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April 3, 2007, 10:49 PM CT

How Lead Exposure Produces Learning Deficits

How Lead Exposure Produces Learning Deficits Tomas R. Guilarte, PhD
A study of young adult rats by scientists from the Johns Hopkins Bloomberg School of Public Health provides evidence that explains exactly how exposure to lead during brain development produces learning deficits. The study shows that exposure to levels of lead that are similar to those measured in lead-intoxicated children reduces the birth and survival of new neurons (neurogenesis) in the brain. Lead also alters the normal development of newly born neurons in a part of the brain (hippocampus) known to be important for learning and memory. The study is reported in the March 30, 2007, issue of Neuroscience.

"There was a dogma in neuroscience that you were born with all the neurons you would ever have, but that thinking has changed dramatically in the last 20 years," said Tomás R. Guilarte, PhD, senior author of the study and professor of environmental health sciences at the Johns Hopkins Bloomberg School of Public Health. "The exciting idea is that researchers have discovered ways to increase the number of new neurons, and this may facilitate learning in the hippocampus portion of the brain".

The scientists studied young adult rats, using a group of lead-treated and non-treated (control) rats. When they examined the brains of lead-exposed rats, they observed that fewer neurons were born and those neurons that were born survived for a shorter amount of time and had abnormal development.........

Posted by: JoAnn      Read more         Source


April 3, 2007, 10:40 PM CT

Parkinson drugs for stroke-related disability

Parkinson drugs for stroke-related disability
Researchers have untangled two similar disabilities that often afflict stroke patients, in the process revealing that one may be treatable with drugs for Parkinson's disease.

Scientists at Washington University School of Medicine in St. Louis showed that stroke damage in a brain region known as the putamen is strongly associated with motor neglect, a condition that makes patients slow to move toward the left side.

Like stroke patients with motor neglect, Parkinson's patients are also slow to initiate responses involving movement. Researchers attribute this deficit in Parkinson's disease to loss of neurons that use the neurotransmitter dopamine to regulate activity in the putamen.

"Earlier attempts to treat stroke patients with neglect with dopamine-like compounds have produced mixed results," says lead author Ayelet Sapir, Ph.D., postdoctoral researcher in neurology. "It's possible, though, that those unfavorable outcomes resulted from an inability to identify the patients most likely to benefit from the intervention. Our data indicate that patients with damage to the putamen may respond differently to this therapy than patients who have neglect from stroke damage to other parts of brain".

Sapir describes the research, which appears in The Journal of Neuroscience, as part of a broader effort to precisely determine how strokes in different parts of the brain's right hemisphere affect patients. She and others want to closely link damage in a given right brain region to a particular set of symptoms.........

Posted by: Daniel      Read more         Source


April 1, 2007, 9:35 PM CT

How a traumatic memory can be wiped out

How a traumatic memory can be wiped out
French CNRS researchers in collaboration have shown that a memory of a traumatic event can be wiped out, eventhough other, associated recollections remain intact. This is what a scientist in the Laboratory for the Neurobiology of Learning, Memory and Communication (CNRS/Orsay University), working with an American team, has recently demonstrated in the rat. This result could be used to cure patients suffering from post-traumatic stress.

Recalling an event stored in the long-term memory triggers a reprocessing phase: the recollection then becomes sensitive to pharmacological disturbances before being once more stored in the long-term memory. Is drug treatment capable of wiping out the initial memory, and only that memory?

The researchers trained rats to be frightened of two distinct sounds, making them listen to these sounds just before sending an electric shock to their paws. The next day, they gave half of the rats a drug known to cause amnesia for events recalled from memory, and played just one of the sounds again. When they played both sounds to the rats on the next day, those which had not received the drug were still frightened of both sounds, while those which had received the drug were no longer afraid of the sound they had heard under its influence. Recalling the memory of the electric shock linked to the sound played while rats were under the influence of a drug thus meant that the memory was wiped out by the drug, leaving intact the memory linked to the other sound.........

Posted by: Daniel      Read more         Source


April 1, 2007, 9:32 PM CT

The formation of social memories

The formation of social memories
Is there a specific memory for events involving people? Scientists in the Vulnerability, Adaptation and Psychopathology Laboratory (CNRS/University Paris VI France ) and a Canadian team at Douglas Hospital, McGill University (Montreal), have identified the internal part of the prefrontal cortex as being the key structure for memorising social information. Published in Journal of Cognitive Neuroscience, February 2007.

Social events such as a party with friends, a work meeting or an argument with a partner form an integral part of daily life. Our ability to remember these events, and more precisely to remember the people and the relationships we had with them, is essential to ensure satisfactory adaptation to our social existence. At a cerebral level, various regions of the brain, and especially the hippocampus, are directly involved in learning and memory. Some of these regions are specialised in learning certain types of information, such as the amygdale and our memory for emotions.

The Canadian and French teams (the latter led by Philippe Fossati ) have recently identified a precise region in the frontal cortex which may be specialised in recording and learning social information. Using a functional magnetic resonance imaging technique, the researchers measured cerebral activity in 17 volunteers while they accomplished a memory task involving pictures of social scenes (interacting individuals) and non-social scenes (landscapes with no people). They thus identified the internal part of the prefrontal cortex, called the medial prefrontal cortex, as being the key structure in memorising social information from a picture.........

Posted by: Daniel      Read more         Source


April 1, 2007, 9:21 PM CT

Actigraphy to assess and manage sleep disorders

Actigraphy to assess and manage sleep disorders
Actigraphy, the use of a portable device that records movement over extended periods of time, and has been used extensively in the study of sleep and circadian rhythms, provides an acceptably accurate estimate of sleep patterns in normal, healthy adult populations and in-patients suspected of certain sleep disorders, as per practice parameters reported in the April 1st issue of the journal SLEEP.

The practice parameters, authored by the American Academy of Sleep Medicines (AASM) Standards of Practice Committee, were developed as a guide to the appropriate use of actigraphy, both as a diagnostic tool in the evaluation of sleep disorders and as an outcome measure of therapy efficacy in clinical settings with appropriate patient populations.

Actigraphy is indicated to assist in the evaluation of patients with advanced sleep phase syndrome, delayed sleep phase syndrome, and shift work disorder. Additionally, there is some evidence to support the use of actigraphy in the evaluation of patients suspected of jet lag disorder and non-24 hour sleep/wake syndrome. Further, when polysomnography is not available, actigraphy is indicated to estimate total sleep time in patients with obstructive sleep apnea.

In patients with insomnia and hypersomnia, there is evidence to support the use of actigraphy in the characterization of circadian rhythms and sleep patterns and disturbances. In assessing response to treatment, actigraphy has proven useful as an outcome measure in patients with circadian rhythms and insomnia.........

Posted by: JoAnn      Read more         Source


March 29, 2007, 10:03 PM CT

Omega-3 Fatty Acid And Alzheimer's Disease?

Omega-3 Fatty Acid And Alzheimer's Disease? Eating fish may help reduce the risk for dementia.
Nutritionists have long endorsed fish as part of a heart-healthy diet, and now some studies suggest that omega-3 fatty acids found in the oil of certain fish may also benefit the brain by lowering the risk of Alzheimer's disease. In order to test whether docosahexaenoic acid (DHA), an omega-3 fatty acid, can impact the progression of Alzheimer's disease, scientists at Washington University School of Medicine and Saint Louis University School of Medicine will evaluate DHA in a clinical trial sponsored by the National Institute on Aging (NIA).

The local effort is part of a nationwide consortium of leading Alzheimer's disease scientists supported by the NIA and coordinated by the University of California, San Diego. The trial will take place at 52 sites across the United States. It seeks 400 participants age 50 and older with mild to moderate Alzheimer's disease. Joseph Quinn, M.D., associate professor of neurology at Oregon Health and Science University, is directing the national study. James Galvin, M.D., M.P.H., at Washington University School of Medicine, and George Grossberg, M.D., at Saint Louis University School of Medicine, will conduct the study locally.

Scientists will primarily evaluate whether taking DHA over a number of months slows both cognitive and functional decline in people with mild to moderate Alzheimer's. During the 18-month clinical trial, researchers will measure the progress of the disease using standard tests for functional and cognitive change.........

Posted by: Daniel      Read more         Source


March 28, 2007, 10:02 PM CT

Possible Genetic Trigger For Schizophrenia

Possible Genetic Trigger For Schizophrenia
A study led by researchers from the University of North Carolina at Chapel Hill may have identified a molecular mechanism involved in the development of schizophrenia.

In studying the postmortem brain tissue of adults who had been diagnosed with schizophrenia, the scientists observed that levels of certain gene-regulating molecules called microRNAs were lower among schizophrenia patients than in persons who were free of psychiatric illness.

"In a number of genetic diseases, such as Huntington's disease or cystic fibrosis, the basis is a gene mutation that leads to a malformed protein. But with other complex inherited disorders such as schizophrenia, a number of cancers, and diabetes we find not mutated proteins, but correctly formed proteins in incorrect amounts," said study lead author and UNC professor of psychiatry Dr. Diana Perkins.

The research appears this week in the online edition of the journal Genome Biology. "To our knowledge this study is the first to associate altered expression of microRNAs with schizophrenia," the authors stated.

Since the 1950s, researchers have known that the genetic code stored in DNA is first transcribed into messenger RNA (mRNA) which is then the template from which the body's protein building blocks are made. MicroRNAs are a newly discovered class of mRNA that does not carry the code for a protein. Instead, these tiny strands of RNA act by binding to matching pieces of the protein coding mRNA, thus preventing the translation of mRNA to protein. When a cell needs certain proteins, the microRNAs may disconnect, thus allowing protein expression to resume.........

Posted by: JoAnn      Read more         Source


March 27, 2007, 8:58 PM CT

It's only a game of chance

It's only a game of chance
The validity of a leading theory that has held a glimmer of hope for unraveling the intricacies of the brain has just been called into question. Dr. Ilan Lampl of the Weizmann Institute of Science's Neurobiology Department has produced convincing evidence to the contrary. His findings recently appeared in the journal Neuron.

Cells in the central nervous system tend to communicate with each other via a wave of electrical signals that travel along neurons. The question is: How does the brain translate this information to allow us to perceive and understand the world before us?

It is widely believed that these electrical signals generate spiked patterns that encode different types of cognitive information. As per the theory, the brain is able to discriminate between, say, a chair and a table because each of them will generate a distinct sequence of patterns within the neural system that the brain then interprets. Upon repeated presentation of that object, its pattern is reproduced in a precise and controlled manner. Prior experiments had demonstrated repeating patterns lasting up to one second in duration.

But when Lampl and colleagues recorded the activity of neurons in the brain region known as the cortex in anaesthetized rats and analyzed the data, they found no difference in the number of patterns produced or the time it takes for various patterns to repeat themselves, compared with data that was randomized. They therefore concluded that the patterns observed could not be due to the deterministically controlled mechanisms posited in the theory, but occur purely by chance.........

Posted by: Daniel      Read more         Source


March 27, 2007, 8:56 PM CT

Pulsing Light Silences Overactive Neurons

Pulsing Light Silences Overactive Neurons
Researchers at the MIT Media Lab have invented a way to reversibly silence brain cells using pulses of yellow light, offering the prospect of controlling the haywire neuron activity that occurs in diseases such as epilepsy and Parkinson's disease.

Such diseases often must be treated by removing neurons that fire incorrectly. The new MIT research could lead to the development of optical brain prosthetics to control neurons, eliminating the need for irreversible surgery.

"In the future, controlling the activity patterns of neurons may enable very specific therapys for neurological and psychiatric diseases, with few or no side effects," said Edward Boyden, assistant professor in the Program in Media Arts and Sciences and leader of the Media Lab's new Neuroengineering and Neuromedia Group.

Boyden and Media Lab research affiliate Xue Han published their results in the March 21 issue of the online journal Public Library of Science ONE (PLOS One).

The work takes advantage of a gene called halorhodopsin found in a bacterium that grows in extremely salty water, such as the Great Salt Lake in Utah. In the bacterium, Natronomas pharaonis, the gene codes for a protein that serves as a light-activated chloride pump, which helps the bacterium make energy.........

Posted by: Daniel      Read more         Source


March 22, 2007, 10:36 PM CT

Experience affects new neuron survival

Experience affects new neuron survival
Experience in the early development of new neurons in specific brain regions affects their survival and activity in the adult brain, new research shows. How these new neurons store information about these experiences may explain how they can affect learning and memory in adults.

A team of scientists headed by Fred Gage, PhD, of the Salk Institute, observed that experience enhances the survival of new neurons in a brain area called the dentate gyrus, and that more of these new neurons were activated when exposed to the same experience later. This change in function may be a mechanism for long-term memory. The findings appear in the March 21 issue of The Journal of Neuroscience

"The results identify a critical period for experience-induced enhancement of new neuron survival in the hippocampus," says Elizabeth Gould, PhD, of Princeton University, who was not affiliated with the study. The hippocampus contains the dentate gyrus.

After injecting mice with a chemical used to mark proliferating cells, the scientists exposed the animals to an "enriched cage" environment, containing tunnels, shelters, and a running wheel. After several weeks, the scientists again exposed the mice in the same enriched experience. They discovered that the enriched experience increased new neuron survival and that more new neurons were activated by re-exposure to the same environment. To determine if the increase in neuronal activity was due to having the same experience or if any new experience was sufficient to achieve this effect, the scientists exposed mice to the enriched cage first and then a water maze task. While both cases promoted new neuron survival, more new neurons were activated in mice that had repeated the same experience but not in those that were exposed to the different experience (the water maze).........

Posted by: Daniel      Read more         Source



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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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