Tuesday, May 17, 2011

One way to study the schizophrenic brain: Build one

Researchers at Yale and the University of Texas used a neural network -- a computer brain -- to test out medical theories of what causes schizophrenia. The result was a computer brain that can't tell the difference between stories about itself and fanciful stories about gangsters, and claims responsibility for terrorist acts.
Brain scans to detect cancer
Brain scans to detect cancer (iStockPhotos)
What can we learn from a "schizophrenic" computer brain?
In a paper published today in the journal Biological Psychiatry, researchers started with a neural network: a computer program that replicates, as best we know how, an actual human brain. It can take in information, learn from it, combine it, talk back to you.
Then they applied to their computer brain a medical hypothesis about schizophrenia: that memories are encoded too quickly on the brain, something the researchers call "hyper-learning."
"What the model suggests is if this process is accelerated unduly, that bad things happen and that stuff going into memory gets intermingled, corrupted, kind of like a bad sector in a hard drive," says Dr. Ralph Hoffman, a psychiatrist at the Yale School of Medicine. The brain takes in too much information, too quickly, "can't organize it and sift it. And somehow something to do with that process may be running amok."
Then Hoffman and his colleagues began telling their computer brain "stories." Some were meant to be autobiographical, about a young doctor working in a New York City hospital.
Then there was a second set of stories, some of which had parallel narrative structures to the autobiographical ones, involving "crime and crime-fighting, mafia activities and assassination and things of that sort," Hoffman says.
Next step: Have the neural network -- the computer brain -- try to retell the stories. Uli Grasemann, a computer scientist at the University of Texas at Austin, says the stories came out much differently than they went in.
"We get stories where the content is changed, but the local structure and the grammar remain intact," says Grasemann. "So for example there might be a story about one gangster killing another gangster, and the network will basically leave the story intact and replace one of the gangsters with itself.
"There was a story about a terrorist bombing, and the network consistently replaced the terrorist with 'I'. Which is an interesting result because these confusions among actors, and inserting oneself into shared cultural stories like movies or legends, that's something that happens a lot with delusions or schizophrenia."
The researchers tweaked the neural network in a number of ways they though might mimic schizophrenia. But this hyperlearning -- taking in too much information too fast -- emerged as the most promising.
Hoffman says the next step is to keep comparing the results with actual schizophrenic people. "If there is validation there, then a real exciting possibility is we might be able to use these artificial brains or networks to test out novel treatments that we haven't really thought of yet."

Top brain specialist calls for ban on antipsychotic in elders

A senior neurologist at Beth Israel Deaconess Medical Center says many hospitals inappropriately use the antipsychotic Haldol "like water" in agitated elderly patients, putting them at risk for serious complications.
Dr. Louis Caplan, a neurology professor at Harvard Medical School, said a recent government report that found pervasive use of antipsychotic medications in elderly nursing home patents underscores the "overuse" problem with this class of drugs.
Caplan said Haldol is typically given to agitated patients to calm them quickly, but he said older patients, especially, can become over-sedated and stiff, putting them at risk for pulmonary and urinary infections, because they have trouble moving and couging.

"I would love to see Haldol banned from use in hospitals," Caplan said. "It has no role to play in hospitalized, agitated patients."
A report released this month by the Inspector General's Office of the federal Department of Health and Human Services found that 51 percent of Medicare claims for a newer class of antipsychotics, known as atypical, were prescribed inappropriately to nursing home patients.
The Inspector General reviewed medical records from 2007 and and found that 83 percent of Medicare claims for atypical antipsychotic drugs for elderly nursing home residents were associated with conditions not intended for that use. The report also found that 88 percent were associated with a condition that could produce serious side-effects, conditions for which federal regulators had specifically warned against such usage.
The use of such drugs is especially worrisome in nursing homes because a substantial number of residents suffer from dementia, a condition that puts them at greater risk of death when given antipsychotic medications.
The drugs were developed to treat people with severe mental illnesses such as schizophrenia, not dementia, which is the progressive loss of memory or other intellectual function than can result from aging or Alzheimer's disease.
Fderal regulators have issued nationwide alerts about troubling and sometimes fatal side effects when antipsychotics are taken by people with dementia, including increased confusion, sedation, and weight gain
Haldol is an earlier class of antipsychotic drugs, but Caplan said it's just as problematical.
During the 14 year period that Caplan was chairman of the Neurology department at Tufts Medical Center and the Neurologist-in-chief, the hospital eliminated completely the use of Haldol in hospitalized patients in its neurology service, Caplan said in a letter he wrote to the Alliance for Human Research Protection, a patient group that has lobbied against the overuse of antipsychotic drugs.
Complications from the use of Haldol was one of the most common reasons for neurological referral for consultation at Tufts, Caplan said.
"It is also a common reason for referral at the Beth Israel Deaconess Medical Center," Caplan said.

Aging Brain Degradation Harms Memory

It's something we just accept: the fact that the older we get, the more difficulty we seem to have remembering things. We can leave our cars in the same parking lot each morning, but unless we park in the same space each and every day, it's a challenge eight hours later to recall whether we left the SUV in the second or fifth row. Or, we can be introduced to new colleagues at a meeting and will have forgotten their names before the handshake is over. We shrug and nervously reassure ourselves that our brains' "hard drives" are just too full to handle the barrage of new information that comes in daily.

According to a Johns Hopkins neuroscientist, however, the real trouble is that our aging brains are unable to process this information as "new" because the brain pathways leading to the hippocampus- the area of the brain that stores memories- become degraded over time. As a result, our brains cannot accurately "file" new information (like where we left the car that particular morning), and confusion results.

"Our research uses brain imaging techniques that investigate both the brain's functional and structural integrity to demonstrate that age is associated with a reduction in the hippocampus's ability to do its job, and this is related to the reduced input it is getting from the rest of the brain," says Michael Yassa, assistant professor of psychological and brain sciences in Johns Hopkins' Krieger School of Arts and Sciences. "As we get older, we are much more susceptible to 'interference' from older memories than we are when we are younger."

In other words, when faced with an experience similar to what it has encountered before, such as parking the car, our brain tends to recall old information it already has stored instead of filing new information and being able to retrieve that. The result? You can't find your car immediately and find yourself wandering the parking lot.

"Maybe this is also why we tend to reminisce so much more as we get older: because it is easier to recall old memories than make new ones," Yassa speculated.

The study appears in the May 9 Early Online edition of the Proceedings of the National Academy of Sciences and is available at www.pnas.org/content/early/2011/05/05/1101567108.

Yassa and his team used MRI scans to observe the brains of 40 healthy young college students and older adults, ages 60 to 80, while these participants viewed pictures of everyday objects such as pineapples, test tubes and tractors and classified each -- by pressing a button -- as either "indoor" or "outdoor." (The team used three kinds of MRI scans in the study: structural MRI scans, which detect structural abnormalities; functional MRI scans, which document how hard various regions of the brain work during tasks; and diffusion MRIs, which monitor how well different regions of the brain communicate by tracking the movement of water molecules along pathways.)

Some of the pictures were similar but not identical, and others were markedly different. The team used functional MRI to watch the hippocampus when participants saw items that were exactly the same or slightly different to ascertain how this region of the brain classified that item: as familiar or not.

"Pictures had to be very distinct from each other for an older person's hippocampus to correctly classify them as new. The more similar the pictures were, the more the older person's hippocampus struggled to do this. A young person's hippocampus, on the other hand, treated all of these similar pictures as new," Yassa explained.

Later, the participants viewed a series of completely new pictures (all different) and again were asked to classify them as either "indoor" or "outdoor." A few minutes later, the researchers presented the participants with the new set of pictures and asked whether each item was "old," "new" or "similar."

"The 'similar' response was the critical response for us, because it let us know that participants could distinguish between similar items and knew that they're not identical to the ones they'd seen before," Yassa says. "We found that older adults tended to have fewer 'similar' responses and more 'old' responses instead, indicating that they could not distinguish between similar items."

Yassa says that this inability among older adults to recognize information as "similar" to something they had seen recently is linked to what is known as the "perforant pathway," which directs input from the rest of the brain into the hippocampus. The more degraded the pathway, the less likely the hippocampus is to store similar memories as distinct from old memories.

"We are now closer to understanding some of the mechanisms that underlie memory loss with increasing age," Yassa says. "These results have possible practical ramifications in the treatment of Alzheimer's disease, because the hippocampus is one of the places that deteriorate very early in the course of that disease."

The team's next step would be to conduct clinical trials in early Alzheimer's disease patients using the mechanisms that they have isolated as a way to measure the efficacy of therapeutic medications.

"Basically, we will now be able to investigate the effect of a drug on hippocampal function and pathway integrity," he says. "If the drug slows down pathway degradation and hippocampal dysfunction, it's possible that it could delay the onset of Alzheimer's by five to 10 years, which may be enough for a large proportion of older adults to not get the disease at all. This would be a huge breakthrough in the field."

Beads for your brain

Concentrating hard: Engrossed with the abacus. Photo: Special Arrangement
Concentrating hard: Engrossed with the abacus. Photo: Special Arrangement
Abacus has the power to stimulate your brain and thereby enhance your academic and creative endeavours.
The capabilities of the human brain are almost magical. However, studies have proved that hardly anyone makes use of even 10 per cent of its amazing faculties.
What does it take to increase this percentage and unlock the door to the miraculous powers of our brain? Research shows that giving proper exercise at the right time to our brain can create wonders in enhancing its prospects and potential.
Mental enhancement
Education experts and researchers in this area say that abacus is a wonderful device, which can help to achieve this task.
Abacus, in simple terms, is a calculating device to be used manually with movable beads on thin bars, fixed on a rectangular frame. Its size, colour and materials can be varied according to convenience. But when it comes to its use, abacus is known across the world as a ‘brain development device'.
According to Saji Tomy, an abacus trainer in Kozhikode and Kannur for the last nine years, its possibilities are incredible. “It not only helps to increase listening skill, concentration, memory power, speed and accuracy of young children but also enhances confidence and triggers the faculty of creativity and imagination in young students,” she says.
Abacus training is in no way a burden on children. “Rather its fun and quite enjoyable,” vouches Ms. Saji. She says many parents have told her that the kids find spending time with the abacus more enjoyable than watching cartoon programmes on TV.
To achieve a desirable result, a child needs a daily practice of minimum 15 minutes after regular classes of two hours. The training, according to her, activates the dormant cells in the brain helping to increase the brain power and thereby making all subjects, especially mathematics easy for them to learn. “We can see noticeable change in students by the time they finish level three of their training,” says, another abacus trainer in the city.
Starting early
According to experts, the age between five and 15 years is the most suitable time to learn to use the abacus as this will be the time when the brain will be most pliable to adapt to changes. “As children are made to use both the hands while using the abacus, both sides of the brain get stimulated and prepared to be active,” says Ms. Saji, who has trained more than 1000 students in Kerala over a period of several years. “I have seen abacus working wonders in young children,” she says.
However, for a better result, the parents of students also need to be given a basic understanding about the abacus, feel trainers. “They (parents) need to be personally convinced and aware of the astonishing changes this training can bring to their kids,” says Ms. Saji. According to her, abacus is a widely accepted tool among education experts in developed countries such Japan and China. “Our people are yet to understand the magic abacus can work in young ones,” she says.

Team makes breakthrough in development of artificial brain

Researchers have built a synthetic synapse in work that could one day lead to a fully-functioning artificial brain.
A team at the University of California Viterbi has built a carbon nanotube synapse circuit whose behavior in tests reproduces the function of a neuron input, or synapse.
The work could lead to devices that could be used in brain prostheses – or that could be combined into massive networks of synthetic neurons to create an artificial brain.
"This is a necessary first step in the process. We wanted to answer the question: Can you build a circuit that would act like a neuron?"  says Professor Alice Parker, who's been working on the problem since 2006.
"The next step is even more complex. How can we build structures out of these circuits that mimic the neuron, and eventually the function of the brain, which has 100 billion neurons and 10,000 synapses?”
The synapse her team created is simplified, and Parker says the actual development of a synthetic brain is decades away. The next stage, she says, is to reproduce brain plasticity in the circuits.
The human brain continually produces new neurons and adapts throughout life, and creating this process through analog circuits will be a major task. But, says Parker, the research could have long-term promise for everything from prosthetic nanotechnology that would heal traumatic brain injuries to intelligent, safer cars.

Perceptions of justice built into the brain

A new study suggests that our brains have a built-in mechanism that causes an automatic reaction when we deal with someone who refuses to share.
The study comes from the Karolinska Institute and Stockholm School of Economics and it will be published in the online open access journal PLoS Biology next week. In the research the subjects’ sense of justice was challenged in a two-player monetary fairness game (monetary fairness, in economics?), and then their brain activity was instantaneously measured using functional magnetic resonance imaging (fMRI).
When bidders in the game made unfair suggestions as to how to share the money, they were regularly punished by their partners even if it cost them. This reaction to unfairness could be reduced by targeting one particular brain region, the amygdala.
The justice study is based on the universal human behavior to react with immediate hostility when another person behaves unfairly and in a way that doesn’t put the best interests of the group first. The social researchers had 35 subjects participate in a money-based fairness game, where on player proposes to another how a fixed sum of cash is to be shared between them; the other player can either accept the suggestion and get the money, or say no, in which case neither player receives any money.
"If the sum to be shared is 100 SEK kronor and the suggestion is 50 each, everyone accepts it as it is seen as fair," says Dr Katarina Gospic. "But if the suggestion is that you get 20 and I take 80, it's seen as unfair. In roughly half the cases it ends up with the player receiving the smaller share rejecting the suggestion, even though it costs them 20 SEK."
Earlier research has put forward the idea that the area controlling the ability to analyze and make financial decisions is located in the prefrontal cortex and insula. But, using fMRI, the researchers saw that the brain area that directs fast financial decisions was really located in the amygdala, an evolutionary old and hence more primitive part of the brain that regulates feelings of anger and fear.
To examine these results further, the test subjects were given the anti-anxiety tranquillizer Oxazepam or a placebo while playing the game. The research team found out that those who had received the drug showed smaller amygdala activity and a stronger tendency to accept an unfair distribution of the money –despite the fact that when asked, they still considered the suggestion unfair.
The control group showed the tendency to act aggressively and reprimand the player who had suggested the unfair distribution of money was directly linked to an increase in activity in the amygdala. A gender difference was also seen, where men responded more aggressively to imbalanced suggestions than women did by showing a consistently higher rate of amygdalic activity. This gender difference was not found in the group that was happily dosed with Oxazepam.
"This is an incredibly interesting result that shows that it isn't just processes in the prefrontal cortex and insula that determine this kind of decision about financial equitability, as was previously thought," says Professor Martin Ingvar. "Our findings, however, can also have ethical implications since the use of certain drugs can clearly affect our everyday decision-making processes."
The concept of monetary fairness is pretty interesting when talking about a sense of justice that is built into the brain. While the results of this study are indeed interesting, there is also reason to believe that the way that it was constructed is flawed.
When dealing with economics it is important to understand that people have a lot of emotional feelings when talking about wealth distribution. Some people take a socialist perspective and some believe in free markets without government intervention.
I believe that fairness in money is open to interpretation from person to person and that this study may want to present their research in a way that eliminates the influence that emotions has on monetary fairness. Plus they doped the subjects up on what I like to call "happy pills".
But hey what do I know; I’m just a graduate student who just took a class in research methods.
The good news is that the research article is in a journal that has no academic pay wall! So if this is a topic that interests or concerns you, you are free to access this information that was put together by the academic scholars. Open access journals are a step in the right direction. They allow the public more involvement in important fields of study. And these are fields of study that impact us all.

Women have two pathways to sexual pleasure

Women have two pathways to sexual pleasure

A new study has found that women have two pathways to sexual pleasure.

Researchers from Rutgers University in New Jersey used brain scanners to look at which parts of a woman's brain become active when they are aroused.

They found one of the ''pathways'' is activated when a woman is alone and fantasising, while the other gets charged when she is physically stimulated by a lover, reports the Daily Mail.

The research team, led by Barry Komisaruk from Rutgers, analysed MRI scans of women reaching climax to investigate the role of imagination and 'top-down control' in triggering a physiological response.

They found heightened activity in more than 30 parts of the brain, including the prefrontal cortex, an area which controls functions such as decision-making, controlling urges and imagination.

In contrast, when scientists observed women being stimulated by a partner, they found that the same brain region had 'switched off' during orgasm.

"It is possible there is a difference between someone trying to mentalise sexual stimulation as opposed to receiving it from a partner," said Janniko Georgiadis of the University of Groningen in Holland.

This suggests that an orgasm is achieved with a partner when the woman 'lets go' and reaches an 'altered state of consciousnesses.'

The study also concludes that an inability to do this may prevent women from reaching their climax.

How Parkinson's disease harms the brain and how it's treated

Parkinson's researchers in Cleveland play important role in search for a cure

Mouse over labels on the graphic below to see descriptions. (For best results, wait for the page to load completely.)


The chemical ‘short circuit’

In Parkinson’s disease, dopamine-producing nerve cells begin to die off, leaving too little of the chemical. That causes the brain’s motion control center to “short circuit” and overstimulate its target neurons. This causes the muscle tremors symptomatic of Parkinson’s.

Scientists learn about the brain’s ability to reorganize itself

A new study from The University of Michigan has found that after being disrupted, mouse brains are able to shift important functions tied to learning and memory.
So when Geoffrey Murphy, Ph.D., begins to talk about plastic structures, it’s important to know that he’s not talking about the actual plastics we use in our everyday lives. To Murphy, an associate professor of molecular and integrative physiology at the University of Michigan Medical School, plasticity is a reference to the brain’s ability to change as we learn.
According to a University of Michigan Health System press release, Murphy’s lab, in cooperation with U-M’s Neurodevelopment and Regeneration Laboratory run by Jack Parent, M.D., recently displayed how the plasticity of the brain permitted mice to reestablish important functions related to learning and memory after the scientists inhibited the animals’ ability to make certain new brain cells.
The research results, published online in the Proceedings of the National Academy of Sciences, bring scientists a bit closer to separating the ways which the brain deals with interferences and redirects neural functioning .
This could eventually lead to treatments for cognitive impairments in humans, which are caused by disease and aging.
“It’s amazing how the brain is capable of reorganizing itself in this manner,” says Murphy, co-senior author of the study and researcher at U-M’s Molecular and Behavioral Neuroscience Institute. “Right now, we’re still figuring out exactly how the brain accomplishes all this at the molecular level, but it’s sort of comforting to know that our brains are keeping track of all of this for us.”
In research that was conducted previously, the scientists had discovered that restricting cell division in the hippocampuses of mice using radiation or genetic manipulation led to reduced functionality in a cell mechanism important to memory formation known as long-term potentiation.
In this study though, the researchers proved that the interruption is temporary and within six weeks, the mouse brains were able to compensate for the disruption and reestablish plasticity, says Parent, the study’s other senior author, a researcher with the VA Ann Arbor Healthcare System and associate professor of neurology at the U-M Medical School.
When the ongoing growth of key brain cells in adult mice was stopped, the researchers found the brain circuitry compensated for the disruption by enabling existing neurons to be more active. The remaining neurons also had longer life spans than when new cells were constantly being made.
“The results suggest that the birth of brain cells in the adult, which was experimentally disrupted, must be really important – important enough for the whole system to reorganize in response to its loss,” Parent says.

Alzheimer’s Gene May Damage Brain Long Before Symptoms

Alzheimers Gene May Damage Brain Long Before SymptomsThe genetic link to Alzheimer’s is well-known in the scientific community. New research suggests one of the risk-related genes begins to do damage to the brain 50 years before Alzheimer’s is seen.

Paul Thompson , a UCLA professor, reports his work in the current online edition of the Journal of Neuroscience. Thompson and his colleagues report that a particular form of the CLU gene impairs the development of myelin, the protective covering around the neuron’s axons in the brain, making it weaker and more vulnerable to the onset of Alzheimer’s much later in life.
The research team scanned the brains of 398 healthy adults ranging in age from 20 to 30 using a high-magnetic-field diffusion scan (called a 4-Tesla DTI), a newer type of MRI that maps the brain’s connections. They compared those carrying a C-allele variant of the CLU gene with those who had a different variant, the CLU T-allele.
They found that carriers of the CLU-C gene risk variant showed a distinct profile of lower white matter integrity that may increase vulnerability to developing the disease later in life. The discovery of what this gene does is interesting on several levels, said Thompson, the senior author of the study.
“For example, Alzheimer’s has traditionally been considered a disease marked by neuronal cell loss and widespread gray-matter atrophy,” he said.
“But degeneration of myelin in white-matter fiber pathways is more and more being considered a key disease component and another possible pathway to the disease, and this discovery supports that.”
Thompson said four things are surprising with the discovery of this gene’s function:
    1. This risk gene damages the brain a full 50 years before people normally get Alzheimer’s. The damage can be seen on an MRI scan, but there are no symptoms yet.
    2. It’s now known what this mysterious gene does — namely, make your brain wiring vulnerable to attack by impairing the wiring before any senile plaques or tangles develop.
    3. Rather than being a gene that few people have, a whopping 88 percent of Caucasians have it. “So I guess you could say the other 12 percent have an ‘Alzheimer’s resistance gene’ that protects their brain wiring,” said Thompson.
    4. Finally, he said, knowing the role of this gene is useful in predicting a person’s risk of the disease and in seeing if you can step in and protect the brain in the 50-year time window before the disease begins to develop.
Of course, the obvious question is if most of us have this “bad” gene, why isn’t Alzheimer’s rampant in young people?
Less myelination in CLU-C carriers may not translate into poorer cognition in youth, said Thompson, because the brain can compensate. “The brain has a lot of built-in redundancy — miles and miles of brain connections,” he said.
Still, he said, with the passage of time — and when exacerbated by other factors, such as normal neuron death as we age and plaque and tangle development in the early stages of Alzheimer’s — reduced myelin integrity could contribute to cognitive impairment.
“So it’s unlikely we are seeing the earliest possible signs of Alzheimer’s-associated brain changes in these young people,” Thompson said. “It’s more likely the reduced fiber integrity represents an early developmental vulnerability that may reduce brain resilience to later Alzheimer’s disease pathology.”
Knowing that an individual is at a genetic risk for Alzheimer’s is important for evaluating treatment and prevention strategies.
“We know that many lifestyle factors, such as regular exercise and a healthful diet, may reduce the risk of cognitive decline, particularly in those genetically at risk for Alzheimer’s, so this reminds us how important that is,” he said.

Maintain your brain

The average weight of the adult brain is three pounds, about the size of a medium head of cauliflower. But the value of the brain's amazing capabilities lies in the billions of neurons (brain cells) and the trillion synapses, which are the connections that occur between those neurons. The complexity of the human brain surpasses the most sophisticated computer.
Eighty to ninety percent of the physical growth of the human brain takes place by the age of three years old. The brain size continues to grow up into the twenties. After that adults begin to lose brain cells.
On a positive note research proves that the adult brain contains cells capable of dividing and building healthy new neurons. There are many things that adults can do to stimulate those brain cells and form new connections to kept the brain waves active.
People who engage in intellectually stimulating activities can sharpen their mental acuity and maintain it well into old age.
Three factors have been indentified as reasons some people have lifeline long mental sharpness.
Education seems to be formost in stimulating brain cell growth. Learning a new skill as you age keeps the brain challenged and active. Reading, traveling, playing word games and other mentally challenging activities throughout life is very beneficial.
Physical activity is very important for all parts of your body including the brain! The brain requires more oxygen than any other organ. It uses about 25 percent of all the oxygen taken in by the lungs. Regular physical activity provides the supply of oxygen-laden blood the brain needs.
Your emotional well-being is the third major factor which has been identified as a reason people maintain mental sharpness. Having a strong sense of purpose and meaning in life seems to be a key characteristic of people who thrive in their later years.
Contact with family and friends, community activities, good general health and relative financial comfort are helpful.
Eating a well balanced diet and drinking plenty of fluids to keep the body hydrated helps to keep the brain cells healthy and functioning well.
Get plenty of sleep to help brain functioning. Go easy on the amount of food eaten after dinner and avoid alcohol and caffeine before going to sleep. And going to bed at the same time every night will be helpful.
Understand what causes stress and eliminate or modify stressful situations in your life.
Try to do things that promote inner peace for you.
Keep a positive attitude and add humor to your life. Humor relives tension. Some experts say laughing is like jogging on the inside. A thankful attitude encourages physical, mental and spiritual well-being.
Just as physical activity keeps the body strong, mental activity keeps the mind sharp and agile. Regardless of age, an active brain can produce new neurons and connections that aid you in maintaining your brain capacity.

HP moves closer to brain-like computing

Researchers at Hewlett Packard and UC Santa Barbara say they've made a breakthrough in the development of a device that could revolutionize computing by mimicking the brain.

It's thought that memristors, which have the ability to 'remember' the total electronic charge that passes through them, will be able to act like synapses within electronic circuits - mimicking the brain's network of neurons,  which enables perception, thought and memory. They are believed to hold promise for a wide range of applications, including semi-autonomous robots.
Memristors are seen as a basic component of electronics, alongside resistors, capacitors and inductors, and have been suggested as a replacement for Flash and DRAM memory.
But while they have been created in the lab, scientists didn't fully understand their bahavior.
Now, though, a team has mapped out the nanoscale physical and chemical properties of memristors. They were able to study the exact channel where the resistance switching of memristors occurs through a combination of techniques.
Highly focused X-rays were used to locate and image the approximately one hundred nanometer-wide channel where the switching of resistance takes place, which could then be fed into a mathematical model of how the memristor heats up.
"One of the biggest hurdles in using these devices is understanding how they work: the microscopic picture for how they undergo such tremendous and reversible change in resistance," says John Paul Strachan of the nano Electronics Research Group at Hewlett-Packard Labs.
"We now have a direct picture for the thermal profile that is highly localized around this channel during electrical operation, and is likely to play a large role in accelerating the physics driving the memristive behavior."

Researchers say math anxiety starts young, has wide-reaching implications for performance

CHICAGO — Math problems make more than a few students — and even teachers — sweat, but new brain research is providing insights into the earliest causes of the anxiety so often associated with mathematics.
Experts argue that “math anxiety” can bring about widespread, intergenerational discomfort with the subject, which could lead to anything from fewer students pursuing math and science careers to less public interest in financial markets.
“People are very happy to say they don’t like math,” said Sian L. Beilock, a University of Chicago psychology professor and the author of “Choke,” a 2010 book on brain responses to performance pressure. “No one walks around bragging that they can’t read, but it’s perfectly socially acceptable to say you don’t like math.”
Mathematics anxiety is more than just disliking math, however; someone with math anxiety feels negative emotions when engaging in an activity that requires numerical or math skills. In one forthcoming study by Ms. Beilock, simply suggesting to college students that they would be asked to take a math test triggered a stress response in the hypothalamus of students with high math anxiety.
Ms. Beilock and other experts at a Learning and the Brain conference held here May 5-7 are searching for the earliest problems in a child’s math career that can grow into lifelong fears and difficulties. The conference, put on by the Needham, Mass.-based Public Information Resources, Inc., brought together several hundred educators and administrators with researchers in educational neuroscience and cognitive science.
Stress in the Brain
Anxiety has become a hot topic in education research, as educators and policymakers become increasingly focused on test performance and more-intensive curricula, and neuroscience has begun to provide a window into how the brain responds to anxiety.
Anxiety can literally cut off the working memory needed to learn and solve problems, according to Dr. Judy Willis, a Santa Barbara, Calif.-based neurologist, former middle school teacher, and author of the 2010 book “Learning to Love Math.”
When first taking in a problem, a student processes information through the amygdala, the brain’s emotional center, which then prioritizes information going to the prefrontal cortex, the part responsible for the brain’s working memory and critical thinking. During stress, there is more activity in the amygdala than the prefrontal cortex; even as minor a stressor as seeing a frowning face before answering a question can decrease a student’s ability to remember and respond accurately.
“When engaged in mathematical problem-solving, highly math-anxious individuals suffer from intrusive thoughts and ruminations,” said Daniel Ansari, the principal investigator for the Numerical Cognition Laboratory at the University of Western Ontario, in London, Ontario. “This takes up some of their processing and working memory. It’s very much as though individuals with math anxiety use up the brainpower they need for the problem” on worrying.