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January 4, 2006

Advances in brain cancer treatment

Advances in brain cancer treatment
With an equal rate of incidence and mortality-the number of those who get the disease and those who die from it-Glioblastoma Multiforme (GBM) is a brain cancer death sentence.

Of the approximately 12,000 people who are diagnosed with GBM annually in the U.S., half will die within a year, and the rest within 3 years. Currently, the only therapys that stretch survival limits are exceptionally invasive surgeries to remove the tumor and radiation therapy with the maximum tolerated dose - all of which leads to a painfully low quality of life. Because of this, scientists are racing to find better therapies to stop or slow GBM.

In the Jan. 1, 2006 issue of the journal Clinical Cancer Research, Gelsomina "Pupa" De Stasio, professor of physics at UW-Madison, and his colleagues report on research into using a new radiotherapy technique for fighting GBM with the element gadolinium. The approach might lead to less invasive therapys that offer greater promise of alleviating the disease.

"It's the most lethal cancer there is. The only good thing about it is that, if left untreated, death is relatively quick and pain-free, since this tumor does not form painful metastases in other parts of the body," says De Stasio.

The treatment, called Gadolinium Synchrotron Stereotactic Radiotherapy (GdSSR), requires a gadolinium compound to find tumor cells and penetrate them, down into their nuclei, while sparing the normal brain. Then, the patient's head is irradiated with x-rays. For these x-ray photons the whole brain is transparent, while gadolinium is opaque. Then, where gadolinium is localized-in the nuclei of the cancer cells only-what's known as "the photoelectric effect" takes place.

"Exactly 100 years after Einstein first explained this effect, we have found a way to make it useful in medicine," De Stasio says. "In this effect, atoms absorb photons and emit electrons. The emitted electrons are very destructive for DNA, but have a very short range of action. Therefore, to induce DNA damage that the cancer cells cannot repair, and consequently cell death, gadolinium atoms must be localized in the nuclei of cancer cells".........

Daniel      Permalink


January 2, 2006, 10:09 PM CT

New Drug Target For Alzheimer's Disease

New Drug Target For Alzheimer's Disease
Gladstone scientists identify new drug target for Alzheimer's disease.

Scientists at the Gladstone Institute of Neurological Disease have identified a potential new way to stop brain cell death related to Alzheimer's disease.

Working with cell cultures, the researchers investigated how amyloid beta (A?) proteins, which build up in the brain tissue of people with Alzheimer's disease, kill neurons. The cell cultures were established from brain tissue of laboratory rats. Study findings showed that A? could be prevented from causing neuronal cell death with a compound called resveratrol, which is also found as a natural ingredient in red wine.

"Our study suggests that resveratrol and related compounds may protect against neuronal loss associated with Alzheimer's disease," explains senior author Li Gan, PhD, a staff research investigator at the Gladstone Institute of Neurological Disease and an assistant professor of neurology at UC San Francisco. "This could certainly open up new avenues for drug development".

The research results are reported in the December 2 issue of the Journal of Biological Chemistry.

According to the research team, it was especially interesting that the beneficial effect of resveratrol was not due to a direct effect on A? or on neurons but on other types of brain cells, called microglia.

Microglia are the immune cells of the brain. They can protect or hurt neurons, depending on which of their powerful defense or attack pathways are activated. The researchers found that A? triggers a pathway in microglia that makes them attack neurons with poisonous chemicals.

A key mediator in this pathway is a protein called NF?B, which resveratrol happens to block. Without resveratrol, A??activates NF?B in microglia, turning them into powerful neuron killing machines.........

Scott      Permalink


January 2, 2006, 9:59 PM CT

How Brain Understands Language

How Brain Understands Language
UC Irvine cognitive neuroscientist has been awarded a National Institutes of Health grant for $2.4 million over five years to unlock the secrets of how the brain translates sound waves into meaningful language.

Greg Hickok, professor of cognitive sciences, will lead a team of researchers from UCI, UC San Diego, the University of Southern California and the University of Iowa in this research that may one day help those with language disorders caused by stroke, Alzheimer's disease and autism. The grant is a renewal from the National Institute on Deafness and Other Communication Disorders (NIDCD), a component of the NIH, and will allow Hickok to continue the work he has done in this field since 1999.

"When we listen to speech, what hits our ears is nothing more than tiny fluctuations in air pressure, or sound waves," Hickok said. "The ability of humans to turn these sound waves into meaningful language is a complex task, one that we have not managed to replicate yet with computer voice recognition systems. This project will help us better understand how brain circuits can do what computers circuits so far cannot".

It is estimated that acquired language disorders, also known as aphasia, affect approximately 1 million people in the U.S., with 80,000 new cases diagnosed each year. Aphasia generally results from a stroke. Language ability is also often affected in those who suffer from neurodegenerative diseases such as Alzheimer's and from disorders such as autism. Understanding the basic circuitry of how speech is processed could help in treating these disorders.

Following on his prior work, Hickok, along with his colleagues, will use functional magnetic resonance imaging (fMRI) technology, which measures blood flow and allows researchers to map which brain regions become active during a task involving speech or language use. The team plans to conduct 200 fMRIs on healthy subjects, primarily at UCI.........

Scott      Permalink


January 2, 2006, 9:48 PM CT

Obesity And Alzheimer's Disease

Obesity And Alzheimer's Disease
If heart disease and diabetes aren't bad enough, now comes another reason to watch your weight. As per a studyjust released, packing on too a number of pounds can increase the risk of developing Alzheimer's disease.

A team led by scientists at the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia and Edith Cowan University in Joondalup, Western Australia has shown that being extremely overweight or obese increases the likelihood of developing Alzheimer's. They found a strong correlation between body mass index and high levels of beta-amyloid, the sticky protein substance that builds up in the Alzheimer's brain and is thought to play a major role in destroying nerve cells and in cognitive and behavioral problems associated with the disease.

"We looked at the levels of beta-amyloid and found a relationship between obesity and circulating amyloid," says Sam E. Gandy, M.D., Ph.D., director of the Farber Institute for Neurosciences. "That's almost certainly why the risk for Alzheimer's is increased," says Dr. Gandy, who is also professor of neurology, and biochemistry and molecular biology at Jefferson Medical College of Thomas Jefferson University. "Heightened levels of amyloid in the blood vessels and the brain indicate the start of the Alzheimer's process." The researchers reported their findings this month in the Journal of Alzheimer's Disease.

According to, Dr. Gandy, evidence has emerged over the last five years that a number of of the conditions that raise the risk for heart disease such as obesity, uncontrolled diabetes, high blood pressure and hypercholesterolemia also increase the risk for Alzheimer's. Yet exactly how such factors made an individual more likely to develop Alzheimer's remained a mystery.........

Daniel      Permalink


January 2, 2006, 9:42 PM CT

Meditation Course Works to Reduce Anxiety

Meditation Course Works to Reduce Anxiety
Mindfulness Meditation, the popular course that helps participants learn to relieve pain, reduce stress and enhance wellness, is once again being offered by the Jefferson-Myrna Brind Center for Integrative Medicine at Thomas Jefferson University Hospital.

"Mindfulness meditation is a process that quiets the mind and releases physical distress. Through mindfulness, you can experience greater vitality and well-being," explains Diane Reibel, Ph.D., research associate professor of Physiology at Jefferson Medical College of Thomas Jefferson University and director of the Stress Reduction Program. "Participants learn how to quiet the mind and relax the body. They learn to identify early signs of stress and how to respond in healthier ways to stressful situations.

"The only requirements for the program are that an individual has a strong commitment to making a healthy change," Dr. Reibel, who is also a research associate professor of Emergency Medicine at Jefferson Medical College of Thomas Jefferson University, explains.

The Mindfulness Meditation program has been particularly helpful for individuals facing the challenges of illness such as chronic pain, headaches, gastrointestinal disorders, heart disease, cancer, HIV or other chronic conditions.

The next eight-week course schedule is as follows:

Tuesday evenings from 6:30 - 9:00 p.m., running from January 31 - March 21. Classes will be held at Thomas Jefferson University in Room 101 of the Bluemle Building, located on 10th and Locust Streets, Philadelphia.

Wednesday mornings from 9:30 a.m. - noon, running from February 1 - March 22. Classes will be held at Thomas Jefferson University in Room 218 of the Curtis Building, located at 1015 Walnut Street, Philadelphia.........

JoAnn      Permalink


December 27, 2005

Steroids Increase Death Risk

Steroids Increase Death Risk
The common use of anti-inflammatory steroids for traumatic head injuries like those from car crashes may actually increase the risk of death, according to a new review of studies about the therapy.

A prior review found there was not enough evidence to recommend that routine use of steroids be stopped. This newer analysis published by the British-based Cochrane Library draws heavily from a recent study of corticosteroid therapy for brain injury, including coma and concussion, that included 10,008 patients, more than all similar studies combined.

The large study found that patients treated with corticosteroids were 18 percent more likely to die from their brain injury than those who did not take the drugs. Among the patients who received steroid therapy, 21 percent ,or 1,052 of the 4,985 treated, died, compared to 18 percent who received a placebo.

"The significant increase in death with steroids found in this trial suggests that steroids should no longer be routinely used in people with traumatic head injury," says Dr. Phil Alderson, lead author of the Cochrane study.

The review appears in the recent issue of The Cochrane Library, a publication of the Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.

Corticosteroids are anti-inflammatory hormones used to treat all kinds of inflammation, from joint injury to asthma. They differ from anabolic steroids, the sex hormones like androgen, which are typically used to increase muscle mass and improve athletic performance.

Corticosteroids are "widely used in medicine to treat inflammation," Alderson explains. "It is thought that some of the damage after a brain injury results from inflammation following the initial injury and that reducing inflammation might reduce this secondary injury".........

Daniel      Permalink


December 27, 2005

Blocking The Nerve Receptor Reduces Brain Damage

Blocking The Nerve Receptor Reduces Brain Damage
Scientists at Johns Hopkins have discovered how to block a molecular switch that triggers brain damage caused by the lack of oxygen during a stroke. The Hopkins study, conducted on mice, is believed to be the first to demonstrate that a protein on the surface of nerve cells called the EP1 receptor is the switch, and that a specific compound, known as ONO-8713, turns it off.

The finding holds promise for the development of effective alternatives to anti-inflammatory drugs called COX inhibitors, which have potentially lethal side effects that limit their use, says Sylvain Dore, Ph.D., an associate professor in the departments of Anesthesiology and Critical Care Medicine and Neuroscience at The Johns Hopkins University School of Medicine. Dore is senior author of the paper, published in the recent issue of Toxicological Sciences. "Our work has shifted the focus from drugs that inhibit COX-2 to drugs that block the EP1 receptor," Dore said.

Receptors are protein-docking sites on cells into which "signaling" molecules such as nerve chemicals or hormones insert themselves. This binding activates the receptor, which transfers the signal into the cell to produce a specific response.

COX inhibitors block the ability of the enzyme cyclooxygenase-2 (COX-2) to make prostaglandin E2 (PGE2), a hormonelike substance long linked to inflammation and other effects. The Hopkins study results suggest that PGE2 causes brain damage following stroke by binding to the EP1 receptor on nerve cells. Therefore, blocking PGE2 activity directly rather than inhibiting COX-2 could reduce brain damage in individuals who have a stroke while avoiding the side effects of COX-2 inhibitors, the Hopkins researchers say.

Prior work by others had shown that certain events, such as cerebral ischemia (stroke) and seizures, that interrupt oxygen flow to the brain also cause excessive activation of so-called NMDA receptors by the nerve chemical glutamate. Other work had suggested that activation of NMDA receptors by glutamate causes an increase in the production of COX-2, which then produces PGE2.........

Daniel      Permalink


December 26, 2005

Arthritis Drug Effective for Depression

Arthritis Drug Effective for Depression
Etanercept (trade name Enbrel), approved for treating rheumatoid arthritis, effectively reduces not only the symptoms of the disease, but also depression and fatigue in psoriasis sufferers, according to a multi-university research team that includes a scientist at Duke University Medical Center. Etanercept, an antibody that blocks tumor necrosis factor-alpha, significantly improved the symptoms and depression associated with the disorder, the scientists reported in an article published online Dec. 14, 2005 by The Lancet.

High concentrations of pro-inflammatory substances called cytokines, such as tumor necrosis factor-alpha (TNF-alpha), have been associated with major depression. According to Ranga Krishnan, M.D., the study author based at Duke, scientists have long hypothesized that reducing the effects of the cytokines may reverse depressive symptoms. Until now, no research team has examined the effects of a tumor necrosis factor receptor on depression in humans.

The phase III clinical trial was primarily designed to test the effectiveness of etanercept in improving the clinical symptoms of psoriasis, a chronic skin disease characterized by silvery, scaling bumps and raised patches of very dry skin. In severe cases, people can experience joint pain similar to that of rheumatoid arthritis. Psoriasis sufferers frequently experience problems with both depression and fatigue as a result of their disease.

"It has been shown that when you are sick or depressed, tumor necrosis factor concentration increases," said Krishnan, chief of psychiatry and behavioral sciences at Duke. "When TNF-alpha goes up, the symptoms are very similar to what is termed 'sickness behavior' and prior studies have shown that when a person is depressed, TNF-alpha levels are increased in blood".........

JoAnn      Permalink


December 26, 2005

Antidepressants Boost Brain Growth

Antidepressants Boost Brain Growth
The beneficial effects of a widely used class of antidepressants might be the result of increased nerve-fiber growth in key parts of the brain, according to a Johns Hopkins study being published in the January 2006 issue of the Journal of Neurochemistry.

The study on rats, led by Vassilis E. Koliatsos, M.D., a neuropathologist at the Johns Hopkins University School of Medicine, found that selective serotonin reuptake inhibitors (SSRIs) increase the density of nerve-impulse-carrying axons in the frontal and parietal lobes of the neocortex and part of the limbic brain which control the sense of smell, emotions, motivation, and organs that work reflexively such as the heart, intestines and stomach. "It appears that SSRI antidepressants rewire areas of the brain that are important for thinking and feeling, as well as operating the autonomic nervous system," said Koliatsos.

Axons are long, filament-shaped extensions of neurons that, together with myelin, are the main constituents of nerves. Axons conduct chemically driven nerve impulses away from the cell body toward a narrow gap known as a synapse. Among the chemicals involved are such monoamines as norepinephrine and serotonin, which, at the synapse, are transferred to another neuron.

Antidepressants, such as Prozac, Zoloft and Paxil, have long been thought to exert their clinical effects by increasing synaptic concentrations of serotonin and norepinephrine, enhancing or stimulating their transference.

"But our findings -- that serotonin reuptake modulators increase the density of nerve synapses, particularly in the front part of the brain - may offer a better explanation of why antidepressants are effective and why they take time to work," according to Koliatsos.

For example, antidepressants increase synaptic monoamines within hours, and the regulatory effects on receptors are complete within a few days, yet clinically meaningful results from antidepressants commonly require a two- to four-week delay.........

JoAnn      Permalink


December 25, 2005

Compounds prevens brain cell death

Compounds prevens brain cell death
Spanish chemists have developed a promising set of synthetic compounds that one day could help slow or perhaps halt the progression of Alzheimer's disease and other neurological disorders. The preliminary finding, based on test tube studies by scientists at the Universidad de Granada and others, appears in the Dec. 29 issue of the American Chemical Society's Journal of Medicinal Chemistry.

The compounds, especially a synthesized metabolite of the hormone melatonin, all inhibit an enzyme called inducible nitric oxide synthase (iNOS), which is needed to produce nitric oxide (NO). NO, a signaling molecule that can activate the immune system, plays an important role in the brain, according to the researchers. But too much NO can trigger the death of brain cells and some researchers theorize the compound is involved in the development of Alzheimer's and Parkinson's diseases.

Like melatonin, the new synthetic compounds apparently can cross biological barriers, suppress iNOS production, and, in turn, prevent NO-induced brain damage, the scientists say. However, they caution that additional research will be needed to verify these results.........

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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