December 16, 2005
Tongue Sensors Taste Fat
As you stand at buffet tables during holiday parties this year, it might cheer you up to know most people don't gain as much weight over the holidays as once was thought. Instead of five or 10 pounds, most of us actually gain only a pound or two. But it might depress you to know that weight gain happens one pound at a time and in the long run, it may be hard to avoid - particularly for some of us, because some of the taste buds in our tongues are programmed to make us crave fatty food - and fat is everywhere in our diets.
French scientists recently reported that mice have a receptor in their tongues that can sense fat, and the presence of that receptor seems to drive the mice to crave fat in their diets. The work was based on research from Nada A. Abumrad, Ph.D., the Dr. Robert C. Atkins Professor of Medicine and Obesity Research at Washington University School of Medicine in St. Louis. She previously had identified a protein receptor for fat and documented its function in recognizing and using fatty food. This led the French scientists from the Taste Institute in Dijon, France, to wonder whether the protein also may have a role in actually tasting fat.
"Fat sensing has been very controversial," Abumrad says. "It once was thought that we could sense five different tastes: sweet, salty, sour, bitter and what researchers refer to as umami, which is the taste of a protein like monosodium glutamate. There was some indirect evidence that the tongue might be able to identify fat, too, but a number of researchers thought that involved sensation of texture more than the actual taste of fat."
Abumrad adds that several researchers had proposed people might not only sense the texture of fat, but also might have fatty acid receptors that lead them to prefer foods containing fat. She studies the molecular mechanisms regulating utilization of fatty acids, and she was the first to identify a protein called CD36 that facilitates the uptake of fatty acids. The CD36 receptor protein is located on the surface of cells and distributed in a number of tissues, including fat cells, the digestive tract, heart tissue, skeletal muscle tissue and, as it happens, the tongue.........Daniel Permalink
December 16, 2005
antioxidant linked to Alzheimer's and Parkinson's
Raymond Swanson, MD
A study conducted at the San Francisco VA Medical Center has identified a protein found in both mice and humans that appears to play a key role in protecting neurons from oxidative stress, a toxic process linked to neurodegenerative illnesses including Alzheimer's and Parkinson's diseases.
The study, led by Raymond Swanson, MD, chief of neurology and rehabilitation services at SFVAMC, identified the protein - known as EAAC1 in mice and as EAAT3 in humans - as the main mechanism through which the amino acid cysteine is transported into neurons. Cysteine is an essential component of glutathione, which Swanson terms "the most important antioxidant in the brain".
It had been thought previously that the main function of the protein was to remove excess glutamate, a neurotransmitter, from brain cells.
"It's known that neurons don't take up cysteine directly, and it's never been clear exactly how it gets there," says Swanson, who is also professor and vice chair of neurology at the University of California, San Francisco. "This study provides the first evidence that EAAC1 is the mechanism by which cysteine gets into neurons - and that transporting cysteine is probably its chief function".
Study findings are currently available in the Advance Online Publication section of Nature Neuroscience.
Antioxidants such as glutathione provide protection from oxidative stress, which kills cells through the "uncontrolled reaction of lipids in the cells with oxygen-basically, burning them out," says Swanson. Since the brain uses a lot of oxygen and is "chock full of lipids," it is especially vulnerable to oxidative stress, he notes.
In the first part of the study, Swanson and his co-authors observed a colony of mice deficient in the gene responsible for the production of EAAC1 and compared their behavior with that of a colony of normal, or "wild type," mice. They noticed that around the age of 11 months - old age for a mouse - the gene-deficient mice began to act listlessly, not groom themselves properly, and exhibit other signs of senility. In contrast, the wild type mice "looked and acted totally normal," according to Swanson.........Daniel Permalink
December 15, 2005
Cerebral Cortex Suggested As Genesis Of Tremors
Parkinson's disease, first described nearly 200 years ago by a British clinician for whom the disease is named (and who dubbed it the "shaking palsy"), is widely thought to show abnormalities in the basal parts of the brain - causing the characteristic tremors, stiffness of the limbs and poor balance.
Now new research led by John Caviness, M.D., Professor of Neurology at Mayo Clinic in Arizona, suggests that the cerebral cortex of the brain is also responsible for significant abnormal muscle activity in Parkinson's disease. The study results were published in the October 2005 edition of Movement Disorders Journal.
Typically parkinson's disease, part of a group of conditions known as motor system disorders, is characterized by tremor of the hands and arms, as well as stiffness of the limbs and slowness of movement.
Nearly 50,000 Americans generally over age 50 are affected by the progressive disease each year, and medical science has struggled to pinpoint exact causes in the vast majority of cases.
The basal portion of the human brain is thought to regulate movement in a place called basal ganglia. It has long been thought that the abnormal basal ganglia in Parkinson's disease patients produce the movement problems. The cerebral cortex, the outermost layer of the brain considered the most complex portion, is also involved in voluntary movement execution and regulates planning, problem-solving, language and speech.
In the study, Dr. Caviness - along with authors from Barrows Neurological Institute, Phoenix, and Sun Health Research Institute, Sun City, Ariz., - examined the significance of postural tremors in patients with Parkinson's. Postural tremor, as opposed to "rest" tremor in Parkinson's, is observed when a patient attempts to "hold" or "posture" against gravity - such as holding one's arms out in front.........Daniel Permalink
December 15, 2005
Immunosuppressive Drug Effective In MS
A medicine that reduces relapse rates in patients with multiple sclerosis (MS) appears to be effective in reducing new brain inflammatory lesions and is well tolerated, as per a studyin the recent issue of the Archives of Neurology, one of the JAMA/Archives journals.
The drug is azathioprine, an immunosuppressive agent that is well tolerated, easy to administer and monitor, and has been used for a number of years in the therapy of transplant rejections and autoimmune diseases. Azathioprine reduces relapse rates in MS patients, but its effects on the frequency and accumulation of new brain inflammatory lesions has not been studied in MS, according to background information in the article. MS is a disease of the central nervous system, marked by numbness, weakness, loss of muscle coordination, and problems with vision, speech, and bladder control.
Luca Massacesi, M.D., and his colleagues at the University of Florence, Italy, conducted an open-label therapy study to evaluate the effect of azathioprine treatment on new brain lesion suppression in MS. They used magnetic resonance imaging (MRI) to evaluate brain lesions of 14 patients with relapse-remitting MS (RRMS) of short duration. RRMS is a form of the disease characterized by relapses, when new symptoms can appear and old ones resurface or worsen, followed by periods of remission, when the person fully or partially recovers from the deficits acquired during the relapse. The patients were evaluated for six months before and six months during therapy with azathioprine, and new lesions were evaluated during the same periods and after an additional six months.
"The results of this study show, for the first time, that the immunosuppressive agent azathioprine suppresses new brain lesions evaluated using MRI in patients with RRMS," the authors report.........Daniel Permalink
December 15, 2005, 7:46 PM CT
Neuron Sprouts Its Branches
Michael D. Ehlers, M.D., Ph.D.
Neurobiologists have gained new insights into how neurons control growth of the intricate tracery of branches called dendrites that enable them to connect with their neighbors. Dendritic connections are the basic receiving stations by which neurons form the signaling networks that constitute the brain's circuitry.
Such basic insights into neuronal growth will help scientists better understand brain development in children, as well as aid efforts to restore neuronal connections lost to injury, stroke or neurodegenerative disease, said the researchers.
In a paper published in the Dec. 8, 2005, issue of Neuron, Howard Hughes Medical Institute investigator Michael Ehlers and colleagues reported that structures called "Golgi outposts" play a central role as distribution points for proteins that form the building blocks of the growing dendrites.
Besides Ehlers, who is at Duke University Medical Center, other co-authors were April Horton in Ehlers' laboratory; Richard Weinberg of the University of North Carolina at Chapel Hill.; Bence Rácz in Weinberg's laboratory; and Eric Monson and Anna Lin of Duke's Department of Physics. The research was sponsored by The National Institutes of Health.
The Golgi apparatus is a cellular warehouse responsible for receiving, sorting and shipping cargoes of newly synthesized molecules needed for cell growth and function. Until the new findings, scientists believed that only a central Golgi apparatus played a role in such distribution, said Ehlers.
"In most mammalian cells, the Golgi has a very stereotyped structure, a stacked system that resides near the cell nucleus in the middle of the cell," he said. "But mammalian neurons in the brain are huge, with a surface area about ten thousand times that of the average cell. So, it was an entirely open question where all the membrane components came from to generate the complex surface of growing dendrites. And we thought these remote structures we had discovered in dendrites called Golgi outposts might play a role."........Daniel Permalink
December 14, 2005, 8:12 PM CT
Depression Improves After Epilepsy Surgery
Depression and anxiety are common problems for people whose epilepsy cannot be controlled by medication. A new study found that depression and anxiety improve significantly after epilepsy surgery.
The study, which is published in the December 13, 2005, issue of Neurology, the scientific journal of the American Academy of Neurology, found that the rate of depression and anxiety disorders decreased by more than 50 percent up to two years after the surgery. People who no longer experienced any seizures after surgery were even more likely to be free of depression and anxiety.
"These results are important because depression and anxiety can significantly affect the quality of life," said study author Orrin Devinsky, MD, Professor of Neurology, Neurosurgery, and Psychiatry at New York University School of Medicine and Director of the NYU Comprehensive Epilepsy Center. "For people with refractory epilepsy, studies show that depression is more likely to affect their quality of life than how often they have seizures or how a number of drugs they have to take.".
The study involved 360 people in seven U.S. epilepsy centers who were undergoing epilepsy surgery to remove the area of the brain producing the seizures. Epilepsy surgery is generally reserved for those whose seizures cannot be adequately controlled by medication. The majority of participants had surgery on the brain's temporal lobe. The participants' mental health and any symptoms of depression and anxiety were evaluated before surgery and at three months, one year, and two years after surgery.
Previous to the surgery, 22 percent of the participants met the criteria for a diagnosis of depression, compared to 9 percent two years after the surgery. For anxiety disorders, 18 percent met the criteria for a diagnosis before the surgery, compared to 10 percent two years after the surgery.........JoAnn Permalink
December 12, 2005
Re-opening Of Blocked Internal Carotid Arteries In Acute Stroke
Tudor Jovin, M.D.
University of Pittsburgh scientists report a high level of effectiveness in re-opening completely blocked internal carotid arteries (ICA) as late as two to three days after acute stroke symptoms by using stents. The study at the University of Pittsburgh School of Medicine Department of Neurology and University of University of Pittsburgh Medical Center (UPMC) Stroke Institute, is in the recent issue of Stroke, a peer-reviewed publication of the American Heart Association.
"This report breaks new ground in that it contradicts the conventional wisdom that a completely blocked or occluded carotid cannot be opened," said the study's lead author, Tudor Jovin, M.D., assistant professor of neurology and neurosurgery at Pitt's School of Medicine, and co-director of the Center for Endovascular Therapy at UPMC.
Dr. Jovin's team, which consisted of members of the UPMC Stroke Institute, retrospectively studied 25 patients with acute carotid occlusion who underwent angiography with the intent to revascularize the occlusion from January 2002 to March 2005.
Scientists concluded that recanalization, or re-opening of the artery, was successful in 23 of the 25 patients, and that the procedure was done safely.
"The main finding of the report was that endovascular revascularization of occluded ICA in the setting of acute or subacute ischemic stroke carries a high-revascularization rate and is safe in selected patients," Dr. Jovin reported.
"Management of stroke because of acute internal carotid artery occlusion continues to represent a challenge because it may result in significant disability in 40 percent and death in 20 percent of cases," Dr. Jovin said. "Our results are significant because they offer an opportunity for patients who may need more aggressive therapy. Future prospective studies are necessary to determine which patients are most likely to benefit from this form of treatment.".........Daniel Permalink
December 12, 2005
About Trust-building Hormone
Functional magnetic resonance imaging data (red) superimposed on structural MRI scans. Frightful faces triggered a dramatic reduction in amygdala activity in subjects who had sniffed oxytocin, suggesting that oxytocin mediates social fear and trust via the amygdala and related circuitry.
brain chemical recently found to boost trust appears to work by reducing activity and weakening connections in fear-processing circuitry, a brain imaging study at the National Institutes of Health's (NIH) National Institute of Mental Health (NIMH) has discovered. Scans of the hormone oxytocin's effect on human brain function reveal that it quells the brain's fear hub, the amygdala, and its brainstem relay stations in response to fearful stimuli. The work at NIMH and a collaborating site in Gera number of suggests new approaches to treating diseases thought to involve amygdala dysfunction and social fear, such as social phobia, autism, and possibly schizophrenia, report Andreas Meyer-Lindenberg, M.D., Ph.D., NIMH Genes Cognition and Psychosis Program, and his colleagues, in the December 7, 2005 issue of the Journal of Neuroscience.
"Studies in animals, pioneered by now NIMH director Dr. Thomas Insel, have shown that oxytocin plays a key role in complex emotional and social behaviors, such as attachment, social recognition and aggression" noted NIH Director Elias Zerhouni, M.D. "Now, for the first time, we can literally see these same mechanisms at work in the human brain."
"The observed changes in the amygdala are exciting as they suggest that a long-acting analogue of oxytocin could have therapeutic value in disorders characterized by social avoidance," added Insel.
Inspired by Swiss researchers who last summer reported1 that oxytocin increased trust in humans, Meyer-Lindenberg and his colleagues quickly mounted a brain imaging study that would explore how this works at the level of brain circuitry. British scientists had earlier linked increased amygdala activity to decreased trustworthiness2. Having just discovered decreased amygdala activity (http://www.nimh.nih.gov/press/williamspathway.cfm) in response to social stimuli in people with a rare genetic brain disorder that rendered them overly trusting of others, Meyer-Lindenberg hypothesized that oxytocin boosts trust by suppressing the amygdala and its fear-processing networks.........Daniel Permalink
Missing Link In Taste
(December 11, 2005)
Researchers funded by the National Institute on Deafness and Other Communication Disorders (NIDCD), one of the National Institutes of Health, are a step closer to unraveling the mystery of taste. As per a research findings published in the December 2, 2005, issue of Science, scientists have pinpointed the chemical responsible for transmitting signals from the taste buds - small sensory bumps on the tongue, throat, and roof of the mouth - to the taste nerves leading to the brain. Today's findings provide researchers with a more complete picture of this complicated process, helping advance the study of taste and taste disorders.
Hole in Heart Does Not Make Stroke Always
(December 11, 2005)
Mayo Clinic scientists have found that -- contrary to current thinking by some in the medical community -- a patent foramen ovale (PFO), a small hole between the two upper chambers of the heart, does not predestine an individual to a stroke later in life. Findings will appear online on Friday, Dec. 9 in the Journal of the American College of Cardiology.
Month Following Heart Attack
(December 11, 2005)
A Mayo Clinic research team discovered that heart attack patients have a 44-fold increased risk of stroke in the 30 days following the heart attack, compared with the general population, according to findings published in the current Annals of Internal Medicine. About 22.6 strokes occurred within the first 30 days of the heart attack for every 1,000 patients followed.
First "Wingspan Stent" Procedure (December 8, 2005)