Posts tagged neuroscience
Articles and news from the latest research reports.
Scientists identify new gene linked to PTSD
August 7, 2012
Investigators at Boston University School of Medicine (BUSM) and Veterans Affairs (VA) Boston Healthcare System have identified a new gene linked to post-traumatic stress disorder (PTSD). The findings, published online in Molecular Psychiatry, indicate that a gene known to play a role in protecting brain cells from the damaging effects of stress may also be involved in the development of PTSD.
The article reports the first positive results of a genome-wide association study (GWAS) of PTSD and suggests that variations in the retinoid-related orphan receptor alpha (RORA) gene are linked to the development of PTSD.
Mark W. Miller, PhD, associate professor at BUSM and a clinical research psychologist in the National Center for PTSD at VA Boston Healthcare System was the study’s principal investigator. Mark Logue, PhD, research assistant professor at BUSM and Boston University School of Public Health and Clinton Baldwin, PhD, professor at BUSM, were co-first authors of the paper.
PTSD is a psychiatric disorder defined by serious changes in cognitive, emotional, behavioral and psychological functioning that can occur in response to a psychologically traumatic event. Previous studies have estimated that approximately eight percent of the U.S. population will develop PTSD in their lifetime. That number is significantly greater among combat veterans where as many as one out of five suffer symptoms of the disorder.
Previous GWAS studies have linked the RORA gene to other psychiatric conditions, including attention-deficit hyperactivity disorder, bipolar disorder, autism and depression.
"Like PTSD, all of these conditions have been linked to alterations in brain functioning, so it is particularly interesting that one of the primary functions of RORA is to protect brain cells from the damaging effects of oxidative stress, hypoxia and inflammation," said Miller.
Participants in the study were approximately 500 male and female veterans and their intimate partners, all of whom had experienced trauma and approximately half of whom had PTSD. The majority of the veterans had been exposed to trauma related to their military experience whereas their intimate partners had experienced trauma related to other experiences, such as sexual or physical assault, serious accidents, or the sudden death of a loved one. Each participant was interviewed by a trained clinician, and DNA was extracted from samples of their blood.
The DNA analysis examined approximately 1.5 million genetic markers for signs of association with PTSD and revealed a highly significant association with a variant (rs8042149) in the RORA gene. The researchers then looked for evidence of replication using data from the Detroit Neighborhood Health Study where they also found a significant, though weaker, association between RORA and PTSD.
"These results suggest that individuals with the RORA risk variant are more likely to develop PTSD following trauma exposure and point to a new avenue for research on how the brain responds to trauma," said Miller.
Provided by Boston University Medical Center
Source: medicalxpress.com
More Kids Taking Antipsychotics for ADHD: Study
Use of powerful antipsychotic medications such as Abilify and Risperdal to control youngsters with attention-deficit/hyperactivity disorder (ADHD) and other behavior problems has skyrocketed in recent years, a new study finds.
Antipsychotics are approved to treat bipolar disorder, schizophrenia, other serious mental problems and irritability related to autism. But they don’t have U.S. Food and Drug Administration approval for ADHD or other childhood behavior problems, and their use for this purpose is considered “off label.”
"Only a small proportion of antipsychotic treatment of children (6 percent) and adolescents (13 percent) is for FDA-approved clinical indications," said lead researcher Dr. Mark Olfson, a professor of clinical psychiatry at Columbia University Medical Center in New York City.
Making it easier to learn to read: Dyslexia caused by signal processing in the brain
August 06, 2012
To participate successfully in life, it is important to be able to read and write. Nevertheless, many children and adults have difficulties in acquiring these skills and the reason is not always obvious. They suffer from dyslexia which can have a variety of symptoms. Thanks to research carried out by Begoña Díaz and her colleagues at the Max Planck Institute for Human Cognitive and Brain Sciences in Leipzig, a major step forward has been made in understanding the cause of dyslexia. The scientists have discovered an important neural mechanism underlying dyslexia and shown that many difficulties associated with dyslexia can potentially be traced back to a malfunction of the medial geniculate body in the thalamus. The results provide an important basis for developing potential treatments.
This figure compares the situation in the brain of dyslexics and the control group. The blue area depicts the auditory cortices and the green area represents the medial geniculate bodies. © MPI for Human Cognitive and Brain Sciences
People who suffer from dyslexia have difficulties with identifying speech sounds in spoken language. For example, while most children are able to recognise whether two words rhyme even before they go to school, dyslexic children often cannot do this until late primary school age. Those affected suffer from dyslexia their whole lives. However, there are also always cases where people can compensate for their dyslexia. “This suggests that dyslexia can be treated. We are therefore trying to find the neural causes of this learning disability in order to create a basis for improved treatment options,” says Díaz.
Between five and ten percent of the world’s children suffer from dyslexia, yet very little is know about its causes. Even though those affected do not lack intelligence or schooling, they have difficulties in reading, understanding and explaining individual words or entire texts. The researchers showed that dyslexic adults have a malfunction in a structure that transfers auditory information from the ear to the cortex is a major cause of the impairment: the medial geniculate body in the auditory thalamus does not process speech sounds correctly. “This malfunction at a low level of language processing could percolate through the entire system. This explains why the symptoms of dyslexia are so varied,” says Díaz.
Under the direction of Katharina von Kriegstein, the researchers conducted two experiments in which several volunteers had to perform various speech comprehension tasks. When affected individuals performed tasks that required the recognition of speech sounds, as compared to recognize the voices that pronounced the same speech, magnetic resonance tomography (MRT) recordings showed abnormal responses in the area around the medial geniculate body. In contrast, no differences were apparent between controls and dyslexic participants if the tasks involved only listening to the speech sounds without having to perform a specific task. “The problem, therefore, has nothing to do with sensory processing itself, but with the processing involved in speech recognition,” says Díaz. No differences could be ascertained between the two test groups in other areas of the auditory signalling path.
The findings of the Leipzig scientists combine various theoretical approaches, which deal with the cause of dyslexia and, for the first time, bring together several of these theories to form an overall picture. “Recognising the cause of a problem is always the first step on the way to a successful treatment,” says Díaz. The researchers’ next project is now to study whether current treatment programmes can influence the medial geniculate body in order to make learning to read easier for everyone in the long term.
Source: Max Planck Institute
Inside a Hoarder’s Brain: Why They Can’t Ditch Their Stuff
Hoarders, or people who can’t bear to throw away even the most useless of junk, often can’t see that they have a problem. But now new research pinpoints that problem in the brains of these individuals.
A new study finds abnormal activity in brain regions of people with hoarding disorder who were asked to make decisions about keeping something versus tossing it. The brain regions involved are known to be involved with decision-making under uncertain conditions as well as risk assessment and emotional choices.
"Hoarding seems to be characterized by problems in the decision-making process that can be seen in patterns of brain activity," said David Tolin, the director of the anxiety disorders center at the Connecticut-based mental health center The Institute of Living.
Brain might not stand in the way of free will
Advocates of free will can rest easy, for now. A 30-year-old classic experiment that is often used to argue against free will might have been misinterpreted.
Our decision-making process remains hazy (Image: Jannes Glas/Getty)
In the early 1980s, Benjamin Libet, a neuroscientist at the University of California in San Francisco, used electroencephalography (EEG) to record the brain activity of volunteers who had been told to make a spontaneous movement. With the help of a precise timer that the volunteers were asked to read at the moment they became aware of the urge to act, Libet found there was a 200 millisecond delay, on average, between this urge and the movement itself.
But the EEG recordings also revealed a signal that appeared in the brain even earlier, 550 milliseconds, on average, before the action. Called the readiness potential, this has been interpreted as a blow to free will, as it suggests that the brain prepares to act well before we are conscious of the urge to move.
This conclusion assumes that the readiness potential is the signature of the brain planning and preparing to move. “Even people who have been critical of Libet’s work, by and large, haven’t challenged that assumption,” says Aaron Schurger of the National Institute of Health and Medical Research in Saclay, France.
One attempt to do so came in 2009. Judy Trevena and Jeff Miller of the University of Otago in Dunedin, New Zealand, asked volunteers to decide, after hearing a tone, whether or not to tap on a keyboard. The readiness potential was present regardless of their decision, suggesting that it did not represent the brain preparing to move. Exactly what it did mean, though, still wasn’t clear.
Crossing a threshold
Now, Schurger and colleagues have an explanation. They began by posing a question: how does the brain decide to make a spontaneous movement? They looked to other decision-making scenarios for clues. Previous studies have shown that when we have to make a decision based on visual input, for example, assemblies of neurons start accumulating visual evidence in favour of the various possible outcomes. A decision is triggered when the evidence favouring one particular outcome becomes strong enough to tip its associated assembly of neurons across a threshold.
Schurger’s team hypothesised that something similar happens in the brain during the Libet experiment. Volunteers, however, are specifically asked to ignore any external signals before they make a spontaneous movement, so the signal must be internal.
There are random fluctuations of neural activity in the brain. Schurger’s team reasoned that movement is triggered when this neural noise accumulates and crosses a threshold.
To probe the idea, the team first built a computer model of such a neural accumulator. In the model, each time the neural noise crossed a threshold it signified a decision to move. They found that when they ran the model numerous times and looked at the pattern of the neural noise that led up to the decision it looked like a readiness potential.
Next, the team repeated Libet’s experiment, but this time if, while waiting to act spontaneously, the volunteers heard a click they had to act immediately. The researchers predicted that the fastest response to the click would be seen in those in whom the accumulation of neural noise had neared the threshold – something that would show up in their EEG as a readiness potential.
This is exactly what the team found. In those with slower responses to the click, the readiness potential was absent in the EEG recordings.
Spontaneous brain activity
"Libet argued that our brain has already decided to move well before we have a conscious intention to move," says Schurger. "We argue that what looks like a pre-conscious decision process may not in fact reflect a decision at all. It only looks that way because of the nature of spontaneous brain activity."
So what does this say about free will? “If we are correct, then the Libet experiment does not count as evidence against the possibility of conscious will,” says Schurger.
Cognitive neuroscientist Anil Seth of the University of Sussex in Brighton, UK, is impressed by the work, but also circumspect about what it says about free will. “It’s a more satisfying mechanistic explanation of the readiness potential. But it doesn’t bounce conscious free will suddenly back into the picture,” he says. “Showing that one aspect of the Libet experiment can be open to interpretation does not mean that all arguments against conscious free will need to be ejected.”
According to Seth, when the volunteers in Libet’s experiment said they felt an urge to act, that urge is an experience, similar to an experience of smell or taste. The new model is “opening the door towards a richer understanding of the neural basis of the conscious experience of volition”, he says.
Source: NewScientist
Robot Learns to Pick the Sweetest, Ripest Strawberries
Richard Dudley imagines a world where strawberries grow in perfect rows and every day a robot army tastes their colors before harvesting the ripe ones. No, that isn’t LSD talking. The research scientist at the United Kingdom’s National Physical Laboratory is building a bot that uses multiple wavelengths of electromagnetic radiation to identify the sweetest, ripest fruit — then plucks it from the vine.
Brain’s Stem Cells “Eavesdrop” to Find out When to Act
Release Date: 08/06/2012
Working with mice, Johns Hopkins researchers say they have figured out how stem cells found in a part of the brain responsible for learning, memory and mood regulation decide to remain dormant or create new brain cells. Apparently, the stem cells “listen in” on the chemical communication among nearby neurons to get an idea about what is stressing the system and when they need to act.
A single parvalbumin-expressing interneuron (red) surrounded by many adult neural stem cells (green) in the brain’s hippocampus. Credit: Gerry Sun
The researchers say understanding this process of chemical signaling may shed light on how the brain reacts to its environment and how current antidepressants work, because in animals these drugs have been shown to increase the number of brain cells. The findings are reported July 29 in the advance online publication of Nature.
“What we learned is that brain stem cells don’t communicate in the official way that neurons do, through synapses or by directly signaling each other,” says Hongjun Song, Ph.D., professor of neurology and director of Johns Hopkins Medicine’s Institute for Cell Engineering’s Stem Cell Program. “Synapses, like cell phones, allow nerve cells to talk with each other. Stem cells don’t have synapses, but our experiments show they indirectly hear the neurons talking to each other; it’s like listening to someone near you talking on a phone.”
The “indirect talk” that the stem cells detect is comprised of chemical messaging fueled by the output of neurotransmitters that leak from neuronal synapses, the structures at the ends of brain cells that facilitate communication. These neurotransmitters, released from one neuron and detected by a another one, trigger receiving neurons to change their electrical charges, which either causes the neuron to fire off an electrical pulse propagating communication or to settle down, squelching further messages.
To find out which neurotransmitter brain stem cells can detect, the researchers took mouse brain tissue, attached electrodes to the stem cells and measured any change in electrical charge after the addition of certain neurotransmitters. When they treated the stem cells with the neurotransmitter GABA – a known signal-inhibiting product the stem cells’ electrical charges changed, suggesting that the stem cells can detect GABA messages.
To find out what message GABA imparts to brain stem cells, the scientists used a genetic trick to remove the gene for the GABA receptor — the protein on the surface of the cell that detects GABA — only from the brain stem cells. Microscopic observation of brain stem cells lacking the GABA receptor over five days showed these cells replicated themselves, or produced glial cells — support cells for the neurons in the brain. Brain stem cells with their GABA receptors intact appeared to stay the same, not making more cells.
Next, the team treated normal mice with valium, often used as an anti-anxiety drug and known to act like GABA by activating GABA receptors when it comes in contact with them. The scientists checked the mice on the second and seventh day of valium use and counted the number of brain stem cells in untreated mice and mice treated with the GABA activator. They found the treated mice had many more dormant stem cells than the untreated mice.
“Traditionally GABA tells neurons to shut down and not continue to propagate a message to other neurons,” says Song. “In this case the neurotransmitter also shuts off the stem cells and keeps them dormant.”
The brain stem cell population in mice (and other mammals, including humans) is surrounded by as many as 10 different kinds of intermingled neurons, says Song, and any number of these may be keeping stem cells dormant. To find out which neurons control the stem cells, the researchers inserted special light-activating proteins into the neurons that trigger the cells to send an electrical pulse, as well as to release neurotransmitter, when light shines on them. By shining light to activate a specific type of neuron and monitoring the stem cells with an electrode, Song’s team showed that one of the three types of neurons tested transmitted a signal to the stem cells causing a change in electrical charge in the stem cells. The neurons messaging the stem cells are parvalbumin-expressing interneurons.
Finally, to see if this stem cell control mechanism aligns with what an animal may be experiencing, the scientists created stress for normal mice by socially isolating them, and did the same in mice lacking GABA receptors in their brain stem cells. After a week, socially isolated normal mice had an increase in the number of stem cells and glial cells. But the socially isolated mice without GABA receptors did not show increases.
“GABA communication clearly conveys information about what brain cells experience of the outside world, and, in this case, keeps the brain stem cells in reserve, so if we don’t need them, we don’t use them up,” says Song.
Source: Johns Hopkins Medicine
Disney researchers add sense of touch to augmented reality applications
Technology developed by Disney Research, Pittsburgh, makes it possible to change the feel of real-world surfaces and objects, including touch-screens, walls, furniture, wooden or plastic objects, without requiring users to wear special gloves or use force-feedback devices. Surfaces are not altered with actuators and require little if any instrumentation.
Instead, Disney researchers employ a newly discovered physical phenomenon called reverse electrovibration to create the illusion of changing textures as the user’s fingers sweep across a surface. A weak electrical signal, which can be applied imperceptibly anywhere on the user’s body, creates an oscillating electrical field around the user’s fingers that is responsible for the tactile feedback.
The technology, called REVEL, could be used to create “please touch” museum displays, add haptic feedback to games, apply texture to projected images on surfaces of any size and shape, provide customized directions on walls for people with visual disabilities and enhance other applications of augmented reality.
3D-printed sugar network to help grow artificial liver
Researchers have moved a step closer to creating a synthetic liver, after a US team created a template for blood vessels to grow into, using sugar.
Scientists have long been experimenting with the 3D printing of cells and blood vessels, building up tissue structure layer by layer with artificial cells. But the synthetically engineered cells often die before the tissue is formed. The technology, in which a 3D printer uses sugar as its building material, could one day be used for transplants. The study appears in the journal Nature Materials.
Study examines effects of growth hormone-releasing hormone on cognitive function
6-Aug-2012
Treatment with growth hormone-releasing hormone appears to be associated with favorable cognitive effects among both adults with mild cognitive impairment and healthy older adults, according to a randomized clinical trial published Online First by Archives of Neurology, a JAMA Network publication.
"Growth hormone-releasing hormone (GHRH), growth hormone and insulinlike growth factor 1 have potent effects on brain function, their levels decrease with advancing age, and they likely play a role in the pathogenesis of Alzheimer disease," the authors write as background information in the study.
To examine the effects of GHRH on cognitive function in healthy older adults and in adults with mild cognitive impairment (MCI), Laura D. Baker, Ph.D., of the University of Washington School of Medicine and Veterans Affairs Puget Sound Health Care System, Seattle, and colleagues, conducted a randomized, double-blind, placebo-controlled trial in which participants self-administered daily injections of a form of human GHRH (tesamorelin), or placebo.
The authors enrolled 152 adults ranging in age from 55 to 87 years (average age, 68 years) and 137 participants (76 healthy patients and 61 patients with MCI) successfully completed the study. At baseline, at 10 and 20 weeks of treatment, and after a 10-week washout (30 weeks total), the authors collected blood samples and administered parallel versions of cognitive tests.
Among the original 152 patients enrolled in the study, analysis indicated a favorable effect of GHRH on cognition, which was comparable in adults with MCI and healthy older adults. Analysis among the 137 patients who successfully completed the trial also showed that treatment with GHRH had a favorable effect on cognition among both groups of patients. Although the healthy adults outperformed those with MCI overall, the cognitive benefits relative to placebo was comparable among both groups.
Treatment with GHRH also increased insulin like growth factor 1 levels by 117 percent, which remained within the physiological range, and increased fasting insulin levels within the normal range by 35 percent in adults with MCI but not in healthy adults.
"Our results replicate and expand our earlier positive findings, demonstrating that GHRH administration has favorable effects on cognitive function not only in healthy older adults but also in adults at increased risk of cognitive decline and dementia," the authors conclude. "Larger and longer-duration treatment trials are needed to firmly establish the therapeutic potential of GHRH administration to promote brain health in normal aging and ‘pathological aging.’"
Source: EurekAlert!