Neuroscience
Month
ScienceDaily (July 31, 2012) — New research demonstrates that blocking the delta opioid receptor in mice created resistance to weight gain and stimulated gene expression promoting non-shivering thermogenesis.
Imagine eating all of the sugar and fat that you want without gaining a pound. Thanks to new research published in The FASEB Journal, the day may come when this is not too far from reality. That’s because researchers from the United States and Europe have found that blocking one of three opioid receptors in your body could turn your penchant for sweets and fried treats into a weight loss strategy that actually works. By blocking the delta opioid receptor, or DOR, mice reduced their body weight despite being fed a diet high in fat and sugar. The scientists believe that the deletion of the DOR gene in mice stimulated the expression of other genes in brown adipose tissue that promoted thermogenesis.
"Our study provided further evidence that opioid receptors can control the metabolic response to diets high in fat and sugar, and raise the possibility that these gene products (or their respective pathways) can be targeted specifically to treat excess weight and obesity," said Traci A. Czyzyk, Ph.D., a researcher involved in the work from the Department of Physiology at the Mayo Clinic in Scottsdale, Arizona.
Scientists studied mice lacking the delta opioid receptor (DOR KO) and wild type (WT) control mice who were fed an energy dense diet (HED), high in fat and sugar, for three months. They found that DOR KO mice had a lean phenotype specifically when they were fed the HED. While WT mice gained significant weight and fat mass on this diet, DOR KO mice remained lean even though they consumed more food. Researchers then sought to determine how DOR might regulate energy balance and found that DOR KO mice were able to maintain their energy expenditure levels, in part, due to an increase in non-shivering thermogenesis. This was evidenced by an increase in thermogenesis-promoting genes in brown adipose tissue, an increase in body surface temperature near major brown adipose tissue depots, and the ability of DOR KO mice to maintain higher core body temperatures in response to being in a cold environment.
"Don’t reach for the ice cream and doughnuts just yet," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “We don’t know how all this works in humans, and of course, a diet of junk food causes other health problems. This exciting research identifies genes that activate brown adipose tissue to increase our burning of calories from any source. It may lead to a safe diet pill in the future.”
Source: Science Daily
July 31, 2012
Wayne State University School of Medicine researchers, working with colleagues in Canada, have found that one or more substances produced by a type of immune cell in people with multiple sclerosis (MS) may play a role in the disease’s progression. The finding could lead to new targeted therapies for MS treatment.
B cells, said Robert Lisak, M.D., professor of neurology at Wayne State and lead author of the study, are a subset of lymphocytes (a type of circulating white blood cell) that mature to become plasma cells and produce immunoglobulins, proteins that serve as antibodies. The B cells appear to have other functions, including helping to regulate other lymphocytes, particularly T cells, and helping maintain normal immune function when healthy.
In patients with MS, the B cells appear to attack the brain and spinal cord, possibly because there are substances produced in the nervous system and the meninges — the covering of the brain and spinal cord — that attract them. Once within the meninges or central nervous system, Lisak said, the activated B cells secrete one or more substances that do not seem to be immunoglobulins but that damage oligodendrocytes, the cells that produce a protective substance called myelin.
The B cells appear to be more active in patients with MS, which may explain why they produce these toxic substances and, in part, why they are attracted to the meninges and the nervous system.
The brain, for the most part, can be divided into gray and white areas. Neurons are located in the gray area, and the white parts are where neurons send their axons — similar to electrical cables carrying messages — to communicate with other neurons and bring messages from the brain to the muscles. The white parts of the brain are white because oligodendrocytes make myelin, a cholesterol-rich membrane that coats the axons. The myelin’s function is to insulate the axons, akin to the plastic coating on an electrical cable. In addition, the myelin speeds communication along axons and makes that communication more reliable. When the myelin coating is attacked and degraded, impulses — messages from the brain to other parts of the body — can “leak” and be derailed from their target. Oligodendrocytes also seem to engage in other activities important to nerve cells and their axons.
The researchers took B cells from the blood of seven patients with relapsing-remitting MS and from four healthy patients. They grew the cells in a medium, and after removing the cells from the culture collected material produced by the cells. After adding the material produced by the B cells, including the cells that produce myelin, to the brain cells of animal models, the scientists found significantly more oligodendrocytes from the MS group died when compared to material produced by the B cells from the healthy control group. The team also found differences in other brain cells that interact with oligodendrocytes in the brain.
"We think this is a very significant finding, particularly for the damage to the cerebral cortex seen in patients with MS, because those areas seem to be damaged by material spreading into the brain from the meninges, which are rich in B cells adjacent to the areas of brain damage," Lisak said.
The team is now applying for grants from several sources to conduct further studies to identify the toxic factor or factors produced by B cells responsible for killing oligodendrocytes. Identification of the substance could lead to new therapeutic methods that could switch off the oligodendrocyte-killing capabilities of B cells, which, in turn, would help protect myelin from attacks.
Provided by Wayne State University
Source: medicalxpress.com
July 31, 2012
(HealthDay) — For patients with dementia with Lewy bodies (DLB), treatment with 5 or 10 mg/day donepezil is associated with significant cognitive, behavioral, and global function improvements, according to research published in the July issue of the Annals of Neurology.
Etsuro Mori, M.D., Ph.D., of the Tohoku University Graduate School of Medicine in Sendai, Japan, and colleagues conducted a randomized, double-blind, placebo-controlled trial involving 140 patients with DLB who received either placebo or 3, 5, or 10 mg of donepezil hydrochloride per day for 12 weeks (35, 35, 33, and 37 patients, respectively). Cognitive function was measured using the Mini-Mental State Examination (MMSE); behavioral changes were measured using the Neuropsychiatric Inventory; global function was evaluated using the Clinician’s Interview-Based Impression of Change-plus Caregiver Input (CIBIC-plus); and caregiver burden was also assessed.
The researchers found that, compared with placebo treatment, the MMSE scores were significantly better with donepezil 5 mg (mean difference, 3.8) and 10 mg (mean difference, 2.4), but the 3 mg/day dose was not significantly better than placebo (P = 0.017). Donepezil at doses of 3, 5, and 10 mg/day correlated with significant improvements versus placebo on CIBIC-plus. Both the 5 and 10 mg doses of donepezil resulted in significant improvements in behavioral measures. Caregiver burden also improved, but only with the 10 mg/day dose. The safety results were similar among the groups and were consistent with the known profile.
"Donepezil at 5 and 10 mg/day produces significant cognitive, behavioral, and global improvements that last at least 12 weeks in DLB patients, reducing caregiver burden at the highest dose," the authors write. Several authors disclosed financial ties to pharmaceutical companies, including Eisai Co., which funded the study and manufactures donepezil.
Source: medicalxpress.com
Jul 31, 2012 by Laura Bailey
Concussions and even lesser head impacts may speed up the brain’s natural aging process by causing signaling pathways in the brain to break down more quickly than they would in someone who has never suffered a brain injury or concussion.
The photos compare images of two brains, one with and without head injury. The red areas indicates electrical activity in response to the task researchers asked study participants to perform, and non-injured brains show more red, thus more electrical activity during the task. Image courtesy of Steven Broglio
Researchers from the University of Michigan School of Kinesiology and the U-M Health System looked at college students with and without a history of concussion and found changes in gait, balance and in the brain’s electrical activity, specifically attention and impulse control, said Steven Broglio, assistant professor of kinesiology and director of the Neurotrauma Research Laboratory.
The declines were present in the brain injury group up to six years after injury, though the differences between the study groups were very subtle, and outwardly all of the participants looked and acted the same.
Broglio, who is also affiliated with Michigan NeuroSport, stressed that the studies lay out a hypothesis where concussions and head impacts accelerate the brain’s natural aging process.
The study, “Cognitive decline and aging: The role of concussive and subconcussive impacts,” appears in the July issue of journal Exercise and Sport Sciences Reviews.
"The last thing we want is for people to panic. Just because you’ve had a concussion does not mean your brain will age more quickly or you’ll get Alzheimer’s," Broglio said. "We are only proposing how being hit in the head may lead to these other conditions, but we don’t know how it all goes together just yet."
Broglio stressed that other factors, such as lifestyle choices, smoking, alcohol consumption, physical exercise, family history and whether or not you “exercise” your brain also impact the brain’s aging process. Concussion may only be one small factor.
To begin to understand how concussions might impact brain activity and its signaling pathways, researchers asked the participants to perform certain tasks in front of a computer, and took images of their brains. The brains of the nonconcussed group showed a greater area of electrical activation than the participants with a history of brain injury.
The signaling pathways in our brains are analogous to a five-lane highway. On a new highway, traffic runs smoothly and quickly as all lanes are in top shape. However, during normal aging, the asphalt deteriorates and lanes might become bumpy or even unusable. Traffic slows.
Similarly, our brains start with all pathways clear to transfer electrical signals rapidly. As we age, the brain’s pathways break down and can’t transfer the information as quickly. Concussive and other impacts to the head may result in a ‘pothole’ on the brain’s highway, causing varying degrees of damage and speeding the pathway’s natural deterioration.
"What we don’t know is if you had a single concussion in high school, does that mean you will get dementia at age 50?" Broglio said. "Clinically, we don’t see that. What we think is it will be a dose response.
"So, if you played soccer and sustained some head impacts and maybe one concussion, then you may have a little risk. If you went on and played in college and took more head balls and sustained two more concussions, you’re probably at a little bigger risk. Then if you play professionally for a few years, and take more hits to the head, you increase the risk even more. We believe it’s a cumulative effect."
In the next phase of study, researchers will look at people in their 20s, 40s and 60s who did and did not sustain concussions during high school sports. They hope to learn if there is an increasing effect of concussion as the study subjects age. If interested in participating in the study, email neurotraumalab.umich@gmail.com.
Researchers from the departments of Physical Medicine and Rehabilitation, and Neurology, and the Michigan Alzheimer’s Disease Center also participated in the study.
Source: University of Michigan
July 31, 2012
The presence of specific autoantibodies of the immune system is associated with blood vessel damage in the brain. These findings were made by Marion Bimmler, a graduate engineer of medical laboratory diagnostics at the Max Delbrück Center for Molecular Medicine Berlin-Buch and Dr. Peter Karczewski of the biotech company E.R.D.E.-AAK-Diagnostik GmbH in studies on a rat model. The researchers’ results suggest that autoimmune mechanisms play a significant role in the pathogenesis and progression of Alzheimer’s and vascular dementia.
(MR Angiography/Copyright: MDC)
Antibodies are the defense molecules of the body’s immune system against foreign invaders. If the antibodies cease to distinguish between “foreign” and “self”, they attack the cells of the own body, and are thus referred to as autoantibodies. These can trigger autoimmune diseases. Using MR angiography and other methods, Marion Bimmler and her colleagues have now shown that the autoantibodies bind to specific surface proteins (alpha1 andrenergic receptors) of vascular cells and thereby damage the blood vessels of the brain. The reason: The autoantibodies generate a continual stimulation of the receptor and at the same time trigger an increase in intracellular calcium ion levels. As a result, the blood vessel walls thicken, and blood flow to the brain is disturbed.
First Encouraging Results after Removal of Autoantibodies by Immunoadsorption
In earlier studies, Marion Bimmler and her research team examined blood samples of patients with Alzheimer’s or vascular dementia and showed that half of them had comparable autoantibodies. A first clinical trial together with Charité – Universitätsmedizin Berlin is currently ongoing with a collective of patients with Alzheimer’s or vascular dementia. The patients were divided into two groups – a small group whose autoantibodies were removed from the blood via immunoadsorption and a control group that did not receive this treatment. Until now, over an observation period of 6 and subsequently 12 months, the patient group who had undergone immunoadsorption improved in their memory performance and in their ability to cope with their everyday lives. In contrast, the condition of the patients who did not receive immunoadsorption treatment and continued to have autoantibodies in their blood deteriorated dramatically. Now the researchers are planning further clinical trials with larger numbers of patients.
Provided by Helmholtz Association of German Research Centres
Source: medicalxpress.com
Tuesday, July 31, 2012
TAU researchers develop bioactive coating to “camouflage” neutral electrodes
Brain-computer interfaces are at the cutting edge for treatment of neurological and psychological disorder, including Parkinson’s, epilepsy, and depression. Among the most promising advance is deep brain stimulation (DBS) — a method in which a silicon chip implanted under the skin ejects high frequency currents that are transferred to the brain through implanted electrodes that transmit and receive the signals. These technologies require a seamless interaction between the brain and the hardware.
But there’s a catch. Identified as foreign bodies by the immune system, the brain attacks the electrodes and forms a barrier to the brain tissue, making it impossible for the electrodes to communicate with brain activity. So while the initial implantation can diminish symptoms, after a few short years or even months, the efficacy of this therapy begins to wane.
Now Aryeh Taub of Tel Aviv University's School of Psychological Sciences, along with Prof. Matti Mintz, Roni Hogri and Ari Magal of TAU’s School of Psychological Sciences and Prof. Yosi Shacham-Diamand of TAU’s School of Electrical Engineering, has developed a bioactive coating which not only “camouflages” the electrodes in the brain tissue, but actively suppresses the brain’s immune response. By using a protein called an “interleukin (IL)-1 receptor antagonist” to coat the electrodes, the multi-disciplinary team of researchers has found a potential resolution to turn a method for short-term relief into a long-term solution. This development was reported in the Journal of Biomedical Materials Research.
Limiting the immune response
To overcome the creation of the barrier between the tissue and the electrode, the researchers sought to develop a method for placing the electrode in the brain tissue while hiding the electrode from the brain’s immune defenses. Previous research groups have coated the electrodes with various proteins, says Taub, but the TAU team decided to take a different approach by using a protein that is active within the brain itself, thereby suppressing the immune reaction against the electrodes.
In the brain, the IL-1 receptor antagonist is crucial for maintaining physical stability by localizing brain damage, Taub explains. For example, if a person is hit on the head, this protein works to create scarring in specific areas instead of allowing global brain scarring. In other words, it stops the immune system from overreacting. The team’s coating, the first to be developed from this particular protein, not only integrates the electrodes into the brain tissue, but allows them to contribute to normal brain functioning.
In pre-clinical studies with animal models, the researchers found that their coated electrodes perform better than both non-coated and “naïve protein”-coated electrodes that had previously been examined. Measuring the number of damaged cells at the site of implantation, researchers found no apparent difference between the site of electrode implantation and healthy brain tissue elsewhere, Taub says. In addition, evidence suggests that the coated electrodes will be able to function for long periods of time, providing a more stable and long-term treatment option.
Restoring brain function
Approximately 30,000 people worldwide are currently using deep brain stimulation (DBS) to treat neurological or psychological conditions. And DBS is only the beginning. Taub believes that, in the future, an interface with the ability to restore behavioral or motor function lost due to tissue damage is achievable — especially with the help of their new electrode coating.
"We duplicate the function of brain tissue onto a silicon chip and transfer it back to the brain," Taub says, explaining that the electrodes will pick up brain waves and transfer these directly to the chip. "The chip then does the computation that would have been done in the damaged tissue, and feeds the information back into the brain — prompting functions that would have otherwise gotten lost."
Source: Tel Aviv University
July 30, 2012
In the first human study of its kind, researchers found that using stem cells to re-grow craniofacial tissues—mainly bone—proved quicker, more effective and less invasive than traditional bone regeneration treatments.
Researchers from the University of Michigan School of Dentistry and the Michigan Center for Oral Health Research partnered with Ann Arbor-based Aastrom Biosciences Inc. in the clinical trial, which involved 24 patients who required jawbone reconstruction after tooth removal.
Patients either received experimental tissue repair cells or traditional guided bone regeneration therapy. The tissue repair cells, called ixmyelocel-T, are under development at Aastrom, which is a U-M spinout company.
"In patients with jawbone deficiencies who also have missing teeth, it is very difficult to replace the missing teeth so that they look and function naturally," said Darnell Kaigler, principal investigator and assistant professor at the U-M School of Dentistry. "This technology and approach could potentially be used to restore areas of bone loss so that missing teeth can be replaced with dental implants."
William Giannobile, director of the Michigan Center for Oral Health Research and chair of the U-M Department of Periodontics and Oral Medicine, is co-principal investigator on the project.
The treatment is best suited for large defects such as those resulting from trauma, diseases or birth defects, Kaigler said. These defects are very complex because they involve several different tissue types—bone, skin, gum tissue—and are very challenging to treat.
The main advantage to the stem cell therapy is that it uses the patient’s own cells to regenerate tissues, rather than introducing man-made, foreign materials, Kaigler said.
The results were promising. At six and 12 weeks following the experimental cell therapy treatment, patients in the study received dental implants. Patients who received tissue repair cells had greater bone density and quicker bone repair than those who received traditional guided bone regeneration therapy.
In addition, the experimental group needed less secondary bone grafting when getting their implants.
The cells used for the therapy were originally extracted from bone marrow taken from the patient’s hip. The bone marrow was processed using Aastrom’s proprietary system, which allows many different cells to grow, including stem cells. These stem cells were then placed in different areas of the mouth and jaw.
Stem cell therapies are still probably 5-10 years away from being used regularly to treat oral and facial injuries and defects, Kaigler said. The next step is to perform more clinical trials that involve larger craniofacial defects in a larger number of patients.
The study, “Stem cell therapy for craniofacial bone repair: A randomized, controlled clinical trial,” appears this month in the journal Cell Transplantation.
See the video here
Source: University of Michigan
July 30, 2012
UC Irvine scientists have discovered intriguing differences in the brains and mental processes of an extraordinary group of people who can effortlessly recall every moment of their lives since about age 10.
The phenomenon of highly superior autobiographical memory – first documented in 2006 by UCI neurobiologist James McGaugh and colleagues in a woman identified as “AJ” – has been profiled on CBS’s “60 Minutes” and in hundreds of other media outlets. But a new paper in the peer-reviewed journal Neurobiology of Learning & Memory’s July issue offers the first scientific findings about nearly a dozen people with this uncanny ability.
All had variations in nine structures of their brains compared to those of control subjects, including more robust white matter linking the middle and front parts. Most of the differences were in areas known to be linked to autobiographical memory, “so we’re getting a descriptive, coherent story of what’s going on,” said lead author Aurora LePort, a doctoral candidate at UCI’s Center for the Neurobiology of Learning & Memory.
Surprisingly, the people with stellar autobiographical memory did not score higher on routine laboratory memory tests or when asked to use rote memory aids. Yet when it came to public or private events that occurred after age 10½, “they were remarkably better at recalling the details of their lives,” said McGaugh, senior author on the new work.
"These are not memory experts across the board. They’re 180 degrees different from the usual memory champions who can memorize pi to a large degree or other long strings of numbers," LePort noted. "It makes the project that much more interesting; it really shows we are homing in on a specific form of memory."
She said interviewing the subjects was “baffling. You give them a date, and their response is immediate. The day of the week just comes out of their minds; they don’t even think about it. They can do this for so many dates, and they’re 99 percent accurate. It never gets old.”
The study also found statistically significant evidence of obsessive-compulsive tendencies among the group, but the authors do not yet know if or how this aids recollection. Many of the individuals have large, minutely catalogued collections of some sort, such as magazines, videos, shoes, stamps or postcards.
UCI researchers and staff have assessed more than 500 people who thought they might possess highly superior autobiographical memory and have confirmed 33 to date, including the 11 in the paper. Another 37 are strong candidates who will be further tested.
"The next step is that we want to understand the mechanisms behind the memory," LePort said. "Is it just the brain and the way its different structures are communicating? Maybe it’s genetic; maybe it’s molecular."
McGaugh added: “We’re Sherlock Holmeses here. We’re searching for clues in a very new area of research.”
Provided by University of California, Irvine
Source: medicalxpress.com
30 July 2012
Researchers from The University of Queensland’s Institute for Molecular Bioscience have discovered a potential new approach to treating chronic inflammatory diseases such as arthritis.
Professor David Fairlie and his colleagues have developed an experimental treatment that has proven effective at reducing symptoms and stopping the progression of the disease in models of arthritis.
“Human enzymes called proteases stimulate the secretion of immune cells that, when the correct amount is released, play important roles in digestion, fighting infections and healing wounds,” Professor Fairlie said.
“But in chronic inflammatory diseases such as arthritis, these enzymes continuously stimulate the release of immune cells, which cause inflammation when present at high levels. This leads to ongoing tissue damage.”
Professor Fairlie and his team have developed experimental compounds that block this stimulation and successfully reduce chronic inflammatory arthritis in experimental models.
If the treatment could be transferred to humans, it has the potential to reduce both the health and economic impacts of chronic inflammatory diseases.
Almost four million Australians suffer from chronic joint pain and disability caused by various forms of arthritis, including osteoarthritis, rheumatoid arthritis and gout.
Related healthcare and loss of employment cost Australia over $20 billion per year, an amount that is expected to increase dramatically as our population ages.
These promising new findings are published in the current hard-copy edition of The Federation of American Societies For Experimental Biology Journal, the world’s most cited scientific journal in biology.
Journal subscribers can access the paper at this address: http://bit.ly/Pg8lgk
Source: The University of Queensland
July 30, 2012
Is attention-deficit/hyperactivity disorder (ADHD) due to a delay in brain development or the result of complete deviation from typical development? In the current issue of Biological Psychiatry, Dr. Philip Shaw and colleagues present evidence for delay based on a study by the National Institutes of Health.
The cerebral cortex is the folded gray tissue that makes up the outermost portion of the brain, covering the brain’s inner structures. This tissue has left and right hemispheres and is divided into lobes. Each lobe performs specific and vitally important functions, including attention, thought, language, and sensory processing.
Two dimensions of this structure are cortical thickness and cortical surface area, both of which mature during childhood as part of the normal developmental process. This group of scientists had previously found that the thickening process is delayed in children diagnosed with ADHD. So in this study, they set out to measure whether surface area development is similarly delayed.
They recruited 234 children with ADHD and 231 typically developing children and scanned each up to 4 times. The first scan was taken at about age 10, and the final scan was around age 17. Using advanced neuroimaging technology, they were able to map the trajectories of surface area development at over 80,000 points across the brain.
They found that the development of the cortical surface is delayed in frontal brain regions in children with ADHD. For example, the typically developing children attained 50% peak area in the right prefrontal cortex at a mean age of 12.7 years, whereas the ADHD children didn’t reach this peak until 14.6 years of age.
"As other components of cortical development are also delayed, this suggests there is a global delay in ADHD in brain regions important for the control of action and attention," said Dr. Shaw, a clinician studying ADHD at the National Institute of Mental Health and first author of this study.
"These data highlight the importance of longitudinal approaches to brain structure," commented Dr. John Krystal, Editor of Biological Psychiatry. "Seeing a lag in brain development, we now need to try to understand the causes of this developmental delay in ADHD."
Dr Shaw agrees, adding that this finding “guides us to search for genes that control the timing of brain development in the disorder, opening up new targets for treatment.”
Additional work expanding these measures into adulthood will also be important. Such data would help determine whether or when a degree of normalization occurs, or if these delays translate into long-lasting cortical deficits.
Provided by Elsevier
Source: medicalxpress.com
By Matthew Hutson | July 30, 2012
Why we are biased toward things on our dominant side
Image: GETTY IMAGES
If you are right-handed, chances are you will make different choices than your left-handed friends. A series of recent studies shows that we associate our dominant side with good and our nondominant side with bad, preferring products and people that happen to be on our “good” side over those closer to the other half of our body.
The theory of embodied cognition, widely embraced by cognitive scientists in recent years, holds that our abstract ideas are grounded in our physical experiences in the world. (See above: “embraced,” “holds,” “grounded.”) Daniel Casasanto, a psychologist at the New School for Social Research, began to wonder: If our bodies shape our thinking, do people with different bodies think differently? He has been using handedness as a test bed for this body-specific hypothesis.
In a set of studies published in 2009 Casasanto found that right-handers associate right with good and left with bad and that left-handers make the reverse associations. People prefer objects, job candidates and images of alien creatures on their dominant side to those on their nondominant side. In 2010 he reported that presidential candidates (Kerry, Bush, Obama and McCain) gesture with their dominant hands when making positive points and their weak hands to emphasize darker matters. And he has collected data to suggest that lefties hold higher opinions of their flight attendants when seated on the right side of a plane.
To rule out the possibility that this bias is purely genetic, like handedness is, Casasanto handicapped people’s preferred hands. In a 2011 study he had subjects manipulate dominoes while wearing a bulky ski glove on their good hand. Afterward, they showed a bias against things on that side. The results suggest that we look kindly on half the world because we can interact with that side fluently. Make it a hassle, and opinions flip.
Most recently, Casasanto reported in January in Cognitive Science that children as young as six display a handedness bias. Kids were asked which animal in a series of cartoon pairs looked nicer or smarter. The right-handers more often chose the drawing on the right side, and the left-handers more often chose the animal on the left. They also elected to put away their preferred toys in boxes on their dominant side.
“We all walk around with these lopsided bodies and have to interact with our environment in systematically different ways,” Casasanto notes. Given how broadly those interactions can influence our thinking, he says, “body specificity may be shaping our judgments in the real world in ways that we never suspected.”
Source: Scientific American
July 30, 2012
(Medical Xpress) — A new study by researchers at the Menzies Research Institute Tasmania (Menzies) suggests that one of the main treatments for multiple sclerosis (MS) may also increase the amount of vitamin D patients receive from sun exposure.
More people suffer with MS per capita in Tasmania than in any other state in Australia. There is currently no cure, but treatments are available to ease some of the symptoms.
This observational study published in the prestigious journal Neurology found that patients taking one of the most common treatments for MS, interferon-beta, had higher vitamin D levels than those not on this treatment or those using other forms of treatment for MS.
Around 60 per cent of MS patients with the relapsing-remitting form of MS are treated with interferon-beta. It is derived from a naturally-occurring component of the human immune system and has been found to reduce the frequency of relapse and other specific symptoms of MS.
Despite being a front-line treatment in MS, how interferon-beta actually works in MS is unclear, though it is thought to act by affecting the immune system.
The study used data from the MS Longitudinal Study, from 2002-2005, and this analysis used data from 178 persons with MS living in southern Tasmania.
Menzies researchers Dr. Niall Stewart and Dr. Steve Simpson, Jr. were co-first authors on the paper. Dr. Simpson says the findings suggest that part of the therapeutic effects of interferon-beta on relapse in MS may be through its effects on vitamin D, since vitamin D has the ability to reduce inflammatory pathways in the immune system.
“Not only did we find that persons taking interferon-beta had higher vitamin D levels than those not taking it, we also found that this increase in vitamin D was due to an enhancement of the association between sun and vitamin D, with persons on interferon-beta having nearly three-times as much vitamin D from similar amounts of sun exposure to those not taking interferon-beta,” Dr. Simpson said.
“We have previously shown persons with MS with higher vitamin D levels had lower numbers of relapses. In this analysis, however, we found that vitamin D was only associated with reduced risk of relapse among those using interferon-beta.
“Interestingly, the reciprocal was also true, with interferon-beta only associated with reduced risk of relapse among those with higher levels of vitamin D,” Dr. Simpson said.
Senior author, Professor Bruce Taylor, says the new findings have the potential to markedly affect clinical practice in the treatment of MS, but cautions that more research is required.
“This study adds to the growing body of research into MS, but before we can apply these findings to MS treatment practice, clinical trials must be done to prove these associations. Menzies is planning to undertake such a trial in the future,” Professor Taylor said.
“This study does provide further support for persons with MS to periodically have their vitamin D measured, particularly in winter, and if they are deficient, to seek the advice of their physician as to whether supplementation is appropriate for them.”
Provided by University of Tasmania
Source: medicalxpress.com
26 July 2012
Emotional problems in childhood are common. Approximately 8 to 22 percent of children suffer from anxiety, often combined with other conditions such as depression. However, most existing therapies are not designed to treat coexisting psychological problems and are therefore not very successful in helping children with complex emotional issues.
To develop a more effective treatment for co-occurring youth anxiety and depression, University of Miami psychologist Jill Ehrenreich-May and her collaborator Emily L. Bilek analyzed the efficacy and feasibility of a novel intervention created by the researchers, called Emotion Detectives Treatment Protocol (EDTP). Preliminary findings show a significant reduction in the severity of anxiety and depression after treatment, as reported by the children and their parents.
“We are very excited about the potential of EDTP,” says Ehrenreich-May, associate professor of psychology in the College of Arts and Sciences at UM and principal investigator of the study. “Not only could the protocol better address the needs of youth with commonly co-occurring disorders and symptoms, it may also provide additional benefits to mental health professionals,” she says. “EDTP offers a more unified approach to treatment that, we hope, will allow for an efficient and cost-effective treatment option for clinicians and clients alike.”
Emotion Detectives Treatment Program is an adaptation of two treatment protocols developed for adults and adolescents, the Unified Protocols. The program implements age-appropriate techniques that deliver education about emotions and how to manage them, strategies for evaluating situations, problem-solving skills, behavior activation (a technique to reduce depression), and parent training.
In the study, 22 children ages 7 to 12 with a principal diagnosis of an anxiety disorder and secondary issues of depression participated in a 15-session weekly group therapy of EDTP. Among participants who completed the protocol (18 out of 22), 14 no longer met criteria for an anxiety disorder at post-treatment. Additionally, among participants who were assigned a depressive disorder before treatment (5 out of 22), only one participant continued to meet such criteria at post-treatment.
Unlike results from previous studies, the presence of depressive symptoms did not predict poorer treatment response. The results also show a high percentage of attendance. The findings imply that EDTP may offer a better treatment option for children experiencing anxiety and depression.
“Previous research has shown that depressive symptoms tend to weaken treatment response for anxiety disorders. We were hopeful that a broader, more generalized approach would better address this common co-occurrence,” says Bilek, doctoral candidate in clinical psychology at UM and co-author of the study. “We were not surprised to find that the EDTP had equivalent outcomes for individuals with and without elevated depressive symptoms, but we were certainly pleased to find that this protocol may address this important issue.”
The study, titled “An Open Trial Investigation of a Transdiagnostic Group Treatment for Children with Anxiety and Depressive Symptoms,” is published online ahead of print in the journal Behavior Therapy.
The team is currently recruiting participants for a randomized controlled trial comparing the EDTP to another group treatment protocol for anxiety disorders. For more information, please contact the study coordinators at www.miami.edu/childanxiety.
Source: ScienceBlog
July 25, 2012
A University study has shown how our minds unconsciously respond to threats.
Researchers studying how our minds develop fears in response to danger found that people can quickly learn to recognise a threat even when they are unaware of it.
However, they also found that this learning is swiftly forgotten. In contrast, when people are aware of the threat, they take longer to learn to be afraid of it, but retain the fear in the long term.
Scientists from the University of Edinburgh and New York University, who carried out the study, say the finding may be a key insight into the differences between conscious and nonconscious mental processes.
Researchers measured physiological fear responses - the amount of sweat on the fingertips - in groups of people who looked at pictures and were given mild electric shocks whenever one of these pictures was shown.
All the people who participated in the study saw the pictures with just one eye. But whereas some of them were allowed to see the pictures clearly, the researchers suppressed the pictures from other subjects’ awareness by showing colourful, dynamic images to the other eye.
The study found that subjects who were prevented from consciously seeing the pictures learned to be afraid of the image associated with a shock more quickly than those who were allowed to see them without suppression.
However, these subjects quickly forgot this association between the images and the electric shocks as the experiment continued.
In contrast, those subjects who were allowed to see the image clearly formed a stronger association over time.
How the brain reacts to threats is key to understanding how human beings function. This study shows that we are capable of learning very rapidly that something is a threat even when we don’t perceive it consciously. Such learning, however, is fleeting.
-David Carmel, Researcher, Department of Psychology
Source: The University of Edinburgh
By Makini Brice | July 26, 2012
Scientists were surprised, expecting the areas of the brain to age more slowly, or even delayed, than those of men.
Photo: Microsoft
Even though the gap is closing now in many high-income countries, on average, women tend to live longer lives than men do. Despite – or perhaps because of – women’s physical longevity, women tend to battle cognitive decline in much greater numbers than men do. In fact, women are more likely to suffer from various types of dementia, including the much-maligned Alzheimer’s disease. Now researchers think that they have an answer to the cause of this double-edged sword: stress. Specifically, stress ages women’s brains more quickly than it does men.
Scientists, and every-day observers, have noted that some body parts age at different rates than others do. As people become older, some genes become more active while others become less so. These changes in activity can be monitored through a “transcriptome,” which collects data on all the RNA – the transcripts that carry DNA’s instructions to cells. A multinational team from Australia, China, Germany, and the United States set out to analyze the transcriptomes for 55 different men and women of various ages.
The researchers were fascinated by what they found. According to the abstract of their article published in Aging Cell, “In the superior frontal gyrus (SFG), a part of the prefrontal cortex, we observed manifest differences between the two sexes in the timing of age-related changes, i.e.sexual heterochrony. Intriguingly, age-related expression changes predominantly occurred earlier, or at a faster pace, in females compared to males. These changes included decreased energy production and neural function, and up-regulation of the immune response, all major features of brain aging.”
In other words, researchers found that the brains of women aged more quickly than those of men, especially in the prefrontal cortex. Scientists were surprised, expecting the areas of the brain to age more slowly, or even delayed, than those of men.
In the superior frontal gyrus, researchers found 667 genes that were expressed differently by gender during the aging process. Within that number, 98 percent were associated with faster aging in women.
Scientists were not convinced that the reason lay in biological differences. In fact, since only half of women displayed accelerated aging, they were convinced that the difference was environmental. Researchers theorize that stress is the difference-maker, and that it affects women’s brains more severely than it does men. While a researcher unaffiliated with the study said that the difference could also be caused by inflammation,
Mehmet Somel and his team have conducted similar research on monkeys that confirms their stress theory.
Source: Medical Daily
July 27, 2012
(Medical Xpress) — Johns Hopkins scientists have discovered a “scaffolding” protein that holds together multiple elements in a complex system responsible for regulating pain, mental illnesses and other complex neurological problems.
Preso1 (green) and mGluR5 (red) appear in the same location inside a neuron.
The finding, published in the May 6 issue of Nature Neuroscience, could give researchers a new target for drugs to treat these often-intractable conditions.
The discovery, detailed in a study led by neuroscience professor Paul Worley, M.D., of the Johns Hopkins University School of Medicine, focuses on a family of proteins called group 1 metabotropic glutamate receptors (mGluRs) that lie on the surfaces of nerve cells. When these receptors lock in glutamate, a chemical that neurons use to communicate, it encourages neurons to fire.
Without a way to turn off these receptors, neurons would remain active indefinitely, keeping pain and other responses going long after they’re useful. Previous research suggested that these mGluRs need to bind to another protein called Homer to shut down, and that this binding is stronger after other molecules called protein kinases modify the receptors. However, Worley explains, thus far it’s been unclear exactly how all these different players come together.
Seeking the mechanism behind this phenomenon, Worley and his colleagues started with a series of experiments to see what other proteins the mGluRs and Homer were binding with in rat brains. Their search turned up a third protein called Preso1, which bound to both mGluRs and Homer. A search in genetic databases shows that the gene responsible for making Preso1 is present in animals ranging from fruit flies to people, highlighting its importance in a wide variety of creatures.
To figure out what Preso1 does, the researchers performed another series of experiments to examine behavior of neurons that produced both mGluRs and Homer. They found that when these neurons also expressed Preso1, the mGluRs bound Homer more efficiently, suggesting that Preso1 might somehow increase modification by protein kinases.
Worley’s team received another clue when they found that protein kinases also bind to Preso1.
Genetically modifying mice so that they don’t make any Preso1, the researchers found that binding between mGluRs and Homer in these animals’ neurons was greatly reduced compared to normal mice.
Additionally, when the researchers injected the modified mice with a chemical that causes pain and inflammation, the animals had a significantly greater and longer-lasting response compared to regular mice. A final experiment showed that neurons taken from the modified animals were significantly more responsive to the neurotransmitter glutamate. When the researchers added Preso1 to the cell cultures, this increased activity disappeared, suggesting that Preso1 is pivotal for mGluRs to signal properly.
Taken together, Worley explains, the findings suggest that Preso1 appears to gather all the important elements in this system — Homer, protein kinases and mGluRs — bringing them all together to coordinate the activation and deactivation of the mGluRs.
With Preso1 so pivotal for regulating group 1 mGluR activity, it could prove a useful new target for drugs to treat a variety of health problems in which these receptors are thought to play a role, including chronic pain, schizophrenia, Alzheimer’s disease, and fragile X syndrome, Worley says.
"Because mGluRs play so many important roles in the brain for so many different mental and neurological health conditions, knowledge of their regulatory mechanisms is extremely important. But we really don’t know how they work in great detail," he says. "You need to know all the players before you can understand the system. Here, we’ve identified an important player that no one had previously known had existed. Preso1 and Homer appear essential for desensitization of mGluR signaling, much like beta-adrenergic receptor kinase and arrestin are important for desensitization of adrenergic and opiate receptors."
Provided by Johns Hopkins University
Source: medicalxpress.com
July 27, 2012
Anyone that has ever had trouble sleeping can attest to the difficulties at work the following day. Experts recommend eight hours of sleep per night for ideal health and productivity, but what if five to six hours of sleep is your norm? Is your work still negatively affected? A team of researchers at Brigham and Women’s Hospital (BWH) have discovered that regardless of how tired you perceive yourself to be, that lack of sleep can influence the way you perform certain tasks.
This finding is published in the July 26, 2012 online edition of The Journal of Vision.
"Our team decided to look at how sleep might affect complex visual search tasks, because they are common in safety-sensitive activities, such as air-traffic control, baggage screening, and monitoring power plant operations," explained Jeanne F. Duffy, PhD, MBA, senior author on this study and associate neuroscientist at BWH. "These types of jobs involve processes that require repeated, quick memory encoding and retrieval of visual information, in combination with decision making about the information."
Researchers collected and analyzed data from visual search tasks from 12 participants over a one month study. In the first week, all participants were scheduled to sleep 10-12 hours per night to make sure they were well-rested. For the following three weeks, the participants were scheduled to sleep the equivalent of 5.6 hours per night, and also had their sleep times scheduled on a 28-hour cycle, mirroring chronic jet lag. The research team gave the participants computer tests that involved visual search tasks and recorded how quickly the participants could find important information, and also how accurate they were in identifying it. The researchers report that the longer the participants were awake, the more slowly they identified the important information in the test. Additionally, during the biological night time, 12 a.m. -6 a.m., participants (who were unaware of the time throughout the study) also performed the tasks more slowly than they did during the daytime.
"This research provides valuable information for workers, and their employers, who perform these types of visual search tasks during the night shift, because they will do it much more slowly than when they are working during the day," said Duffy. "The longer someone is awake, the more the ability to perform a task, in this case a visual search, is hindered, and this impact of being awake is even stronger at night."
While the accuracy of the participants stayed the fairly constant, they were slower to identify the relevant information as the weeks went on. The self-ratings of sleepiness only got slightly worse during the second and third weeks on the study schedule, yet the data show that they were performing the visual search tasks significantly slower than in the first week. This finding suggests that someone’s perceptions of how tired they are do not always match their performance ability, explains Duffy.
Provided by Brigham and Women’s Hospital
Source: medicalxpress.com
July 26, 2012 By Mark Wheeler
UCLA researchers say blocking this molecule may improve and speed recovery
FINDINGS:
Researchers at UCLA have identified a novel molecule in the brain that, after stroke, blocks the formation of new connections between neurons. As a result, it limits the brain’s recovery. In a mouse model, the researchers showed that blocking this molecule—called ephrin-A5—induces axonal sprouting, that is, the growth of new connections between the brain’s neurons, or cells, and as a result promotes functional recovery.
IMPACT:
If duplicated in humans, the identification of this molecule could pave the way for a more rapid recovery from stroke and may allow a synergy with existing treatments, such as physical therapy.
UCLA AUTHOR:
Dr. S. Thomas Carmichael, professor of neurology, and colleagues
JOURNAL:
The research appears online this week in the journal PNAS.
MORE:
Stroke is the leading cause of adult disability because of the brain’s limited capacity for repair. An important process in recovery after stroke may be in the formation of new connections, termed axonal sprouting. The adult brain inhibits axonal sprouting and the formation of these connections. In previous work the researchers found, paradoxically, that the brain sends mixed signals after a stroke—activating molecules that both stimulate and inhibit axonal sprouting. In this present work, the researchers have identified the effect of one molecule that inhibits axonal sprouting and determined the new connections in the brain that are necessary to form for recovery.
The researchers also developed a new tissue bioengineering approach for delivering drugs to the brain after stroke. This approach uses a biopolymer hydrogel, or a gel of naturally occurring brain proteins, to release neural repair molecules directly to the target region for recovery in stroke—the tissue adjacent to the center of the stroke.
Last, the paper also shows that the more behavioral activity after stroke, such as the amount an impaired limb is used, the more new connections are directly stimulated to form in the injured brain. This direct link between movement patterns, like those that occur in neurorehabilitation, and the formation of new brain connections, provides a biological mechanism for the effects of some forms of physical therapy after stroke.
Source: UCLA
July 26, 2012
Excitation of neurons depends on the selected influx of certain ions, namely sodium, calcium and potassium through specific channels. Obviously, these channels were crucial for the evolution of nervous systems in animals. How such channels could have evolved their selectivity has been a puzzle until now. Yehu Moran and Ulrich Technau from the University of Vienna together with Scientists from Tel Aviv University and the Woods Hole Oceanographic Institution (USA) have now revealed that voltage-gated sodium channels, which are responsible for neuronal signaling in the nerves of animals, evolved twice in higher and lower animals. These results were published in Cell Reports.
Close-up of nervous system of a transgenic polyp of the sea anemone Nematostella vectensis, in which a red fluorescent reporter gene (mCherry) is driven by the regulatory sequence of the neuronal ELAV gene. The picture shows the diffuse structure of the nervous system, but also reveals the accumulation of longitudinal axonal tracts along the eight gastric tissue folds (mesenteries). Credit: Copyright: U. Technau
The opening and closing of ion channels enable flow of ions that constitute the electrical signaling in all nervous systems. Every thought we have or every move we make is the result of the highly accurate opening and closing of numerous ion channels. Whereas the channels of most lower animals and their unicellular relatives cannot discern between sodium and calcium ions, those of higher animals are highly specific for sodium, a characteristic that is important for fast and accurate signaling in complex nervous system.
Surprising results in sea anemones and jellyfish
However, the researchers found that a group of basal animals with simple nerve nets including sea anemones and jellyfish also possess voltage-gated sodium channels, which differ from those found in higher animals, yet show the same selectivity for sodium. Since cnidarians separated from the rest of the animals more than 600 million years ago, these findings suggest that the channels of both cnidarians and higher animals originated independently twice, from ancient non-selective channels which also transmit calcium.
Since many other processes of internal cell signaling are highly dependent on calcium ions, the use of non-selective ion channels in neurons would accidently trigger various signaling systems inside the cells and will cause damage. The evolution of selectivity for sodium ions is therefore considered as an important step in the evolution of nervous systems with fast transmission. This study shows that different parts of the channel changed in a convergent manner during the evolution of cnidarians and higher animals in order to perform the same task, namely to select for sodium ions.
This demonstrates that important components for the functional nervous systems evolved twice in basal and higher animals, which suggests that more complex nervous systems that rely on such ion-selective channels could have also evolved twice independently.
Source: PHYS.ORG