications may be due to their inhibition of these parasites.........

Posted by: Daniel      Permalink


January 25, 2006, 9:01 PM CT

Defective Synapse Generator Leads To Alzheimer

Defective Synapse Generator Leads To Alzheimer
A new UCLA/Veterans Affairs study implicates defects in the machinery that creates connections between brain cells as responsible for the onset of Alzheimer disease.

The defect in PAK enzyme signaling pathways - vital to creation of these connections, or synapses - is correlation to loss of a synapse protein in certain forms of mental retardation, such as Down syndrome. The new finding suggests therapies designed to address the PAK defect could treat cognitive problems in both patient populations.

The peer-reviewed journal Nature Neuroscience published the study online Jan. 15.

"The emerging lesson is that cognitive problems in Alzheimer disease are correlation to defects in the machinery controlling neuronal connections, not the lesions observed by pathologists," said principal investigator Greg Cole, professor of medicine and neurology at the David Geffen School of Medicine and Alzheimer Disease Research Center at UCLA, and the Geriatric Research Education and Clinical Center at the Veterans Affairs Greater Los Angeles Health Care System and Sepulveda Ambulatory Care Center. "Our findings show that PAK defects in the brains of Alzheimer patients appear sufficient to directly cause cognitive difficulties".

In some families, early-onset Alzheimer disease can be caused by mutations in different genes that all increase the production of a sticky protein called Abeta42 (Ab42). The increase causes the protein to form aggregates, little clusters or long filaments that pile up and make lesions in the brain called plaques.........

Posted by: Daniel      Permalink


January 25, 2006, 8:42 PM CT

Heart And Alzheimer's Disease Protein Imaged

Heart And Alzheimer's Disease Protein Imaged Karl H. Weisgraber, Ph.D.
Scientists for the first time have created a three-dimensional image of apolipoprotein E, a protein long associated with cardiovascular disease and more recently with Alzheimer's disease, as it appears when it is bound to fat-like substances known as lipids.

Using the technique known as x-ray crystallography, researchers at the Gladstone Institute of Cardiovascular Disease (GICD) have created the highest-resolution x-ray structure of a lipoprotein particle to date.

The work focuses apoE4, one of three specific forms of apolipoprotein E, usually known as apoE. The breakthrough has already answered long-standing questions about the configuration of apoE4 in its active, or native, state. A complete understanding of the protein's functioning will be a key factor for development of future therapeutic interventions, as per the researchers.

Details of the works are published in the January 13 edition of the Journal of Biological Chemistry.

"This is the first successful use of x-ray crystallography to reveal the structure of a protein bound to lipids," explains senior author Karl Weisgraber, PhD, a senior investigator at both GICD and the Gladstone Institute of Neurological Disease (GIND). "It's crucial to understand this molecule, since it plays such a pivotal role in both cardiovascular and neurological disease.........

Posted by: Daniel      Permalink


January 18, 2006, 0:08 AM CT

Stress In Infancy May Lead To Addictions

Stress In Infancy May Lead To Addictions
Female rats appear to be affected more than males by stress early in life, leading to a higher likelihood of cocaine addiction and eating disorders as adults, as per a studyby Yale School of Medicine scientists in Neuropsychopharmacology.

"These results differ somewhat from our prior study conducted with male rats," said Therese Kosten, research scientist, Department of Psychiatry, and lead author of the study. "Early life stress produces a greater increase in cocaine self-administration in female versus male rats".

In addition, the neonatal stress enhances responding for food treats in female, but not male, rats, she said. "We believe this may suggest that women with early life stress have an enhanced risk of developing drug addiction, as well as eating disorders," Kosten said.

Of the rats in the research, some were isolated from their mothers as "infants." The rats were studied as adults who had learned to self-administer cocaine and food treats. The scientists found the rats that had been kept in isolation worked harder to obtain food and drug rewards.

"The results of the cocaine self-administration study along with our prior work demonstrating enduring effects of neonatal isolation in female rats point to the possibility that women with early life stress experience may be at increased risk of initiating and maintaining drug addiction," Kosten said. "The fact that early isolation enhances responding for food in female rats, but not male rats, may provide an insight into the role of early life stress on gender differences in vulnerability to develop eating disorders".........

Posted by: JoAnn      Permalink


January 16, 2006, 11:55 PM CT

Physical Activity And Parkinson's Disease

Physical Activity And Parkinson's Disease
Parkinson's disease can be more effectively managed by a regular exercise program, say experts at Baylor College of Medicine in Houston.

"There's no doubt that people who have a positive attitude and exercise generally cope with the disease much better than those who don't," said Dr. Joseph Jankovic, professor of neurology and director of BCM's Parkinson's Disease Center and Movement Disorders Clinic. "Exercise is clearly a positive force in dealing with Parkinson's".

Living proof of the "use it or lose it" adage can be found in one of Jankovic's patients, former Beaumont, Texas, Mayor Maury Meyers, who not only stays physically active, he also embodies advancements in patient care and research.

For over 10 years, Meyers has organized the Dr. Sol and Miriam Rogers Memorial Golf Tournament, which supports a research endowment at the clinic. In spite of the devastation wrought to the Beaumont area by Hurricane Rita, Meyers' charity tournament raised the most money in its history.

"Parkinson's disease keeps on going, hurricanes or not," said Jankovic.

Meyers, who also played in the recent tournament for the first time, currently shoots in the mid-80s for 18 holes in a sport where a number of people with no physical disabilities at all struggle to avoid the three-digit range. It took Meyers five years to overhaul the mechanics of his swing after first being diagnosed with the debilitating disease.........

Posted by: Daniel      Permalink


January 12, 2006, 11:59 PM CT

Brain Volume And Dementia

Brain Volume And Dementia
Reduced volume, or atrophy, in parts of the brain known as the amygdala and hippocampus may predict which cognitively healthy elderly people will develop dementia over a six-year period, as per a studyin the recent issue of the Archives of General Psychiatry, one of the JAMA/Archives journals.

New strategies may be able to prevent or delay the onset of Alzheimer's disease (AD), the most common cause of dementia among older adults, according to background information in the article. Accurate methods of identifying which people are at high risk for dementia in old age would help physicians determine who could benefit from these interventions. There is evidence that adults with AD and mild cognitive impairment, a less severe condition that is considered a risk factor for AD, have reduced hippocampal and amygdalar volumes. However, prior research has not addressed whether measuring atrophy using magnetic resonance imaging (MRI) can predict the onset of AD at an earlier stage, before cognitive symptoms appear.

Tom den Heijer, M.D., Ph.D., of the Erasmus Medical Center, Rotterdam, the Netherlands, and his colleagues used MRI to assess the brain volumes of 511 dementia-free elderly people who were part of the Rotterdam Study, a large population-based cohort study that began in 1990. They screened the participants for dementia at initial visits in 1995 and 1996 and then in follow-up visits between 1997 and 2003, during which they asked about memory problems and performed extensive neuropsychological testing. The authors also monitored the medical records of all participants. During the follow-up, 35 participants developed dementia and 26 were diagnosed with AD.........

Posted by: Daniel      Permalink


January 9, 2006, 10:55 PM CT

Integrating New Neurons In To Adult Brain

Integrating New Neurons In To  Adult Brain
In experiments with mice, researchers from Johns Hopkins' Institute for Cell Engineering have discovered the steps mandatory to integrate new neurons into the brain's existing operations.

For more than a century, researchers thought the adult brain could only lose nerve cells, not gain them, but in fact, new neurons do form during adulthood in all mammals, including humans, and become a working part of the adult brain in mice at the very least.

In the first study to show how these "baby" neurons are integrated into the brain's existing networks, the Johns Hopkins scientists show that a brain chemical called GABA readies baby neurons to make connections to old ones. The discovery is described in the Dec. 11 advance online section of Nature.

"GABA is important during fetal development, but most researchers thought it would have the same role it has with adult neurons, which is to inhibit the cells' signals," says Hongjun Song, Ph.D., an assistant professor in the Neuroregeneration and Repair Program within ICE. "We've shown that GABA instead excites new neurons and that this is the first step toward their integration into the adult brain".

Song added that their discovery might help efforts to increase neuron regeneration in the brain or to make transplanted stem cells form connections more efficiently.........

Posted by: Daniel      Permalink


January 7, 2006, 3:55 PM CT

Gene Therapy For Muscular Dystrophy

Gene Therapy For Muscular Dystrophy Gene defects are often the cause of muscular dystrophy
A new gene treatment technique that has shown promise in skin disease and hemophilia might one day be useful for treating muscular dystrophy, according to a new study by scientists at Stanford University School of Medicine.

In the study, published online in the Proceedings of the National Academy of Sciences the week of Jan. 2, the scientists used gene treatment to introduce a healthy copy of the gene dystrophin into mice with a condition that mimics muscular dystrophy. The dystrophin gene is mutated and as a result produces a defective protein in the roughly 20,000 people in the United States with the most common form of the disease.

Using gene treatment to treat muscular dystrophy isn't a new idea. Thomas Rando, MD, PhD, associate professor of neurology and neurological sciences, said that scientists have tried several different techniques with variable success. One hurdle is getting genes into muscle cells all over the body. Another is convincing those cells to permanently produce the therapeutic protein made by those genes.

The gene treatment technique Rando and postdoctoral fellow Carmen Bertoni, PhD, used was developed by Michele Calos, PhD, associate professor of genetics. One of the main advantages of this method is that it could potentially provide a long-term fix for a variety of genetic diseases, including muscular dystrophy.........

Posted by: Daniel      Permalink


January 7, 2006, 3:06 PM CT

Lack Of Sleep May Impair Learning

Lack Of Sleep May Impair Learning
As the pace of life quickens and it becomes harder to balance home and work, a number of people meet their obligations by getting less sleep.

But sleep deprivation impairs spatial learning -- including remembering how to get to a new destination. And now researchers are beginning to understand how that happens: Learning spatial tasks increases the production of new cells in an area of the brain involved with spatial memory called the hippocampus. Sleep plays a part in helping those new brain cells survive.

A team of scientists from the University of California and Stanford University found that sleep-restricted rats had a harder time remembering a path through a maze compared to their rested counterparts. And unlike the rats that got enough sleep, the sleep-restricted rats showed reduced survival rate of new hippocampus cells.

The scientists used sleep-restricted rats rather than sleep-deprived rats to more closely mimic the common human experience of inadequate sleep during the work week, said lead investigator Ilana Hairston of both the University of California, Berkeley, and Stanford University. The paper, "Sleep restriction suppresses neurogenesis induced by hippocampus-dependent learning," appears in the Journal of Neurophysiology published by the American Physiological Society. Stanford scientists Milton T.M. Little, Michael D. Scanlon, Monique T. Barakat, Theo D. Palmer, Robert M. Sapolsky, and H. Craig Heller co-authored the paper.........

Posted by: Daniel      Permalink


January 4, 2006

Brain Cell Activity Increases Amyloid Beta

Brain Cell Activity Increases Amyloid Beta
Increased communication between brain cells increases levels of amyloid beta, the key ingredient in Alzheimer's brain plaques, researchers at Washington University School of Medicine in St. Louis have found.

The findings showed that turning up brain cell firing rates drove up levels of amyloid beta in the spaces between brain cells. Corresponding drops in amyloid beta levels occurred when brain cells' ability to send messages was dampened or blocked completely.

The results, produced in mouse models of Alzheimer's, will appear in the journal Neuron on Dec. 22. They complement a Washington University study published earlier this year that used functional brain imaging to show that the brain areas that develop Alzheimer's plaques are also the regions that are the most active in healthy young people who are daydreaming or not carrying out a specific cognitive task (http://news-info.wustl.edu/news/page/normal/5621.html).

The two papers have scientists considering the possibility of someday slowing or preventing the development of Alzheimer's disease by using pharmaceuticals to selectively reduce some communication between brain cells. However, scientists still have to determine if increased levels of amyloid beta can be partially linked to particular classes of the nerve cell messengers and receptors that cells use to communicate with each other.

"Ideally, we will be hoping to find a drug or mechanism that could very specifically target the processes that lead to increased amyloid beta levels," says lead author John Cirrito, Ph.D., a postdoctoral research associate in neurology and psychology. "If we can identify these and find ways to modulate them, we'd have new ways of intervening in Alzheimer's disease."

Senior author David Holtzman, M.D., the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology, says that the results do not contradict earlier studies that suggested crossword puzzles, exercise and other mental stimulation can reduce the chances of developing Alzheimer's disease.........

Daniel      Permalink



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Did you know?
The drug Ativan is better than Valium or Dilantin for controlling severe epileptic seizures, according to a new review of studies.Ativan, or lorazepam, and Valium, or diazepam, are both benzodiazepines, the currently preferred class of drugs for treating severe epileptic seizures. Dilantin, or phenytoin, is an anticonvulsant long used for the treatment of epileptic seizures.

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