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August 20, 2006, 9:23 PM CT

A New Tool Against Brain Disease

A New Tool Against Brain Disease A shell from the venomous cone snail Conus omaria, which lives in the Pacific and Indian oceans and eats other snails
Credit: Kerry Matz, University of Utah
University of Utah researchers isolated an unusual nerve toxin in an ocean-dwelling snail, and say its ability to glom onto the brain's nicotine receptors may be useful for designing new drugs to treat a variety of psychiatric and brain diseases.

"We discovered a new toxin from a venomous cone snail that may enable scientists to more effectively develop medications for a wide range of nervous system disorders including Parkinson's disease, Alzheimer's disease, depression, nicotine addiction and perhaps even schizophrenia," says J. Michael McIntosh.

Discovery of the new cone snail toxin will be published Friday, Aug. 25 in The Journal of Biological Chemistry by a team led by McIntosh, a University of Utah research professor of biology, professor and research director of psychiatry, member of the Center for Peptide Neuropharmacology and member of The Brain Institute.

McIntosh is the same University of Utah researcher who as an incoming freshman student in 1979 discovered another "conotoxin" that was developed into Prialt, a drug injected into fluid surrounding the spinal cord to treat severe pain due to cancer, AIDS, injury, failed back surgery and certain nervous system disorders. Prialt was approved in late 2004 in the United States and was introduced in Europe last month.........

Posted by: Daniel      Permalink         Source


August 20, 2006, 2:09 PM CT

Technology For Brain Cooling Unlikely To Help Trauma Patients

Technology For Brain Cooling Unlikely To Help Trauma Patients
Attempts to cool the brain to reduce injury from stroke and other head trauma may face a significant obstacle: current cooling devices can't penetrate very deeply into the brain.

Researchers at Washington University School of Medicine in St. Louis used rats to validate a "cold shielding" effect of blood flow that they previously predicted theoretically. The shielding effect, created by large quantities of warm blood that continually perfuse brain tissue, prevents a drop in temperatures around the head from penetrating beyond a certain depth in the brain.

A number of ongoing clinical trials try to reduce brain temperatures through cooling units incorporated into hats or other devices that surround the head. However, the new findings, published online this month in the Journal of Applied Physiology, suggest in most patients such techniques will be unable to defeat the natural temperature regulation built into the brain via the blood system.

"In adult humans, the characteristic length that this kind of cold assault appears to penetrate is approximately a tenth of an inch, leaving the temperature of approximately 6 inches of brain tissue unchanged," says senior author Dmitriy Yablonskiy, Ph.D., professor of radiology at the School of Medicine and of physics in Arts and Sciences. "Our findings suggest that the reason trials of this kind have so far produced inconsistent results is because we're not cooling enough of the brain."........

Posted by: Daniel      Permalink         Source


August 17, 2006, 11:46 PM CT

Spinal Cord Injury Treatment Progress

Spinal Cord Injury Treatment Progress
The body's spinal cord is like a super highway of nerves. When an injury occurs, the body's policing defenses put up a roadblock in the form of a scar to prevent further injury, but it stops all neural traffic from moving forward.

Scientists from Case Western Reserve University, Drexel University and the University of Arkansas bypassed this roadblock in the spinal cord. First, the scientists regenerated the severed nerve fibers, also called axons, around the initial large lesion with a segment of peripheral nerve taken from the leg of the same animal that suffered the spinal injury. Next, they jump started neural traffic by allowing a number of nerve fibers to exit from the end of the bridge. This was accomplished, for the first time, by using an enzyme that stopped growth inhibitory molecules from forming in the small scar that forms at the exit ramp of the bridge, where it is inserted into the spinal cord on the other side of the lesion. This allowed the growing axons to reconnect with the spinal cord.

Jerry Silver, a professor of neurosciences at the Case School of Medicine, was senior author among the scientists reporting in the Journal of Neuroscience article, "Combining an Autologous Peripheral Nervous System 'Bridge' and Matrix Modification by Chondroitinase Allows Robust Functional Regeneration beyond a Hemisection Lesion of the Adult Rat Spinal Cord." The other scientists were John Houle, the lead author, and Veronica Tom (a Case alum) from Drexel University College of Medicine; and Gail Wagoner and Napoleon Phillips from the University of Arkansas.........

Posted by: Daniel      Permalink         Source


August 17, 2006, 11:24 PM CT

Cause of Ischemic Stroke Analyzed

Cause of Ischemic Stroke Analyzed
In contrast to traditional beliefs that stroke-causing clots derived from arterial and cardiac sources are distinctly different, a new UCLA study shows they are composed of similar components.

Scientists studied clots removed from the brain blood vessels of 25 stroke victims. The clots were retrieved during therapy using a novel mechanical clot-retrieval device called the MERCI (Mechanical Embolus Removal in Cerebral Ischemia) Retriever. The removed clots were analyzed under the microscope to compare their component structures.

"Unexpectedly, no two retrieved clots looked the same, even though all were constructed from the same basic components of fibrin, white cells and red blood cells," said lead author Dr. Victor Marder, professor of hematology and oncology at the David Geffen School of Medicine at UCLA and a UCLA Stroke Center member. "The same components were involved in both the newly formed and mature, enlarging clots. Red blood-cell accumulations had previously been considered to dominate the structure of clots that formed within a heart chamber, but our results suggest that red cells often accumulated on clots after impaction in the brain artery".

The findings could lead to better therapies to prevent clots, clear blockages and reverse strokes in the crucial first hours after they occur.........

Posted by: Daniel      Permalink         Source


August 13, 2006, 6:26 PM CT

Life and death in the hippocampus

Life and death in the hippocampus
Whether newborn nerve cells in adult brains live or die depends on whether they can muscle their way into networks occupied by mature neurons. Neuroresearchers at the Salk Institute for Biological Studies pin-pointed the molecular survival gear mandatory for a young neuron to successfully jump into the fray and hook up with other cells.

As per a research findings published in a forthcoming issue of Nature, scientists in the lab of Fred H. Gage, Ph.D., a professor in the Gene Expression Laboratory and the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Diseases, identify a subunit of the NMDA receptor, a protein complex that transduces signals sent by neighboring cells, as the cells' life-saving equipment that allows them to integrate into the existing brain circuitry.

The NMDA receptor is activated by the neurotransmitter glutamate, a chemical released by neurons in order to transmit information to neighboring cells. Whenever the receptor picks up a glutamate signal it is stimulated and relays the signal. But for newborn neurons that signal means something else entirely -- survival.

"When we removed the NMDA receptor, that is when cells make connections in response to glutamate in the environment, the newborn neurons withered and died at a specific stage of their maturation," explains Gage. " The NMDA receptor modulates synapse formation and determines what pattern of input activity new neurons receive, which in turn determines survival or death".........

Posted by: Daniel      Permalink         Source


August 10, 2006, 6:46 AM CT

Genetics Of Successful Aging

Genetics Of Successful Aging
Researchers have identified genes correlation to reaching age 90 with preserved cognition, as per a research studyreported in the recent issue of the American Journal of Geriatric Psychiatry. The study, which was conducted at the University of Pittsburgh is among the first to identify genetic links to cognitive longevity.

"Successful aging has been defined in a number of ways, however, we focused on individuals who had reached at least 90 without significant decline in mental capacity," said lead researcher George S. Zubenko, M.D., Ph.D., professor of psychiatry and biological sciences at the University of Pittsburgh. "While this is a goal that a number of of us share, such a definition of 'successful aging' can be determined objectively and consistently across subjects--an important requirement of scientific studies."

While prior research has revealed that genes make important contributions to exceptional longevity, the goal of this study was to identify regions of the human genome that contributed, along with lifestyle factors, to reaching age 90 with preserved cognition.

The study involved 100 people age 90 and older who had preserved cognition as measured by clinical and psychometric assessments. Half of the subjects were male, half were female. Using a novel genome survey method, researchers compared the DNA of the study sample with that of 100 young adults, aged 18-25, who were matched for sex, race, ethnicity and geographic location. Particularly, Dr. Zubenko and his research team attempted to identify specific genetic sequences present in older individuals that may be associated with reaching older ages with preserved cognitive abilities, or on the other hand, specific genetic sequences present in younger individuals (and not present in those over age 90) that may impede successful aging. The study also looked at a variety of lifestyle factors, such as smoking and alcohol consumption, with the goal of eventually exploring the interactive effects of genes and lifestyle on successful aging.........

Posted by: Daniel      Permalink         Source


August 9, 2006, 7:06 AM CT

Transcendental Meditation And Pain

Transcendental Meditation And Pain
Twelve healthy long-term meditators who had been practicing Transcendental Meditation for 30 years showed a 40-50% lower brain response to pain in comparison to 12 healthy controls, reported by a latest NeuroReport journal article, published by Lippincott Williams & Wilkins (Vol.17 No.12; 21 August 2006:1359-1363). Further, when the 12 controls then learned and practiced Transcendental Meditation for 5 months, their brain responses to pain also decreased by a comparable 40-50%. www.neuroreport.com Current issue (Aug 9).

Transcendental Meditation could reduce the brain's response to pain because neuroimaging and autonomic studies indicate that it produces a physiological state capable of modifying various kinds of pain. In time it reduces trait anxiety, improves stress reactivity and decreases distress from acute pain.

As per Orme-Johnson, lead author of this research, "Previous research indicates that Transcendental Meditation creates a more balanced outlook on life and greater equanimity in reacting to stress. This study suggests that this is not just an attitudinal change, but a fundamental change in how the brain functions".

Pain is part of everyone's experience and 50 million people worldwide suffer from chronic pain. Transcendental Meditation would have a long term effect in reducing responses in the affective component of the pain matrix. Future research could focus on other areas of the pain matrix and the possible effects of other meditation techniques to relieve pain.........

Posted by: Daniel      Permalink         Source


August 8, 2006, 9:36 PM CT

Exploring Alzheimer's Causes

Exploring Alzheimer's Causes Li-Huei Tsai Photo / Cynthia Henshall, Picower Institute
Some people live to be 100 without falling victim to Alzheimer's disease. Li-Huei Tsai, who joined MIT this spring as Picower Professor of Neuroscience, wants to know why.

Amyloid beta or Abeta (a protein fragment that accumulates in the brains of Alzheimer's patients) is a telltale sign of the disease, which affects 4 million Americans, most over age 65. Normally, the body manages to break down and eliminate these fragments, but in the aging brain, they tend to form insoluble plaques.

To add to the mystery, some people function relatively normally with plaques nestled among their neurons, while others are virtually incapacitated. "There are people with a significant plaque load who can keep up with their daily lives," said Tsai, who has appointments in the Department of Brain and Cognitive Sciences and at the Picower Institute for Learning and Memory. "Obviously, other factors are determining whether they have full-blown Alzheimer's."

Tsai, who as a child in Taipei witnessed her beloved grandmother's descent into dementia, is determined to unravel the thorny questions linked to neurodegenerative and psychiatric disorders.

Tsai uses a combination of molecular, cellular and biochemical approaches to study Alzheimer's disease and psychiatric and developmental disorders. She focuses on a kinase (kinases are enzymes that change proteins) called Cdk5. Cdk5, paired with the protein p35, helps new neurons form and migrate to their correct positions during brain development. But Cdk5, paired with an aberrant form of p35 called p25, also is implicated in age-related neurodegenerative diseases.........

Posted by: Daniel      Permalink         Source


August 8, 2006, 8:46 PM CT

Brain's Visual Area: How Behavior Is Organized

Brain's Visual Area: How Behavior Is Organized
A brain region that focuses on vision also receives signals that may help configure the operation of the brain, neuroresearchers at Washington University School of Medicine in St. Louis report.

If the brain is thought of as an army, the new signals may give researchers a unique opportunity to trace how messages from the high command reach all the way down to individual soldiers in a particular platoon and affect their activities.

That's because the brain region in question, called V1, has already been the focus of detailed studies at the level of individual brain cell interactions and how they encode and analyze data from the eyes.

"To really understand how a control signal works, you first have to know how the mechanism being controlled works, and we already have a fairly detailed feel for that in V1," says Anthony I. Jack, Ph.D., a postdoctoral fellow and lead author of a study that appeared last month in the journal Neuron. "This provides us with a potential way of understanding a major puzzle: on a minute scale, how do control signals change how neurons process incoming information?".

Much of the human brain's power derives from its ability to take one stimulus and process it in different ways to meet a variety of needs. Different parts of the brain have specialized abilities that can contribute in various ways to completion of different tasks. They just need to be told when to shift from one task to the next.........

Posted by: Daniel      Permalink         Source


August 8, 2006, 0:18 AM CT

New Learning Strategy

New Learning Strategy In the Thoroughman laboratory, volunteers play games on a computer screeen using a robotic arm so that Thoroughman and his colleagues can study how people learn motor skills.
Central to being human is the ability to adapt: We learn from our mistakes. Prior theories of learning have assumed that the size of learning naturally scales with the size of the mistake. But now biomedical engineers at Washington University in St. Louis have shown that people can use alternative strategies: Learning does not necessarily scale proportionally with error.

In so doing, Kurt Thoroughman, Ph.D., assistant professor of biomedical engineering at Washington University, and his graduate student, Michael Fine, have discovered a new learning strategy they call categorical adaptation in which steps of learning are sensitive to the direction of error, but do not scale proportionally with the size of the error. Eventually, their findings could have an impact in the rehabilitation of people with neurological ailments such as strokes by making use of different learning environments.

If you make a movement error in one direction, in makes sense that your next movement would correct toward the opposite direction, in exact proportion to the error. An example would be a pitcher correcting to the right, after missing home plate to the left with a pitch.

"We show that learning does not necessarily scale with error," said Thoroughman. "I think we have uncovered a part of human adaptation that certainly doesn't do that. We are not claiming that all prior theories are false in the behaviors that were captured. It's just that we have for the first time found a part of human adaptation that clearly does not scale with the size of the error."........

Posted by: Daniel      Permalink         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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