Posts tagged brain

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

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

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

May 29, 2012

Researchers from South Korea, Sweden, and the United States have collaborated on a project to restore neuron function to parts of the brain damaged by Huntington’s disease (HD) by successfully transplanting HD-induced pluripotent stem cells into animal models.

Induced pluripotent stem cells (iPSCs) can be genetically engineered from human somatic cells such as skin, and can be used to model numerous human diseases. They may also serve as sources of transplantable cells that can be used in novel cell therapies. In the latter case, the patient provides a sample of his or her own skin to the laboratory.

In the current study, experimental animals with damage to a deep brain structure called the striatum (an experimental model of HD) exhibited significant behavioral recovery after receiving transplanted iPS cells. The researchers hope that this approach eventually could be tested in patients for the treatment of HD.

"The unique features of the iPSC approach means that the transplanted cells will be genetically identical to the patient and therefore no medications that dampen the immune system to prevent graft rejection will be needed,” said Jihwan Song, D.Phil. Associate Professor and Director of Laboratory of Developmental & Stem Cell Biology at CHA Stem Cell Institute, CHA University, Seoul, South Korea and co-author of the study.

The study, published online this week in Stem Cells, found that transplanted iPSCs initially formed neurons producing GABA, the chief inhibitory neurotransmitter in the mammalian central nervous system, which plays a critical role in regulating neuronal excitability and acts at inhibitory synapses in the brain. GABAergic neurons, located in the striatum, are the cell type most susceptible to degeneration in HD.

Another key point in the study involves the new disease models for HD presented by this method, allowing researchers to study the underlying disease process in detail. Being able to control disease development from such an early stage, using iPS cells, may provide important clues about the very start of disease development in HD. An animal model that closely imitates the real conditions of HD also opens up new and improved opportunities for drug screening.

"Having created a model that mimics HD progression from the initial stages of the disease provides us with a unique experimental platform to study Huntington’s disease pathology" said Patrik Brundin, M.D., Ph.D., Director of the Center for Neurodegenerative Science at Van Andel Research Institute (VARI), Head of the Neuronal Survival Unit at Lund University, Sweden, and co-author of the study.

Huntington’s disease (HD) is a neurodegenerative genetic disorder that affects muscle coordination and leads to cognitive decline and psychiatric problems. It typically becomes noticeable in mid-adult life, with symptoms beginning between 35 and 44 years of age. Life expectancy following onset of visual symptoms is about 20 years. The worldwide prevalence of HD is 5-10 cases per 100,000 persons. Key to the disease process is the formation of specific protein aggregates (essentially abnormal clumps) inside some neurons.

Provided by Van Andel Research Institute

Source: medicalxpress.com

May 29, 2012

What do physicists, chemists, mathematicians and biologists have in common? One of the answers at Cambridge is a shared interest in unravelling the processes behind neurodegenerative diseases such as Alzheimer’s, Parkinson’s and Motor Neurone Disease.

Dementia. Credit: ©freshidea Fotolia

As more people live to a ripe old age, an increasing number of us will develop neurodegenerative diseases such as Alzheimer’s. Despite the escalating economic costs and human misery associated with these diseases, we still know relatively little about how they develop or how best to tackle them.

Alzheimer’s is the most common neurodegenerative disease. “It’s an enormous problem and we’re not doing very well at the moment in slowing the disease or treating its symptoms effectively,” says Professor Peter St George-Hyslop.

Neurodegenerative diseases such as Alzheimer’s are difficult to study for several reasons. “One is that it’s not easy to get pieces of living brain,” he explains. “It’s also a disease where patients become unable to speak for themselves, so unlike people with AIDS or breast cancer they aren’t demonstrating outside the houses of Parliament demanding funding.”

Although charities and campaigners are doing sterling work raising the profile of Alzheimer’s, until recently attitudes to neurodegenerative disease had much in common with the way we viewed cancer 50 years ago.

“We are, for Alzheimer’s, like where we were for cancer in the 1950s, when people didn’t like to talk about it, were frightened or ashamed of it. And therapeutically we are in the same place; although we are beginning to learn about these diseases we don’t yet have much in the way of effective therapies,” Professor St George-Hyslop says.

One crucial discovery is that proteins misfolding in the brain form clumps or aggregates and these play a major role in causing neurodegenerative diseases. When these proteins misfold they take on certain characteristics that become noxious to cells, but what we need to know now is why these proteins misfold, which aggregates do the damage, and how that damage occurs. Which is where physics, chemistry and mathematics enter the biological picture.

Professor St George-Hyslop leads a group of experts from disparate disciplines, each bringing different tools and different ways of working to the study of neurodegenerative diseases.

What began in late 2008 as a series of meetings has now developed into a 12-strong group funded by a £5.3 million Strategic Award from the Wellcome Trust and Medical Research Council. “It’s a very interesting group of people who came together because they wanted to come together. They each knew they had something to contribute but also that they needed something else – some skills, some knowledge, some point of view – from another member of the group,” he says.

“The biologists among us knew there were techniques that the physicists and chemists had that could help us. They in turn knew we had some biological knowledge that would help them apply, in a sensible way, their very good and insightful physical and chemical tools.”

Among the group is Professor David Klenerman from the Department of Chemistry. One of the inventors of rapid, high-throughput DNA sequencing, he is now applying this knowledge to protein misfolding. From the same department comes Professor Michele Vendruscolo, a theoretical physicist working on the mechanics and thermodynamics of protein misfolding. Professor Chris Dobson, who is also from the Department of Chemistry works on protein misfolding in neurodegenerative diseases, while from the Department of Chemical Engineering and Biotechnology Dr. Clemens Kaminski brings modern laser spectroscopy tools that allow you to watch these proteins misfold inside living cells in real time.

The group has applied these physical tools to study nematode worms in which a mutation produces the same protein misfolding that causes disease in humans. “That ability to see these things as they happen in a living model give us a much greater understanding compared with previous techniques, which essentially involved grinding up biological samples and examining them after these processes had occurred,” Professor St George-Hyslop explains.

“What’s important is the marriage of the physical tool with the biological question,” he says. And he hopes that by revealing where these misfolded proteins act, these new tools could help researchers develop ways of blocking the damage they cause in both Alzheimer’s and other neurodegenerative diseases.

“The primary goal is to understand what the beginning and the middle parts of the process are. We know what the end is – the cell dies and you get a disease – but if you know why the cells get sick and what the mechanisms are then you have a better chance of preventing or halting it,” says Professor St George- Hyslop. “Our goal is to provide that fundamental knowledge of cause and mechanism. Hopefully from that will come some idea of which parts of those pathways you can monitor as a diagnostic and which parts you can block or change as a treatment.”

More recently, the group has been enlarged by a £4.5 million grant from the National Institute of Health Research to support an extension of the Cambridge Biomedical Research Centre via the creation of a Biomedical Research Unit in Dementia for translational research. This has allowed the inclusion of researchers in immunology and in brain imaging from the Department of Medicine and the Wolfson Brain Imaging Centre.

Provided by University of Cambridge

Source: medicalxpress.com

ScienceDaily (May 28, 2012) — A team of researchers from Maastricht, Leuven, Bristol and Cambridge demonstrated the effectiveness of a new tinnitus treatment approach in the journal The Lancet. Tinnitus is the perception of a noxious disabling internal sound without an external source. Roughly fifteen percent of the population suffers from this disorder in varying degrees along with the associated concentration problems, sleep disturbances, anxiety, depression and extreme fatigue.

Tinnitus is the perception of a noxious disabling internal sound without an external source. (Credit: © BildPix.de / Fotolia)

Sometimes this disorder is so disruptive it seriously impairs their daily functioning and, unfortunately, there is no cure.

The research conducted by Rilana Cima and her colleagues, however, indicates that cognitive behavioural therapy can help improve the daily functioning of tinnitus patients.

The study, conducted at Adelante Audiology & Communication, followed 492 adult tinnitus patients for a period of twelve months. The effectiveness of an innovative tinnitus treatment protocol was compared to the standard treatment methods offered throughout the Netherlands. The ground-breaking, stepped treatment plan consists of cognitive behavioural therapy and combines elements from psychology and audiology. The therapy aims at reducing the negative thoughts and feelings surrounding tinnitus, symptoms through exposure techniques, movement and relaxation exercises, and mindfulness-based elements.

This is supplemented with elements from the so-called tinnitus retraining therapy (TRT), which examines the problems on a sound perception level. The treatment is offered by a multidisciplinary team of audiologists, psychologists, speech and movement therapists, physical therapists and social workers. The project was funded by the Netherlands Organisation for Health Research and Development (ZonMW), and directed by Johan Vlaeyen, professor behavioural medicine at KU Leuven and Maastricht University.

The results offer compelling evidence to support the effectiveness of this innovative and specialised tinnitus therapy over more traditional forms of treatment. The overall health of the tinnitus patient improves and the severity of their symptoms and perceived impairment decreases after therapy. Moreover, the new treatment is far more effective in reducing negative mood, dysfunctional beliefs and tinnitus-related fear). The specialised tinnitus treatment is effective for both milder and more severe forms of the disorder. The researchers are therefore advocating a widespread implementation of this new treatment protocol.

Source: Science Daily

May 29, 2012

Human brain functions have been studied in the past using relatively simple stimuli, such as pictures of faces and isolated sounds or words. Researchers from Aalto University Department of Biomedical Engineering and Computational Science have now taken a highly different approach: they have studied brain functions in lifelike circumstances.

In their new study, published in PLoS ONE, the group examined how the brain processes the film The Match Factory Girl by Aki Kaurismäki.

Films have been previously used to study brain activity, but the brain activity patterns have been integrated over the whole duration of the film, and thus time information is lost. This is like compressing a whole film into just one frame. In some studies, scientists have looked at dynamic brain activity, but focusing on a single brain region at a time.

The Aalto University scientists on the other hand study the full brain activity patterns with the time resolution allowed by functional magnetic resonance imaging. This way it possible to find out which events in the film cause changes in the brain activity, and which brain areas are activated at each moment.

This analysis revealed, for example, that parts of a brain network that usually respond to speech also become activated during other types of communication, such as writing. Some other areas of the network were very selective to speech.

The researchers combined two complementary approaches to disclose the brain activity. One based on dependencies of activation in different parts of the brain, and the other begins from detailed analysis of the visual and acoustic features of which the film is composed.

The results revealed brain networks in which activity follows remarkably well the complex model of the auditory and visual features of the film. For example, brain activity in the auditory cortex followed the soundtrack extremely well over the whole length of the film, and viewing the motions of characters’ hands reliably activated widespread areas of the brain.

"Our study opens new ways for studying human brain functions. Many brain areas that process sensory information reveal their principles only if sufficiently complex and naturalistic stimuli are used,” explain researcher Juha Lahnakoski and Professor Mikko Sams from Aalto University Department of Biomedical Engineering and Computational Science.

The new methods also make it possible to study brain mechanisms’ underlying behaviour in normal everyday conditions – by simulating them in films.

Provided by Aalto University

Source: medicalxpress.com

May 28, 2012

Exposure to solvents at work may be associated with reduced thinking skills later in life for those who have less than a high school education, according to a study published in the May 29, 2012, print issue of Neurology, the medical journal of the American Academy of Neurology.

The thinking skills of people with more education were not affected, even if they had the same amount of exposure to solvents.

"People with more education may have a greater cognitive reserve that acts like a buffer allowing the brain to maintain its ability to function in spite of damage," said study author Lisa F. Berkman, PhD, of Harvard University in Cambridge, Mass. "This may be because education helps build up a dense network of connections among brain cells.”

The study involved 4,134 people who worked at the French national gas and electric company. The majority of the people worked at the company for their entire career. Their lifetime exposure to four types of solvents—chlorinated solvents, petroleum solvents, benzene and non-benzene aromatic solvents—was assessed. The participants took a test of thinking skills when they were an average of 59 years old and 91 percent were retired.

A total of 58 percent of the participants had less than a high school education. Of those, 32 percent had cognitive impairment, or problems with thinking skills, compared to 16 percent of those with more education. Among the less-educated, those who were highly exposed to chlorinated and petroleum solvents were 14 percent more likely to have cognitive problems than those with no exposure. People highly exposed to benzene were 24 percent more likely to have cognitive problems, and those highly exposed to non-benzene aromatic solvents were 36 percent more likely to have cognitive problems.

"These findings suggest that efforts to improve quality and quantity of education early in life could help protect people’s cognitive abilities later in life," Berkman said, who worked alongside study author Erika Sabbath, ScD. "Investment in education could serve as a broad shield against both known and unknown exposures across the lifetime. This is especially important given that some evidence shows that federal levels of permissible exposure for some solvents may be insufficient to protect workers against the health consequences of exposure.”

Provided by American Academy of Neurology

Source: medicalxpress.com

May 28, 2012

In a groundbreaking study, researchers from the Czech Republic and the United Kingdom have discovered a link between the déjà vu phenomenon and structures in the human brain, effectively confirming the neurological origin of this phenomenon. Despite past studies investigating this phenomenon in healthy individuals, no concrete evidence had ever emerged … until now. The study is presented in the journal Cortex.

Led by the Central European Institute of Technology, Masaryk University (CEITEC MU) and Masaryk University’s Faculty of Medicine in the Czech Republic, researchers discovered that specific brain structures have a direct impact on the déjà vu experience. The findings of their study showed that the size of these structures are considerably smaller in the brains of the people experiencing déjà vu, compared with individuals who had no personal experience with déjà vu.

The team from CEITEC MU, along with colleagues from other Brno research institutions as well as the University of Exeter in the United Kingdom succeeded in providing huge insight into this phenomenon that has perplexed many over the years.

The team observed how small structures in the brain’s medial temporal lobes, in which memory and recollections originate, were considerably smaller in individuals with the occurrence of déjà vu than in individuals who have not experienced déjà vu. Their findings also showed that the more often the examined individuals experience déjà vu, the smaller the brain structures are.

"One hundred and thirteen healthy subjects underwent a structural examination of their brain by means of magnetic resonance and subsequently by using a new sensitive method for an automatic analysis of brain morphology (source-based morphometry) [and] the size of individual brain regions was compared among the individuals who have never experienced déjà vu and those who have experienced it," said lead author Milan Brázdil from CEITEC.

"Except for the presence of the examined phenomenon, both groups of individuals were fully comparable. When we stimulate the hippocampus, we are able to induce déjà vu in neurological patients. By finding the structural differences in hippocampus in healthy individuals who do and do not experience déjà vu, we have unambiguously proved that déjà vu is directly linked to the function of these brain structures. We think that it is probably a certain small “error in the system” caused by higher excitability of hippocampuses. It is the consequence of changes in the most sensitive brain regions which probably occurred in the course of the development of the neural system.”

Experts say déjà vu, while fascinating, is not an uncommon experience. Between 60% and 80% of healthy individuals have reported occasional occurrences of déjà vu.

Provided by CORDIS

Source: medicalxpress.com