Posts tagged neuroscience

ScienceDaily (May 30, 2012) — Changes to just three genetic letters among billions contributed to the evolution and development of the mammalian motor sensory circuits and laid the groundwork for the defining characteristics of the human brain, Yale University researchers report.

Illustration of neurons. Changes to just three genetic letters among billions contributed to the evolution and development of the mammalian motor sensory circuits and laid the groundwork for the defining characteristics of the human brain. (Credit: © nobeastsofierce / Fotolia)

In a study published in the May 31 issue of the journal Nature, Yale researchers found that a small, simple change in the mammalian genome was critical to the evolution of the corticospinal neural circuits. This circuitry directly connects the cerebral cortex, the conscious part of the human brain, with the brainstem and the spinal cord to make possible the fine, skilled movements necessary for functions such as tool use and speech. The evolutionary mechanisms that drive the formation of the corticospinal circuit, which is a mammalian-specific advance, had remained largely mysterious.

"What we found is a small genetic element that is part of the gene regulatory network directing neurons in the cerebral cortex to form the motor sensory circuits," said Nenad Sestan, professor of neurobiology, researcher for the Kavli Institute for Neuroscience, and senior author of the paper.

Most mammalian genomes contain approximately 22,000 protein-encoding genes. The critical drivers of evolution and development, however, are thought to reside in the non-coding portions of the genome that regulate when and where genes are active. These so-called cis-regulatory elements control the activation of genes that carry out the formation of basic body plans in all organisms.

Sungbo Shim, the first author, and other members of Sestan’s lab identified one such regulatory DNA region they named E4, which specifically drives the development of the corticospinal system by controlling the dynamic activity of a gene called Fezf2 — which, in turn, directs the formation of the corticospinal circuits. E4 is conserved in all mammals but divergent in other craniates, suggesting that it is important to both the emergence and survival of mammalian species. The species differences within E4 are tiny, but crucially drive the regulation of E4 activity by a group of regulatory proteins, or transcription factors, that include SOX4, SOX11, and SOX5. In cooperation, they control the dynamic activation and repression of E4 to shape the development of the corticospinal circuits in the developing embryo.

Source: Science Daily

ScienceDaily (May 30, 2012) — A new method for rapidly solving the three-dimensional structures of a special group of proteins, known as integral membrane proteins, may speed drug discovery by providing scientists with precise targets for new therapies, according to a paper published May 20 in Nature Methods.

Using their new rapid technique, Choe’s team generated the structure of a hIMP known as TMEM14A, shown here in multiple three-dimensional conformations. (Credit: Courtesy of the Salk Institute for Biological Studies)

The technique, developed by scientists at the Salk Institute for Biological Studies, provides a shortcut for determining the structure of human integral membrane proteins (hIMPs), molecules found on the surface of cells that serve as the targets for about half of all current drugs.

Knowing the exact three-dimensional shape of hIMPs allows drug developers to understand the precise biochemical mechanisms by which current drugs work and to develop new drugs that target the proteins.

"Our cells contain around 8,000 of these proteins, but structural biologists have known the three-dimensional structure of only 30 hIMPs reported by the entire field over many years," says Senyon Choe, a professor in Salk’s Structural Biology Laboratory and lead author on the paper. "We solved six more in a matter of months using this new technique. The very limited information on the shape of human membrane proteins hampers structure-driven drug design, but our method should help address this by dramatically increasing the library of known hIMP structures."

Integral membrane proteins are attached to the membrane surrounding each cell, serving as gateways for absorbing nutrients, hormones and drugs, removing waste products, and allowing cells to communicate with their environment. Many diseases, including Alzheimer’s, heart disease and cancer have been linked to malfunctioning hIMPs, and many drugs, ranging from aspirin to schizophrenia medications, target these proteins.

Most of the existing drugs were discovered through brute force methods that required screening thousands of potential molecules in laboratory studies to determine if they had a therapeutic effect. Given a blueprint of the 3D structure of a hIMP involved in a specific disease, however, drug developers could focus only on molecules that are most likely to interact with the target hIMP, saving time and expense.

In the past, it was extremely difficult to solve the structure of hIMPs, due to the difficulty of harvesting them from cells and the difficulty of labeling the amino acids that compose the proteins, a key step in determining their three-dimensional configuration.

"One problem was that hIMPs serve many functions in a cell, so if you tried to engineer cells with many copies of the proteins on their membrane, they would die before you could harvest the hIMPs," says Christian Klammt, a postdoctoral researcher in Choe’s lab and a first author on the paper.

To get around this, the scientists created an outside-the-cell environment, called cell-free expression system, to synthesize the proteins. They used a plexiglass chamber that contained all the biochemical elements necessary to manufacture hIMPs as if they were inside the cell. This system provided the researchers with enough of the proteins to conduct structural analysis.

The cell-free method also allowed them to easily add labeled amino acids into the biochemical stew, which were then incorporated into the proteins. These amino acids gave off telltale structural clues when analyzed with nuclear magnetic resonance spectroscopy, a method for using the magnetic properties of atoms to determine a molecule’s physical and chemical properties.

"It was very difficult and inefficient to introduce labeled amino acids selectively into the protein produced in live cells," says Innokentiy Maslennikov, a Salk staff scientist and co-first author on the paper. "With a cell-free system, we can precisely control what amino acids are available for protein production, giving us isotope-labeled hIMPs in large quantities. Using a proprietary labeling strategy we devised a means to minimize the number of samples to prepare."

Prior methods might take up to a year to determine a single protein structure, but using their new method, the Salk scientists determined the structure of six hIMPs within just 18 months. They have already identified 38 more hIMPs that are suitable for analysis with their technique, and expect it will be used to solve the structure for many more.

Source: Science Daily

May 30, 2012

(Medical Xpress) — A protein produced by the central nervous system’s support cells seems to play two opposing roles in protecting nerve cells from damage, an animal study by Johns Hopkins researchers suggests: Decreasing its activity seems to trigger support cells to gear up their protective powers, but increasing its activity appears to be key to actually use those powers to defend cells from harm.

Seth Blackshaw, Ph.D., an associate professor in the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine, explains that researchers have long suspected that central nervous system cells called glia play an important role in saving nerve cells from almost certain death after either an acute injury, such as a blow to the head, or chronic damage, such as that caused by Alzheimer’s or Parkinson’s disease. Glia — named after the Greek word for glue, since decades ago they were thought to play a very passive role in holding the central nervous system together — respond to an assault on nearby neurons in a dramatic way, puffing up to a larger size and turning off several genes involved in routine maintenance functions.

Previous research in cell cultures containing both neurons and glia showed that when the entire group was exposed to an assault, the reaction of the glia seemed to drive a response that protects cells from subsequent damage. However, Blackshaw says, it’s been unclear exactly what glia are doing when they change in size and gene expression. Even whether this response is actually important for protection was uncertain, he adds, since it’s been impossible to study this so-called glial reactivity without treating whole tissues that include neurons and other types of cells that may exert their own protective effects.

Hoping to find a way to trigger glial reactivity without assaulting entire tissues, Blackshaw and his colleagues searched for proteins that could play an important role in this response. The team used Mueller glia as their model system. These glia are the most abundant type in the retina, and are highly likely to behave like other glia throughout the central nervous system, Blackshaw says.

The researchers’ investigation eventually zeroed in on a protein called Lhx2. When they bred mutant mice that selectively lacked Lhx2 in the glia of the eye, these cells displayed the physical and genetic characteristics of being reactive all the time, even without any damaging stimulus. However, to the researchers’ surprise, hitting the mutant animals’ eyes with extraordinarily bright light caused considerably more damage to their retinas compared to the same stimulus in normal mice.

To understand why these reactive glia didn’t produce the expected protective response, the researchers looked for other pro-survival proteins that glia produce under assault. In the mutant animals, these other proteins were conspicuously missing, Blackshaw says, suggesting that Lhx2 is necessary for glia to produce other protective proteins.

“Lhx2 seems to be a master regulator of glial reactivity, and we’ve shown here that it has two faces,” Blackshaw says of these results, reported in the March 20 issue of the Proceedings of the National Academy of Sciences. While the protein’s absence seems to be critical for triggering the physical and genetic changes glia use to bring their protective proteins to bear to help neurons survive, its presence is vital to produce these proteins in the first place. Levels of Lhx2 activity likely dip and then increase in glia exposed to an attack, he says, explaining both the initial glial reactivity researchers see under a microscope as well as the resulting neural protection.

Once researchers understand this mechanism better, Blackshaw adds, they may be able to craft drugs that stimulate glia to pump out more pro-survival proteins, making novel therapies for neurodegenerative diseases.

Provided by Johns Hopkins University

Source: medicalxpress.com

May 30, 2012

Patients who are blind in one side of their visual field benefit from presentation of sounds on the affected side. After passively hearing sounds for an hour, their visual detection of light stimuli in the blind half of their visual field improved significantly. Neural pathways that simultaneously process information from different senses are responsible for this effect.

"We have embarked on a whole new therapy approach" says PD Dr. Jörg Lewald from the RUB’s Cognitive Psychology Unit. Together with colleagues from the Neurological University Clinic at Bergmannsheil (Prof. Dr. Martin Tegenthoff) and Durham University (PD Dr. Markus Hausmann), he describes the results in PLoS ONE.

To investigate the effectiveness of the auditory stimulation, the research team carried out a visual test before and after the acoustic stimulation. Patients were asked to determine the position of light flashes in the healthy and in the blind field of vision. While performance was stable in the intact half of their field of vision, the number of correct answers in the blind half increased after the auditory stimulation. This effect lasted for 1.5 hours. “In other treatments, the patients undergo arduous and time-consuming visual training” explains Lewald. “The therapeutic results are moderate and vary greatly from patient to patient. Our result suggests that passive hearing alone can improve vision temporarily.”

If strokes or injuries cause damage to the area of the brain that processes the information of the visual sense, this results in a visual field defect. The area most commonly affected is the primary visual cortex, the first processing point for visual input to the cerebral cortex. The more neurons die in this brain area, the bigger the visual deficit. Usually the entire half of the visual field is affected, a condition known as hemianopia. “Hemianopia restricts patients immensely in their everyday life” says Lewald. “When objects or people are missed on the blind side, this can quickly lead to accidents.”

"There is increasing evidence that processing of incoming sensory information is not strictly separated in the brain", says Lewald. "At various stages there are connections between the sensory systems." In particular the nerve cells in the so-termed superior colliculus, part of the midbrain, process auditory and visual information simultaneously. This area is not usually affected by visual field defects, and thus continues to analyse visual stimuli. Therefore, remaining visual functions are retained in the blind half, which the patients, however, are not aware of. “Since the same nerve cells also receive auditory information, we had the idea to use acoustic stimuli to increase their sensitivity to light stimuli” says Lewald.

The team of researchers now aims to further refine their therapy approach in order to reveal sustained improvement in visual functioning. They will also investigate whether the stimulation of the sense of hearing also has an effect on more complex visual functions. Finally, they aim to explore the mechanisms that underlie the effect observed.

Provided by Ruhr-Universitaet-Bochum

Source: medicalxpress.com

May 30, 2012

(Medical Xpress) — Scientists have unlocked the secrets of the zebra fish’s ability to heal its spinal cord after injury, in research that could deliver therapy for paraplegics and quadriplegics in the future.

Scientists discovered the role of a protein in the remarkable self-healing ability of the fish

A team from Monash University’s Australian Regenerative Medicine Institute (ARMI), led by Dr Yona Goldshmit and Professor Peter Currie, discovered the role of a protein in the remarkable self-healing ability of the fish.

The findings, detailed in The Journal of Neuroscience, could eventually lead to ways to stimulate spinal cord regeneration in humans.

When the spinal cord is severed in humans and other mammals, the immune system kicks in, activating specialised cells called glia to prevent bleeding into it, Professor Currie said.

“Glia are the workmen of nervous system. The glia proliferate, forming bigger cells that span the wound site in order to prevent bleeding into it. They come in and try to sort out problems. A glial scar forms,” Professor Currie said.

However, the scar prevents axons, threadlike structures of nerve cells that carry impulses to the brain, of neighbouring nerve cells from penetrating the wound. The result is paralysis.

“The axons upstream and downstream of the lesion sites are never able to penetrate the glial scar to reform. This is a major barrier in mammalian spinal cord regeneration,” Professor Currie said.

In contrast, the zebra fish glia form a bridge that spans the injury site but allow the penetration of axons into it.

The fish can fully regenerate its spinal cord within two months of injury. “You can’t tell there’s been any wound at all,” Professor Currie said.

Scientists discovered the protein, called fibroblast growth factor (fgf), controlled the shape of the glia, and accounted for the difference in the response to spinal cord injury between humans and zebra fish.

The scientists showed the protein could be manipulated in the zebra fish to speed up tissue repair even more.

“The hope is that fgf could eventually be used to promote better results in spinal cord repair in people,” Professor Currie said.

Provided by Monash University

Source: medicalxpress.com

ScienceDaily (May 30, 2012) — Bipolar disorder is a serious and debilitating condition where individuals experience severe swings in mood between mania and depression. The episodes of low or elevated mood can last days or months, and the risk of suicide is high.

Antidepressants are commonly prescribed to treat or prevent the depressive episodes, but they are not universally effective. Many patients still continue to experience periods of depression even while being treated, and many patients must try several different types of antidepressants before finding one that works for them. In addition, it may take several weeks of treatment before a patient begins to feel relief from the drug’s effects.

For these reasons, better treatments for depression are desperately needed. A new study in Biological Psychiatry this week confirms that scientists may have found one in a drug called ketamine.

A group of researchers at the National Institute of Mental Health, led by Dr. Carlos Zarate, previously found that a single dose of ketamine produced rapid antidepressant effects in depressed patients with bipolar disorder. They have now replicated that finding in an independent group of depressed patients, also with bipolar disorder. Replication is an important component of the scientific method, as it helps ensure that the initial finding wasn’t accidental and can be repeated.

In this new study, they administered a single dose of ketamine and a single dose of placebo to a group of patients on two different days, two weeks apart. The patients were then carefully monitored and repeatedly completed ratings to ‘score’ their depressive symptoms and suicidal thoughts.

When the patients received ketamine, their depression symptoms significantly improved within 40 minutes, and remained improved over 3 days. Overall, 79% of the patients improved with ketamine, but 0% reported improvement when they received placebo.

Importantly, and for the first time in a group of patients with bipolar depression, they also found that ketamine significantly reduced suicidal thoughts. These antisuicidal effects also occurred within one hour. Considering that bipolar disorder is one of the most lethal of all psychiatric disorders, these study findings could have a major impact on public health.

"Our finding that a single infusion of ketamine produces rapid antidepressant and antisuicidal effects within one hour and that is fairly sustained is truly exciting," Dr. Zarate commented. "We think that these findings are of true importance given that we only have a few treatments approved for acute bipolar depression, and none of them have this rapid onset of action; they usually take weeks or longer to have comparable antidepressant effects as ketamine does."

Ketamine is an N-methyl-D-aspartate (NMDA) receptor antagonist, which means that it works by blocking the actions of NMDA. Dr. Zarate added, “Importantly, confirmation that blocking the NMDA receptor complex is involved in generating rapid antidepressant and antisuicidal effects offers an avenue for developing the next generation of treatments for depression that are radically different than existing ones.”

Source: Science Daily

May 30, 2012

(Medical Xpress) — The first large non-commercial study to investigate whether the main active constituent of cannabis (tetrahydrocannabinol or THC) is effective in slowing the course of progressive multiple sclerosis (MS) shows that there is no evidence to suggest this; although benefits were noted for those at the lower end of the disability scale.

The CUPID (Cannabinoid Use in Progressive Inflammatory brain Disease) study was carried out by researchers from the Peninsula College of Medicine and Dentistry (PCMD), Plymouth University. The study was funded by the Medical Research Council (MRC) and managed by the National Institute for Health Research (NIHR) on behalf of the MRC-NIHR partnership, the Multiple Sclerosis Society and the Multiple Sclerosis Trust.

The preliminary results of CUPID were presented by lead researcher Professor John Zajicek at the Association of British Neurologists’ Annual Meeting in Brighton on Tuesday 29th May.

CUPID enrolled nearly 500 people with MS from 27 centres around the UK, and has taken eight years to complete. People with progressive MS were randomised to receive either THC capsules or identical placebo capsules for three years, and were carefully followed to see how their MS changed over this period. The two main outcomes of the trial were a disability scale administered by neurologists (the Expanded Disability Status Scale), and a patient report scale of the impact of MS on people with the condition (the Multiple Sclerosis Impact Scale 29).

Overall the study found no evidence to support an effect of THC on MS progression in either of the main outcomes. However, there was some evidence to suggest a beneficial effect in participants who were at the lower end of the disability scale at the time of enrolment but, as the benefit was only found in a small group of people rather than the whole population, further studies will be needed to assess the robustness of this finding. One of the other findings of the trial was that MS in the study population as a whole progressed slowly, more slowly than expected. This makes it more challenging to find a treatment effect when the aim of the treatment is that of slow progression.

As well as evaluating the potential neuroprotective effects and safety of THC over the long-term, one of the aims of the CUPID study was to improve the way that clinical trial research is done by exploring newer methods of measuring MS and using the latest statistical methods to make the most of every piece of information collected. This analysis will continue for several months. The CUPID study will therefore provide important information about conducting further large scale clinical trials in MS.

Professor John Zajicek, Professor of Clinical Neuroscience at PCMD, Plymouth University, said: “To put this study into context: current treatments for MS are limited, either being targeted at the immune system in the early stages of the disease or aimed at easing specific symptoms such as muscle spasms, fatigue or bladder problems. At present there is no treatment available to slow MS when it becomes progressive. Progression of MS is thought to be due to death of nerve cells, and researchers around the world are desperately searching for treatments that may be ‘neuroprotective’. Laboratory experiments have suggested that certain cannabis derivatives may be neuroprotective.”

He added: “Overall our research has not supported laboratory based findings and shown that, although there is a suggestion of benefit to those at the lower end of the disability scale when they joined CUPID, there is little evidence to suggest that THC has a long term impact on the slowing of progressive MS.”

Dr. Doug Brown, Head of Biomedical Research at the MS Society, said: “There are currently no treatments for people with progressive MS to slow or stop the worsening of disability. The MS Society is committed to supporting research in this area and this was an important study for us to fund. While this study sadly suggests THC is ineffective at slowing the course of progressive MS, we will not stop our search for effective treatments. We are encouraged by the possibility shown by this study that THC may have potential benefits for some people with MS and we welcome further investigation in this area.”

Provided by University of Plymouth

Source: medicalxpress.com

ScienceDaily (May 29, 2012) — A specific antioxidant supplement may be an effective therapy for some features of autism, according to a pilot trial from the Stanford University School of Medicine and Lucile Packard Children’s Hospital that involved 31 children with the disorder.

The antioxidant, called N-Acetylcysteine, or NAC, lowered irritability in children with autism as well as reducing the children’s repetitive behaviors. The researchers emphasized that the findings must be confirmed in a larger trial before NAC can be recommended for children with autism.

Irritability affects 60 to 70 percent of children with autism. “We’re not talking about mild things: This is throwing, kicking, hitting, the child needing to be restrained,” said Antonio Hardan, MD, the primary author of the new study. “It can affect learning, vocational activities and the child’s ability to participate in autism therapies.”

The study appears in the June 1 issue of Biological Psychiatry. Hardan is an associate professor of psychiatry and behavioral sciences at Stanford and director of the Autism and Developmental Disabilities Clinic at Packard Children’s. Stanfordis filing a patent for the use of NAC in autism, and one of the study authors has a financial stake in a company that makes and sells the NAC used in the trial.

Finding new medications to treat autism and its symptoms is a high priority for researchers. Currently, irritability, mood swings and aggression, all of which are considered associated features of autism, are treated with second-generation antipsychotics. But these drugs cause significant side effects, including weight gain, involuntary motor movements and metabolic syndrome, which increases diabetes risk. By contrast, side effects of NAC are generally mild, with gastrointestinal problems such as constipation, nausea, diarrhea and decreased appetite being the most common.

The state of drug treatments for autism’s core features, such as social deficits, language impairment and repetitive behaviors, is also a major problem. “Today, in 2012, we have no effective medication to treat repetitive behavior such as hand flapping or any other core features of autism,” Hardan said. NAC could be the first medication available to treat repetitive behavior in autism — if the findings hold up when scrutinized further.

The study tested children with autism ages 3 to 12. They were physically healthy and were not planning any changes in their established autism treatments during the trial. In a double-blind study design, children received NAC or a placebo for 12 weeks. The NAC used was a pharmaceutical-grade preparation donated by the drug manufacturer Bioadvantex Inc. Subjects were evaluated before the trial began and every four weeks during the study using several standardized surveys that measure problem behaviors, social behaviors, autistic preoccupations and drug side effects.

During the 12-week trial, NAC treatment decreased irritability scores from 13.1 to 7.2 on the Aberrant Behavior Checklist, a widely used clinical scale for assessing irritability. The change is not as large as that seen in children taking antipsychotics. “But this is still a potentially valuable tool to have before jumping on these big guns,” Hardan said.

In addition, according to two standardized measures of autism mannerisms and stereotypic behavior, children taking NAC showed a decrease in repetitive and stereotyped behaviors.

"One of the reasons I wanted to do this trial was that NAC is being used by community practitioners who focus on alternative, non-traditional therapies," Hardan said. "But there is no strong scientific evidence to support these interventions. Somebody needs to look at them."

Hardan cautioned that the NAC for sale as a dietary supplement at drugstores and grocery stores differs in some important respects from the individually packaged doses of pharmaceutical-grade NAC used in the study, and that the over-the-counter version may not produce the same results. “When you open the bottle from the drugstore and expose the pills to air and sunlight, it gets oxidized and becomes less effective,” he said.

Although the study did not test how NAC works, the researchers speculated on two possible mechanisms of action. NAC increases the capacity of the body’s main antioxidant network, which some previous studies have suggested is deficient in autism. In addition, other research has suggested that autism is related to an imbalance in excitatory and inhibitory neurotransmitters in the brain. NAC can modulate the glutamatergic family of excitatory neurotransmitters, which might be useful in autism.

The scientists are now applying for funding to conduct a large, multicenter trial in which they hope to replicate their findings.

"This was a pilot study," Hardan said. "Final conclusions cannot be made before we do a larger trial."

Source: Science Daily

ScienceDaily (May 29, 2012) — TAU research finds that existing diabetes medication may ease damage caused by brain-addling explosions.

Although the death toll is relatively low for people who suffer from traumatic brain injury (TBI), it can have severe, life-long consequences for brain function. TBI can impair a patient’s mental abilities, impact memory and behavior, and lead to dramatic personality changes. And long-term medical treatment carries a high economic cost.

Now, in research commissioned by the United States Air Force, Prof. Chaim Pick of Tel Aviv University’s Sackler Faculty of Medicine and Dr. Nigel Greig of the National Institute of Aging in the US have discovered that Exendin-4, an FDA-approved diabetes drug, significantly minimizes damage in TBI animal models when administered shortly after the initial incident. Originally designed to control sugar levels in the body, the drug has recently been found effective in protecting neurons in disorders such as Alzheimer’s disease.

Prof. Pick’s collaborators include his TAU colleagues Dr. Vardit Rubovitch, Lital Rachmany-Raber, and Prof. Shaul Schreiber, and Dr. David Tweedie of the National Institute of Aging in the US. Detailed in the journal Experimental Neurology, this breakthrough is the first step towards developing a cocktail of medications to prevent as much brain damage as possible following injury.

Diabetes medication to halt trauma

Prof. Pick has been researching TBI for many years, beginning with the effects of everyday injuries such as hitting the windshield in a car accident. As a result of his work for the Air Force, he has expanded his research to include trauma sustained when a person is exposed to an explosion, such as during a terrorist attack.

TBI causes long-term damage by changing the chemistry of the brain. During an explosion, increased pressure followed by an intense vacuum shakes the fluid inside the brain and damages the brain’s structure. This damage cannot be reversed, but mapping the injury through behavioral and physical tests is crucial to understanding and quantifying the damage and forming a treatment plan through therapy or medication.

Prof. Pick and his colleagues designed a pre-clinical experiment that exposed mice to controlled explosions from 23 and 33 feet away, and then analyzed the resulting injuries. They also studied the effect of Exendin-4 as an additional parameter in minimizing brain damage.

The researchers divided their mice into four groups: a control group; a second group that was exposed to the blast without medication; a third group that received the medication but was not exposed to the blast; and a fourth group, exposed to the explosion but given the medication within an hour after the blast and continuing for seven days afterwards. The mice were placed under anesthesia before the explosion.

Behavioral and physical tests showed that the mice that had been exposed to the blast had severely impaired brain function compared to the control group. However, the mice that had also received the Exendin-4 treatment were almost on a par with the control group in terms of brain function, proving that Exendin-4 significantly reduced the long-term damage done by an explosion. In separate experiments, the drug was also associated with an improved outcome in mice who sustained TBI by blunt force.

Finding the ideal drug cocktail

Prof. Pick says this promising discovery can help researchers find the ideal combination of medications to minimize the lasting impact of TBI. “We are moving in the right direction. Now we need to find the right dosage and delivery system, then build a cocktail of drugs that will increase the therapeutic value of this concept,” he explains. He adds that in treating such traumatic injuries, one drug is unlikely to be sufficient.

Source: Science Daily

ScienceDaily (May 29, 2012) — New research from the University of Warwick could explain why the evil eyebrows and pointy chin of a cartoon villain make our ‘threat’ instinct kick in.

Triangular-shaped face. Psychologists have found that a downward pointing triangle can be perceived to carry a threat. (Credit: © Viktor Kuryan / Fotolia)

Psychologists have found that a downward pointing triangle can be perceived to carry threat just like a negative face in a crowd.

In a paper published in Emotion, a journal of the American Psychological Association, Dr Derrick Watson and Dr Elisabeth Blagrove have carried out a series of experiments with volunteers to find out if simple geometric shapes can convey positive or negative emotions.

Previous research by these scientists showed that people could pick out a negative face in a crowd more quickly than a positive or neutral face and also that it was difficult to ignore faces in general. The researchers carried out a series of experiments asking volunteers to respond to computer-generated images. They were shown positive, negative and neutral faces, and triangles facing upwards, downwards, inward and outward. This latest study shows that downward triangles are detected just as quickly as a negative face.

Dr Watson said: “We know from previous studies that simple geometric shapes are effective at capturing or guiding attention, particularly if these shapes carry the features present within negative or positive faces.”

"Our study shows that downward pointing triangles in particular convey negative emotions and we can pick up on them quickly and perceive them as a threat."

Dr Blagrove added: “If we look at cartoon characters, the classic baddie will often be drawn with the evil eyebrows that come to a downward point in the middle. This could go some way to explain why we associate the downward pointing triangle with negative faces. These shapes correspond with our own facial features and we are unconsciously making that link.”

Source: Science Daily