July 17, 2012

(Medical Xpress) — You’re headed out the door and you realize you don’t have your car keys. After a few minutes of rifling through pockets, checking the seat cushions and scanning the coffee table, you find the familiar key ring and off you go. Easy enough, right? What you might not know is that the task that took you a couple seconds to complete is a task that computers — despite decades of advancement and intricate calculations — still can’t perform as efficiently as humans: the visual search.

Pictured is part of the research team in front of the magnetic resonance imaging device at the UCSB Brain Imaging Center. From left to right: researcher Tim Preston; associate professor of psychological and brain sciences Barry Giesbrecht; and professor of psychological and brain sciences Miguel P. Eckstein. Not pictured: Koel Das, now a faculty member at the Indian Institute of Science in Bangalore, Karnatka, India; and lead author Fei Guo, now in the software industry. Credit: UCSB

"Our daily lives are comprised of little searches that are constantly changing, depending on what we need to do," said Miguel Eckstein, UC Santa Barbara professor of psychological and brain sciences and co-author of the recently released paper "Feature-Independent Neural Coding of Target Detection during Search of Natural Scenes," published in the Journal of Neuroscience. "So the idea is, where does that take place in the brain?"

A large part of the human brain is dedicated to vision, with different parts involved in processing the many visual properties of the world. Some parts are stimulated by color, others by motion, yet others by shape.

However, those parts of the brain tell only a part of the story. What Eckstein and co-authors wanted to determine was how we decide whether the target object we are looking for is actually in the scene, how difficult the search is, and how we know we’ve found what we wanted.

They found their answers in the dorsal frontoparietal network, a region of the brain that roughly corresponds to the top of one’s head, and is also associated with properties such as attention and eye movements. In the parts of the human brain used earlier in the processing stream, regions stimulated by specific features like color, motion, and direction are a major part of the search. However, in the dorsal frontoparietal network, activity is not confined to any specific features of the object.

"It’s flexible," said Eckstein. Using 18 observers, an MRI machine, and hundreds of photos of scenes flashed before the observers with instructions to look for certain items, the scientists monitored their subjects’ brain activity. By watching the intraparietal sulcus (IPS), located within the dorsal frontoparietal network, the researchers were able to note not only whether their subjects found the objects, but also how confident they were in their finds.

The IPS region would be stimulated even if the object was not there, said Eckstein, but the pattern of activity would not be the same as it would had the object actually existed in the scene. The pattern of activity was consistent, even though the 368 different objects the subjects searched for were defined by very different visual features. This, Eckstein said, indicates that IPS did not rely on the presence of any fixed feature to determine the presence or absence of various objects. Other visual regions did not show this consistent pattern of activity across objects.

"As you go further up in processing, the neurons are less interested in a specific feature, but they’re more interested in whatever is behaviorally relevant to you at the moment," said Eckstein. Thus, a search for an apple, for instance, would make red, green, and rounded shapes relevant. If the search was for your car keys, the interparietal sulcus would now be interested in gold, silver, and key-type shapes and not interested in green, red, and rounded shapes.

"For visual search to be efficient, we want those visual features related to what we are looking for to elicit strong responses in our brain and not others that are not related to our search, and are distracting," Eckstein added. "Our results suggest that this is what is achieved in the intraparietal sulcus, and allows for efficient visual search."

For Eckstein and colleagues, these findings are just the tip of the iceberg. Future research will dig more deeply into the seemingly simple yet essential ability of humans to do a visual search and how they can use the layout of a scene to guide their search.

"What we’re trying to really understand is what other mechanisms or strategies the brain has to make searches efficient and easy," said Eckstein. "What part of the brain is doing that?"

Provided by University of California - Santa Barbara

Source: medicalxpress.com

July 16, 2012 By Maureen Salamon

(HealthDay) — Evidence is building that poor sleep patterns may do more than make you cranky: The amount and quality of shuteye you get could be linked to mental deterioration and Alzheimer’s disease, four new studies suggest.

Inadequate shuteye associated with mental decline in four new studies.

Too little or too much sleep was equated with two years’ brain aging in one study. A separate study concluded that people with sleep apnea — disrupted breathing during sleep — were more than twice as likely to develop mild thinking problems or dementia compared to problem-free sleepers. Yet another suggests excessive daytime sleepiness may predict diminished memory and thinking skills, known as cognitive decline, in older people.

"Whether sleep changes, such as sleep apnea or disturbances, are signs of a decline to come or the cause of decline is something we don’t know, but these four studies … shed further light that this is an area we need to look into more," said Heather Snyder, senior associate director of medical and scientific relations for the Alzheimer’s Association in Chicago, who was not involved in the studies.

The studies are scheduled for presentation Monday at the Alzheimer’s Association annual meeting in Vancouver.

The largest of the studies, which examined data on more than 15,000 women in the U.S. Nurses’ Health Study, suggested that those who slept five hours a day or less, or nine hours a day or more, had lower average mental functioning than participants who slept seven hours per day. Too much or too little sleep was cognitively equivalent to aging by two years, according to the research, which followed the women over 14 years beginning in middle age.

The study also observed that women whose sleep duration changed by two hours or more a day from mid- to later life had worse brain function than participants with no change in sleep duration — a finding that held true regardless of how long they usually slept at the beginning of the study.

Read more …

ScienceDaily (July 16, 2012) — Post-traumatic stress disorder (PTSD) is more treatable than previously thought. A novel method has shown to be remarkably effective. The method, called Narrative Exposure Therapy (NET), is an intervention aimed at reducing symptoms of post-traumatic stress.

In an on-going Norwegian study, exposure therapy has been used with asylum seekers and refugees who have survived the ordeal of torture.

"According to previous studies, these patients do not benefit from traditional psychological therapy. In our study, however, 60 per cent show a marked improvement, and approximately 20 per cent show no symptoms of PTSD after treatment," says Håkon Stenmark, a PhD candidate at the Norwegian University of Science and Technology’s Department of Neuroscience, and has conducted the study in collaboration with colleague and fellow PhD candidate Joar Øverås Halvorsen.

Describing traumatic events

"Narrative" simply means telling a story. In exposure therapy the patient constructs a narration of his life while focusing on a detailed report of traumatic experiences. In a typical therapy session, the patient is given a rope to symbolize his or her life, from early childhood up to the present date.

The patient then describes the events in his life, good and bad, in chronological order. For every good memory the patient places a flower on the rope, and for every bad memory, a stone.

"I was blindfolded and seated in the prison’s interrogation room. I received multiple blows all over my body, and had no way of anticipating where I would be beaten next, the patient recalls with great difficulty."

The therapist is sitting at the opposite end of the table, listening attentively. Everything is written down, as it might prove useful later. The written account may be used in an application for asylum, or even as documentation for Amnesty International.

"Electrodes were fastened to my toes, and I was told I would be given electric shocks. The next thing I knew, a skinny man with a cigarette in his mouth turned the nob. The pain was excruciating, and my whole body tensed up."

"This is just one example. Although the patients are of different nationalities, and have been subjected to different kinds of torture, they share similar stories," Stenmark says.

Flashbacks and learning problems

Torture can result in a range of symptoms, depending on the method of torture as well as the duration of the ordeal. Nonetheless, symptoms typically fall into three main categories: ‘Reliving’ the event, avoidance and arousal. “A patients who is reliving torture may have flashbacks of the event, or episodes of repeated nightmares. Avoidance reactions are typically displayed as an extreme fear of the police or anybody who might resemble the abuser. People with these symptoms will try to isolate themselves and avoid people in general. Symptoms of arousal may result in difficulties concentrating, irritability, or having trouble falling or staying asleep,” Stenmark explains.

The classic symptom of PTSD is an inability to concentrate. As a consequence, sufferers often have learning difficulties and end up losing their jobs.

The brain’s “alarm system”

Existing trials are showing promising results with regards to exposure therapy. But why the method works in the first place, and the exact mechanisms behind it, have yet to be verified.

The most prominent theory is that exposure therapy changes the way fear is ‘wired’ in the memory. Simply stated, there is a part of the brain known as the brain’s ‘alarm system’, which enables us to respond to dangerous stimuli.

"During therapy the patient describes the traumatic event in a safe setting, while re-experiencing his or her emotions. In the process, the patient learns that the memories are not dangerous in themselves. The event was threatening when it occurred, but the memory the patient has today is not," Stenmark explains.

The goal of exposure therapy is to reduce the overall symptoms of PTSD, thereby increasing levels of functioning. Stenmark stresses that this is especially important for asylum seekers and refugees, as they often face additional challenges in Norwegian society.

Narrative exposure therapy was developed by trauma specialists working in refugee camps in Africa and Asia. To date, exposure therapy is not widely used in other parts of the world, which makes Øverås Halvorsen and Stenmark’s study the largest of its kind in the western world.

Source: Science Daily

ScienceDaily (July 16, 2012) — While Spider-Man is capturing the imagination of theatergoers, real-life spider men in Upstate New York are working intently to save a young boy’s life.

UB researchers are developing a treatment for muscular dystrophy using a peptide found in the venom of a Chilean rose tarantula. (Credit: Image courtesy of University at Buffalo)

It all began in 2009, when Jeff Harvey, a stockbroker from the Buffalo suburbs, discovered that his grandson, JB, had Duchenne muscular dystrophy. The disease is fatal. It strikes only boys, causing their muscles to waste away.

Hoping to help his grandson, Harvey searched Google for promising muscular dystrophy treatments and, in a moment of serendipity, stumbled upon University at Buffalo scientist Frederick Sachs, PhD.

Sachs was a professor of physiology and biophysics who had been studying the medical benefits of venom. In the venom of the Chilean rose tarantula, he and his colleagues discovered a protein that held promise for keeping muscular dystrophy at bay. Specifically, the protein helped stop muscle cells from deteriorating.

Within months of getting in touch, Harvey and Sachs co-founded Tonus Therapeutics, a pharmaceutical company devoted to developing the protein as a drug. Though the treatment has yet to be tested in humans, it has helped dystrophic mice gain strength in preliminary experiments.

The therapy is not a cure. But if it works in humans, it could extend the lives of children like JB for years — maybe even decades.

Success can’t come quickly enough.

JB, now four, can’t walk down the stairs alone. When he runs, he waddles. He receives physical therapy and takes steroids as a treatment. While playing tee ball one recent day, he confided to his grandfather, “When I grow up, I want to be a baseball player.” It was a heartbreaking moment.

"Oh, I would be thrilled if you could be a baseball player," Harvey remembers replying. He’s doing everything he can to make sure that JB — and other boys like him — can live out their dreams.

Source: Science Daily

July 16th, 2012

Spinal Muscular Atrophy affects one in 6,000 children and has no known cure.

A team of University of Missouri researchers has found that introducing a missing gene into the central nervous system could help extend the lives of patients with Spinal Muscular Atrophy (SMA) – the leading genetic cause of infantile death in the world.

SMA is a rare genetic disease that is inherited by one in 6,000 children who often die young because there is no cure. Children who inherit SMA are missing a gene that produces a protein which directs nerves in the spine to give commands to muscles.

The MU team, led by Christian Lorson, professor in the Department of Veterinary Pathobiology and the Department of Molecular Microbiology and Immunology, introduced the missing gene into mice born with SMA through two different methods: intravenously and directly into the mice’s central nervous systems. While both methods were effective in extending the lives of the mice, Lorson found that introducing the missing gene directly into the central nervous system extended the lives of the mice longer.

Mice born with spinal muscular atrophy typically only live five or six days. Researchers introduced the SMN gene into the mice’s central nervous systems and were able to extend their lives 10-25 days longer. The mice in the picture have spinal muscular atrophy.

“Typically, mice born with SMA only live five or six days, but by introducing the missing SMN gene into the mice’s central nervous systems, we were able to extend their lives 10-25 days longer than SMA mice who go untreated,” said Lorson, who works in the MU Bond Life Sciences Center and the College of Veterinary Medicine. “While this system is still not perfect, what our study did show is that the direct administration of the missing gene into the central nervous system provides some degree of rescue and a profound extension of survival.”

There are several different types of SMA that appear in humans, depending on the age that symptoms begin to appear. Lorson believes that introducing the missing gene through the central nervous system is a way to potentially treat humans regardless of what SMA type they have.

“This is a treatment method that is very close to being a reality for human patients,” Lorson said. “Clinical trials of SMA treatment using gene therapy are likely to begin in next 12-18 months, barring any unforeseen problems.”

Source: Neuroscience News

July 16, 2012

Can you teach an old dog (or human) new tricks? Yes, but it might take time, practice, and hard work before he or she gets it right, according to Hans Schroder and colleagues from Michigan State University in the US. Their work shows that when rules change, our attempts to control our actions are accompanied by a loss of attention to detail. Their work is published online in the Springer journal Cognitive, Affective, & Behavioral Neuroscience.

In order to adapt to changing conditions, humans need to be able to modify their behavior successfully. Overriding the rules we adhere to on a daily basis requires substantial attention and effort, and we do not always get it right the first time. When we switch between two or more tasks, we are slower and more likely to commit errors, which suggests switching tasks is a costly process. This may explain why it is so hard to learn from our mistakes when rules change.

The authors explain: “Switching the rules we use to perform a task makes us less aware of our mistakes. We therefore have a harder time learning from them. That’s because switching tasks is mentally taxing and costly, which leads us to pay less attention to the detail and therefore make more mistakes.”

A total of 67 undergraduates took part in the study. They were asked to wear a cap, which recorded electrical activity in the brain. They then performed a computer task that is easy to make mistakes on. Specifically, the participants were shown letter strings like “MMMMM” or “NNMNN” and were told to follow a simple rule: if ‘M’ is in the middle, press the left button; if ‘N’ is in the middle, press the right button. After they had followed this rule for almost 50 trials, they were instructed to perform the same task, but with the rules reversed i.e. now if ‘M’ is in the middle, press the right button; and if ‘N’ is in the middle, press the left button.

When the rules were reversed, participants made more consecutive errors. They were more likely to get it wrong twice in a row. This showed they were less apt to bounce back and learn from their mistakes. Reversing the rules also produced greater control-related and less error-awareness brain activity.

These results suggest that when rules are reversed, our brain works harder to juggle the two rules - the new rule and the old rule - and stay focused on the new rule. When we spend brain energy juggling these two rules, we have less brain power available for recognizing our mistakes.

Provided by Springer

Source: medicalxpress.com

ScienceDaily (July 16, 2012) — Far from processing every word we read or hear, our brains often do not even notice key words that can change the whole meaning of a sentence, according to new research from the Economic and Social Research Council (ESRC).

After a plane crash, where should the survivors be buried?

If you are considering where the most appropriate burial place should be, you are not alone. Scientists have found that around half the people asked this question, answer it as if they were being asked about the victims not the survivors.

Similarly, when asked “Can a man marry his widow’s sister?” most people answer “yes” — effectively answering that it would indeed be possible for a dead man to marry his bereaved wife’s sister.

What makes researchers particularly interested in people’s failure to notice words that actually don’t make sense, so called semantic illusions, is that these illusions challenge traditional models of language processing which assume that we build understanding of a sentence by deeply analysing the meaning of each word in turn.

Instead semantic illusions provide a strong line of evidence that the way we process language is often shallow and incomplete.

Professor Leuthold at University of Glasgow led a study using electroencephalography (EEG) to explore what is happening in our brains when we process sentences containing semantic illusions.

By analysing the patterns of brain activity when volunteers read or listened to sentences containing hard-to-detect semantic anomalies — words that fit the general context even though they do not actually make sense — the researchers found that when a volunteer was tricked by the semantic illusion, their brain had not even noticed the anomalous word.

Analyses of brain activity also revealed that we are more likely to use this type of shallow processing under conditions of higher cognitive load — that is, when the task we are faced with is more difficult or when we are dealing with more than one task at a time.

The research findings not only provide a better understanding of the processes involved in language comprehension but, according to Professor Leuthold, knowing what is happening in the brain when mistakes occur can help us to avoid the pitfalls,such as missing critical information in textbooks or legal documents, and communicate more effectively.

There are a number of tricks we can use to make sure we get the correct message across: “We know that we process a word more deeply if it is emphasised in some way. So, for example in a news story, a newsreader can stress important words that may otherwise be missed and these words can be italicised to make sure we notice them when reading,” said Professor Leuthold.

The way we construct sentences can also help reduce misunderstandings, he explained: “It’s a good idea to put important information first because we are more likely to miss unusual words when they are near the end of a sentence. Also, we often use an active sentence construction such as ‘Bob ate the apple’ because we make far more mistakes answering questions about a sentence with a passive construction — for example ‘The apple was eaten by Bob’.”

The study findings also suggest that we should avoid multi-tasking when we are reading or listening to an important message: “For example, talking to someone on the phone while driving on a busy motorway or in town, or doing some homework while listening to the newsmight lead to more shallow processing,” said Professor Leuthold.

Source: Science Daily

July 16, 2012

A nationwide consortium of scientists at 20 institutions, led by a principal faculty member at the Harvard Stem Cell Institute (HSCI), has used stem cells to take a major step toward developing personalized medicine to treat Parkinson’s disease.

This study points the way to screening patients with Parkinson’s for their particular variation of the disease, and then treating them with drugs shown effective to work on that variation, rather than trying to treat all patients with the same drugs, as is generally done now, notes Ole Isacson, a leader of the study. Credit: B. D. Colen/Harvard Staff

In part supported by the Harvard Miller Consortium for the Development of Nervous System Therapies, the team of scientists created induced pluripotent stem cells (iPS cells) from the skin cells of patients and at-risk individuals carrying genetic mutations implicated in Parkinson’s disease, and used those cells to derive neural cells, providing a platform for studying the disease in human cells outside of patients.

In a paper published in the journal Science Translational Medicine, the researchers report that although approximately 15 genetic mutations are linked to forms of Parkinson’s, many seem to affect the mitochondria, the cell unit that produces most of its energy.

“This is the first comprehensive study of how human neuronal cells can be models of Parkinson’s, and how it might be treated,” said Ole Isacson, a leader of the study, an HSCI principal faculty member, and a Harvard Medical School professor of neurology, based at McLean Hospital’s Neuroregeneration Laboratory.

The researchers determined that certain compounds or drugs could reverse some signs of disease in the cultured cells with specific genetic mutations, and not in cells with other types of mutations, making real the concept of developing drugs that would be prescribed to patients or individuals at risk for Parkinson’s.

The study was launched with federal stimulus funding provided by the National Institutes of Health (NIH) and was continued with funding from HSCI.

“These findings suggest new opportunities for clinical trials of Parkinson’s disease, wherein cell reprogramming technology could be used to identify the patients most likely to respond to a particular intervention,” said Margaret Sutherland, a program director at NIH’s National Institute of Neurological Disorders and Stroke, in a press release.

The new research indicates that compounds that previously have shown promise in treating Parkinson’s in animal studies, including the antioxidant coenzyme Q10, together with the immunosuppressant rapamycin, have differing levels of effectiveness on various genetic forms of Parkinson’s.

Researchers hope that such findings can provide the basis for more specific drugs for individuals with sporadic forms of Parkinson’s.

As Isacson explained in an interview, this study points the way to screening patients with Parkinson’s for their particular variation of the disease, and then treating them with drugs shown effective to work on that variation, rather than trying to treat all patients with the same drugs, as is generally done now.

“We believe that using human stem cells to study the disease is the correct way to go,” Isacson said. “We have the cell type most vulnerable to the disease in a dish. We can study the most vulnerable cells and compare them to the least vulnerable cells. Traditionally, in neurology,” he said, “all patients with the same disease get the same drugs. But they may have the disease for different reasons. This gives us a way to tease out those different reasons, and find different ways to treat them.”

Provided by Harvard University

Source: medicalxpress.com