Our belief in the motto ‘good things come to those who wait’ stems from a brain circuit that tells us to refuse instant gratification, say researchers.
The study provides insight into the capacity for ‘mental time travel,’ also known as episodic future thought, that enables humans to make choices with high long-term benefits.
"Humans normally prefer larger over smaller rewards, but this situation can change when the larger rewards are associated with delays," explains lead study author, Dr. Jan Peters from the Department of Systems Neuroscience at the University Medical Center Hamburg-Eppendorf in Germany. "Although there is no doubt that humans discount the value of rewards over time, in general, individuals exhibit a particularly significant ability to delay gratification."
Several models have been proposed to explain the neural basis of assigning relative value to multiple rewards at different points in time (also known as ‘intertemporal decision making’) in humans. However, many questions remain unanswered, and the brain regions and mechanisms involved in this process are unclear. Dr. Peters, and coauthor Professor Christian Büchel, used functional magnetic resonance imaging (fMRI), neural coupling analyses, and extensive behavioral paradigms to examine the interactions between episodic future thought and intertemporal decision making.
Human subjects had to make a series of choices between smaller immediate and larger delayed rewards while brain activity was measured with fMRI. Importantly, in addition to this standard control condition, the participants were presented with ‘cues’ that referred to real subject-specific future events planned for the respective day of reward delivery. The researchers observed that the more the cues induced spontaneous episodic imagery, the more subjects changed their preferences toward patient, future-minded choice behavior.
Further, the neuroimaging data revealed that signals in the anterior cingulate cortex (ACC), a part of the brain implicated in reward-based decision making, and functional coupling of this region with the hippocampus, linked with imagining the future, predicted the degree to which forward thinking modulated individual preference functions.
"Taken together, our results reveal that vividly imagining the future reduced impulsive choice," concludes Dr. Peters. "Our data suggest that the ACC, based on episodic predictions involving the hippocampus, supports the dynamic adjustment of preference functions that enable us to make choices that maximize future payoffs."
The study by the Department of Systems Neuroscience at the University Medical Center , Hamburg-Eppendorf, is published in the journal Neuron this month.
Thursday, April 15, 2010
Why can't we trust what we see?
The human memory can be impressive, but it is equally prone to letting us down. Now groundbreaking research has revealed the extent of just how fragile it can be - and how to use it better.
You're in the pub and trouble starts. There is shouting, someone is stabbed, they die. It happened right in front of your eyes and the police want to speak to you. But what exactly did you see? It's long been accepted that eyewitness testimony may not always be as reliable as it seems. The problem is people simply don't remember exactly what happened, say psychologists. The mind does not work like a video camera, nowhere in the brain is the perfect memory of everything that has been seen, in the order it happened.
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Now research has gone further than ever before to understand the fragile nature of our powers of recall.
The project - involving the Open University, the BBC and Greater Manchester Police (GMP) - is groundbreaking in several ways. The technology it used is cutting edge, including eye trackers - devices for measuring eye positions and eye movement. But just as unparalleled was the realism involved. It's always a big issue with research - how do you accurately test someone's everyday reactions when they know they are part of an experiment and in controlled conditions? Won't they try harder to remember details if they know they are doing a memory test?
'Appalling'
In this case the important action took place when they were least expecting it. The 10 volunteers were put through days of memory tests in a studio and assumed this was the research. In fact, two intricately planned and elaborate mock crimes - a fatal stabbing and an armed robbery - were really what mattered.
On one day the participants went for lunch in a local pub, which was really filled with actors, stuntmen and 10 hidden cameras. A fight broke out and someone appeared to be stabbed and killed. The whole scenario unfolded over 20 minutes.
| Eyewitness Simon Woodthorpe  The whole experience really surprised me. I'd never had a problem with my memory before but had never been in a situation where I'd been asked to recall things in that much detail. I was good at describing the overall situation. But when it came to the real detail of what had happened, I was actually creating a lot of what I thought I'd remembered. I'm not sure I would be confident about saying I'd seen anything after this. I'd be worried about incriminating someone. |
"I always thought I had a good memory, but I was yards away from the incident, saw it all unfold and still got the murderer wrong. I said it was the wrong man."
What was also unprecedented about the project was the access to interviewing techniques used by GMP. Detectives treated each mock crime as if it were real, interviewing the volunteers, but unlike a real case, what they said could be checked against what exactly went on.
During the drama the eye trackers - still being worn by some volunteers during the mock robbery - were able to pinpoint exactly what people were looking at and compared to what they reported. The differences, say those involved, were in some cases staggering.
'Lifeblood'
"One person thought they hadn't seen the crime being committed, they were adamant about it," says Dr Graham Pike, a memory expert involved in the project. "When we reviewed the eye tracker we found they'd actually spent almost the entire time looking at it unfold. It was quite amazing."
| FIND OUT MORE Episode one of the three-part Eyewitness is broadcast on BBC Two beginning on Sunday 18 April at 2250 BST Or listen here later |
"It's not like inputting data into a computer, the mind does not store facts absolutely the way they are and it does not recall them absolutely accurately either."
There are three stages in memory, according to modern pyschology. The first is perception, which is what we see - also what we hear, taste, touch and smell. This in itself is a selective process. From the start we can fail to encode detail or simply not notice something, so the information going in isn't accurate. Secondly there's storage. We know we forget things over time, but we also revise our memories and re-write them to fit in with new ideas.
Finally there's the retrieval stage, where the brain searches out information. When you remember something, lots of different parts of the brain work together and from that emerges the mental representation that is going to be your experience of a memory. Every time you recall something, you reinterpret it all over again. And in every reconstruction process there are many opportunities for error.
'Empty the head'
In a crime situation memory is influenced by many factors such as stress, the presence of a weapon and even just the desire to help police solve the crime.
"Police know how fallible the memory can be," says Steve Retford, a former head of the investigative skills unit at GMP and now specialist interviewing adviser with the force.
"They also know this is usually not through mischievousness on the part of the witnesses, but through stress and shock."
Take the case of Jean Charles de Menezes, shot at Stockwell Tube station in 2005 by police who mistook him for a suicide bomber. Eyewitnesses said he had vaulted a ticket barrier when running away from the police. In fact it was later shown by CCTV that Mr Menezes had walked through the barriers, having picked up a free newspaper, and only ran when he saw his train arriving.
 Memories are reconstructed unconsciously |
What this latest research has proved is the extent of how fallible the memory can be, which is "massively important", say those involved.
"That the memory is vulnerable is not new," says Dr Pike. "But it is so important that we know how fallible it is and in what ways. By understanding this better we can design police techniques that make the most of memory."
For the police, the findings of the project are essential because eyewitnesses are still at the heart of most investigations - even with the growth of CCTV.
"Eyewitnesses are our lifeblood and without them you are usually stuffed," says Mr Retford. "Creating the right environment and using the correct psychological tools to get accurate evidence is vital. You have to be on top of your game and really empty the head of all the detail you need."
Scientists, Creationists Agree: 'Sediba' is No 'Missing Link'
Two fossils that were discovered in South Africa nearly two years ago are causing a stir today after two articles published recently in the journal Science introduced them as members of a new species that “might help reveal the ancestor” of the genus Homo.
While some – mostly media – have been quick to hail the species as the “missing link,” many more have cast their doubts over the discovery, which some say might not even be a new species.
Some critics further say the find expands the cloud of uncertainty rather than “cast new light,” as Science claimed in its introduction of the papers.
"The origins of the genus Homo remain as murky as ever," commented Dr. Daniel E. Lieberman, professor of Human Evolutionary Biology at Harvard.
“[T]he situation seems to grow more convoluted with each newly unearthed specimen,” added Brian Thomas of the anti-evolution Institute for Creation Research.
As for the authors of the two papers, neither claim the new species, Australopithecus sediba, to be a direct ancestor of modern humans. They, like many in the science community, reject the term "missing link" as it implies a chain in evolution rather than the more widely accepted tree model.
But they do claim that “Sediba” shares more derived features with early Homo species than any other australopith species and thus might help reveal the ancestor of that genus.
"They (the fossils), ladies and gentlemen, are potentially a Rosetta stone into the past," paleo-anthropologist Lee R. Berger of South Africa’s University of Witwatersrand told reporters during a press conference last Thursday.
It was Berger’s then-nine-year-old son, Matthew, who first stumbled upon a piece of the first skeleton while playing with his dog in the Cradle of Humankind World Heritage Site in South Africa.
Matthew’s find led Berger and his team to uncover the rest of the skeleton and another nearby, giving them two skeletons “far more complete than the famous Lucy fossil from Ethiopia" and in "extraordinary condition," according to Berger.
"What we have found are arguably the most complete early hominid skeletons ever discovered,” he reported.
Amid all the hype, anti-evolution groups are largely, and not surprisingly, unfazed.
“This fossil has been surrounded by the standard overhype we've come to expect from those on a campaign to evangelize for Darwin,” commented Casey Luskin of the Discovery Institute.
Furthermore, they have on their side skeptical members of the science community who are just as critical of the conclusions drawn so far – particularly those of the press – as they are.
“[T]he bones have been examined by only one group of scientists, and their interpretation may be challenged dramatically as time passes,” stated apologetics ministry Answers in Genesis, recalling how the “missing link” hype over the fossil “Ida” last year “quickly evaporated.”
“The persistent admission of overall confusion about human evolution … is the real story, tucked beneath the fanfare,” added Thomas from the Institute of Creation Research.
“[T]he fine print in the actual scientific studies reveals that each discovery only adds another layer of confusion and forces another rewrite of evolutionary history,” he stated.
Presently, Berger's team of researchers are looking to see if any proteins are preserved in one of the skeletons, which they suspect might contain the remnant of the dried brain.
If the brain yields soft tissue, there is a slim chance the researchers could yield DNA that might unlock the genetic code for Sediba.
"We shall wait and see," said Berger.
The lead scientist said the newly described fossils date between 1.95 million and 1.78 million years in age.
While some – mostly media – have been quick to hail the species as the “missing link,” many more have cast their doubts over the discovery, which some say might not even be a new species.
Some critics further say the find expands the cloud of uncertainty rather than “cast new light,” as Science claimed in its introduction of the papers.
"The origins of the genus Homo remain as murky as ever," commented Dr. Daniel E. Lieberman, professor of Human Evolutionary Biology at Harvard.
“[T]he situation seems to grow more convoluted with each newly unearthed specimen,” added Brian Thomas of the anti-evolution Institute for Creation Research.
As for the authors of the two papers, neither claim the new species, Australopithecus sediba, to be a direct ancestor of modern humans. They, like many in the science community, reject the term "missing link" as it implies a chain in evolution rather than the more widely accepted tree model.
But they do claim that “Sediba” shares more derived features with early Homo species than any other australopith species and thus might help reveal the ancestor of that genus.
"They (the fossils), ladies and gentlemen, are potentially a Rosetta stone into the past," paleo-anthropologist Lee R. Berger of South Africa’s University of Witwatersrand told reporters during a press conference last Thursday.
It was Berger’s then-nine-year-old son, Matthew, who first stumbled upon a piece of the first skeleton while playing with his dog in the Cradle of Humankind World Heritage Site in South Africa.
Matthew’s find led Berger and his team to uncover the rest of the skeleton and another nearby, giving them two skeletons “far more complete than the famous Lucy fossil from Ethiopia" and in "extraordinary condition," according to Berger.
"What we have found are arguably the most complete early hominid skeletons ever discovered,” he reported.
Amid all the hype, anti-evolution groups are largely, and not surprisingly, unfazed.
“This fossil has been surrounded by the standard overhype we've come to expect from those on a campaign to evangelize for Darwin,” commented Casey Luskin of the Discovery Institute.
Furthermore, they have on their side skeptical members of the science community who are just as critical of the conclusions drawn so far – particularly those of the press – as they are.
“[T]he bones have been examined by only one group of scientists, and their interpretation may be challenged dramatically as time passes,” stated apologetics ministry Answers in Genesis, recalling how the “missing link” hype over the fossil “Ida” last year “quickly evaporated.”
“The persistent admission of overall confusion about human evolution … is the real story, tucked beneath the fanfare,” added Thomas from the Institute of Creation Research.
“[T]he fine print in the actual scientific studies reveals that each discovery only adds another layer of confusion and forces another rewrite of evolutionary history,” he stated.
Presently, Berger's team of researchers are looking to see if any proteins are preserved in one of the skeletons, which they suspect might contain the remnant of the dried brain.
If the brain yields soft tissue, there is a slim chance the researchers could yield DNA that might unlock the genetic code for Sediba.
"We shall wait and see," said Berger.
The lead scientist said the newly described fossils date between 1.95 million and 1.78 million years in age.
It's hard to cope with Alzheimer's
Alzheimer's is a most hideous disease, shocking to the moral sense with memory loss also associated with brain damage. One can look up the word Alzheimer's in the dictionary, but words are not enough to explain the disease. One must live with an Alzheimer's person. Notice I didn't say "patient," but "person," as most times the person who is suffering with the disease is hardly treated as a patient, but as someone to avoid.
It's hard to get help and understanding for the caretaker of an Alzheimer's person. One mostly gets "Tsk, tsk." That's as far as their sense of recognition really goes. "Love they neighbor as thyself" is mighty hard when your neighbor has to deal with living and living as an Alzheimer's person.
Try living with someone who is combative most of the time, and you never know when they're in their worst mood. Smile one second and cry the next, or sweet-talk to screaming. You must be very rich or to the point of being broke before there is any help for an Alzheimer's person to be looked upon as an "Alzheimer's patient." Where does one turn? Who cares? "Love thy neighbor" — oh, but you mean when all is going well.
Your neighbor is someone who sits next to you in church, rides with you on the bus taking you all to wherever. But people say, "Don't sit next to so-and-so, they're sort of different." The word is hard to say, but love and hate are so much alike as you're either judged by others in the blink of an eye.
God loves us no matter. We, the people, need others to find a way to love the "unlovable."
It's hard to get help and understanding for the caretaker of an Alzheimer's person. One mostly gets "Tsk, tsk." That's as far as their sense of recognition really goes. "Love they neighbor as thyself" is mighty hard when your neighbor has to deal with living and living as an Alzheimer's person.
Try living with someone who is combative most of the time, and you never know when they're in their worst mood. Smile one second and cry the next, or sweet-talk to screaming. You must be very rich or to the point of being broke before there is any help for an Alzheimer's person to be looked upon as an "Alzheimer's patient." Where does one turn? Who cares? "Love thy neighbor" — oh, but you mean when all is going well.
Your neighbor is someone who sits next to you in church, rides with you on the bus taking you all to wherever. But people say, "Don't sit next to so-and-so, they're sort of different." The word is hard to say, but love and hate are so much alike as you're either judged by others in the blink of an eye.
God loves us no matter. We, the people, need others to find a way to love the "unlovable."
Fish Feeds Your Brain
Why the secret to longevity might be found in pickled herring
Excerpted from Prevention's Brainpower Game Plan book by Cynthia R. Green, Ph.D., and the Editors of Prevention
At age 115, Henrikje van Andel-Schipper was the oldest person in the world at
the time of her death in 2005. Scientists who interviewed the Dutch woman say she remained sharp-witted and just plain witty until her last days. Her secret? When asked, van Andel-Schipper quipped, “Pickled herring.” Then again, maybe she wasn’t joking. Eating plenty of fish and shellfish can help keep your mind in top form and lower your risk of dementia, multiple studies suggest.
What’s so magical about seafood? Most scientists believe it’s the dose of omega-3 fatty acids you get with every bite of tuna or trout. Omega-3 fatty acids are powerful and versatile nutrients. Your body needs fatty acids of all different types, from various foods. One of the most important jobs for fatty acids is forming cell membranes. About 40 percent of the fatty acids in brain cell membranes are docosahexaenoic acid, or DHA, which is one of the main omega-3 fatty acids in fish oil. Experts believe that DHA is probably necessary for transmitting signals between brain cells. Another omega-3, known as eicosapentaenoic acid, or EPA, appears to be important for brain health, too.
Better performance and long-term brain health
Some research hints that enjoying regular servings of broiled salmon or baked haddock may make your brain work more efficiently. In a 2007 study, researchers at Wageningen University in the Netherlands analyzed blood samples from 807 men and women over 50 and found that those with the highest levels of omega-3 fatty acids scored 60 percent to 70 percent better on tests that measured reaction time and speed of processing complex information than people who had low omega-3 levels. Other research suggests that eating fish helps bolster your defense shield against dementia. In a 2006 study involving 899 men and women, researchers at Tufts University found that people who ate fish three times a week and had the highest levels of DHA in their blood slashed their risk of Alzheimer’s disease by 39 percent and other forms
of dementia by 47 percent.
Fish has another important benefit for the brain: it helps prevent strokes. In a 2002 study in the Journal of the American Medical Association (JAMA), researchers studied more than 43,000 men and found that those who ate fish one to three times per month were about half as likely to suffer these potentially devastating “brain attacks” as those who rarely ate fish. Massive strokes can be fatal or leave victims paralyzed or plagued by other severe side effects. However, even “silent strokes”—which may occur unnoticed, without producing obvious symptoms—can cause cognitive problems, including memory loss. As many as one in 10 middle-aged adults has suffered a silent stroke and doesn’t know it.
Studies show that silent strokes more than double the risk of developing dementia. Scientists have made some other discoveries that make the case for eating fish even more compelling. For example, lab rats fed diets rich in omega-3 fatty acids learn more quickly and have better memories than those fed diets high in unhealthy fats and sugar. Studies also show that feeding omega-3s to lab animals increases levels of BDNF, a protein that is needed for the growth and survival of brain cells. Other studies hint that DHA helps brain cells produce energy more efficiently and prevents the formation of cell damage called oxidative stress (which you’ll read more about soon).
Eating seafood regularly will do much more than boost your Brain IQ, of course. After all, studies show that people who eat fish just once a week cut in half the risk of sudden cardiac death, which kills more than 300,000 Americans each year. Eating fish also lowers levels of artery-clogging blood fats called triglycerides and confers a slight drop in blood pressure. Those changes alone could reduce your risk of heart disease and other conditions—including dementia—later in life. As the nutritional benefits of omega-3s have become better known, it’s no wonder that consumption of fish and shellfish has soared 30 percent in the United States over the past generation. However, many people still don’t consume adequate levels of omega-3s. People often ask me if it’s true that fish is “brain food,” like their grandmothers told them. As you can see, the research offers powerful evidence that your grandma was right: eating fish really does seem to be good for the brain. The Brainpower Game Plan gives you plenty of ideas for including this nutritional powerhouse in your weekly meal plan.
Seafood and your mood
Eating fish may be good for your emotional health, too. Several studies have shown that depression rates tend to be low in countries where seafood is a popular menu item. For instance, depression is relatively rare in Iceland, where consumption of seafood is five times higher than in the United States or Canada. Mounting research suggests that fish oil may play a role in combating the blues. For example, University of Pittsburgh researchers showed in a 2007 study that people with the highest blood levels of omega-3 fatty acids were significantly less likely than people with low levels to say they felt mildly or moderately depressed.
Fish benefits for fish haters
Some people who don’t like fish but want to enjoy the brain boost and other health benefits of fish oil turn to other food sources of omega-3 fatty acids, which include flaxseed, walnuts, canola oil, and soybeans. Or they shop for “functional” foods, such as eggs, mayonnaise, breakfast cereal, and others that contain added omega-3 fatty acids. Sounds like a great alternative, but unfortunately, most of those foods do not contain the same omega-3s you get from fish oil, which are known as DHA and EPA. Some of the eggs, mayo, and other food products at your local grocer that are enriched with omega-3s contain a form called alpha-linolenic acid (ALA). That’s the same form found in flaxseed and other non-marine sources.
While nutrition scientists sing the praises of DHA and EPA, far less is known about the health benefits of ALA. Your body does convert ALA to DHA and EPA, but the process is not efficient. Lab studies show that only a small fraction of the ALA you consume ends up as DHA and EPA. (Note to vegetarians: DHA is also found in algae supplements.) Some food products promoted as good sources of omega-3s do contain added DHA and EPA, but usually very little. For instance, according to the Center for Science in the Public Interest (a consumer health watchdog group), a 6-ounce serving of Atlantic salmon has about 100 times more DHA and EPA than a serving of DHA-fortified yogurt or milk. Likewise, one popular brand of yogurt boasts of offering 32 milligrams of DHA per serving. Yet that’s the amount you would get from a small bite of salmon. Including flaxseed, walnuts, canola oil, soybeans, and other sources of ALA in your diet remains a great idea, since they offer other important health benefits. Just keep in mind that eating those foods probably won’t significantly increase your blood levels of DHA and EPA. Eating fish (or taking fish oil supplements) remains the best way to get your dose of omega-3s.
More on Increasing Your Brainpower:
* The Pleasure Principal: Why a Little Indulgence Won’t Hurt Your Health
* Trim Down to Smarten Up
* Best Foods For Focus
* Video: Simple Forgetfulness or Something Serious?
* Purchase the Brainpower Game Plan
Excerpted from Prevention's Brainpower Game Plan book by Cynthia R. Green, Ph.D., and the Editors of Prevention
At age 115, Henrikje van Andel-Schipper was the oldest person in the world at
the time of her death in 2005. Scientists who interviewed the Dutch woman say she remained sharp-witted and just plain witty until her last days. Her secret? When asked, van Andel-Schipper quipped, “Pickled herring.” Then again, maybe she wasn’t joking. Eating plenty of fish and shellfish can help keep your mind in top form and lower your risk of dementia, multiple studies suggest.
What’s so magical about seafood? Most scientists believe it’s the dose of omega-3 fatty acids you get with every bite of tuna or trout. Omega-3 fatty acids are powerful and versatile nutrients. Your body needs fatty acids of all different types, from various foods. One of the most important jobs for fatty acids is forming cell membranes. About 40 percent of the fatty acids in brain cell membranes are docosahexaenoic acid, or DHA, which is one of the main omega-3 fatty acids in fish oil. Experts believe that DHA is probably necessary for transmitting signals between brain cells. Another omega-3, known as eicosapentaenoic acid, or EPA, appears to be important for brain health, too.
Better performance and long-term brain health
Some research hints that enjoying regular servings of broiled salmon or baked haddock may make your brain work more efficiently. In a 2007 study, researchers at Wageningen University in the Netherlands analyzed blood samples from 807 men and women over 50 and found that those with the highest levels of omega-3 fatty acids scored 60 percent to 70 percent better on tests that measured reaction time and speed of processing complex information than people who had low omega-3 levels. Other research suggests that eating fish helps bolster your defense shield against dementia. In a 2006 study involving 899 men and women, researchers at Tufts University found that people who ate fish three times a week and had the highest levels of DHA in their blood slashed their risk of Alzheimer’s disease by 39 percent and other forms
of dementia by 47 percent.
Fish has another important benefit for the brain: it helps prevent strokes. In a 2002 study in the Journal of the American Medical Association (JAMA), researchers studied more than 43,000 men and found that those who ate fish one to three times per month were about half as likely to suffer these potentially devastating “brain attacks” as those who rarely ate fish. Massive strokes can be fatal or leave victims paralyzed or plagued by other severe side effects. However, even “silent strokes”—which may occur unnoticed, without producing obvious symptoms—can cause cognitive problems, including memory loss. As many as one in 10 middle-aged adults has suffered a silent stroke and doesn’t know it.
Studies show that silent strokes more than double the risk of developing dementia. Scientists have made some other discoveries that make the case for eating fish even more compelling. For example, lab rats fed diets rich in omega-3 fatty acids learn more quickly and have better memories than those fed diets high in unhealthy fats and sugar. Studies also show that feeding omega-3s to lab animals increases levels of BDNF, a protein that is needed for the growth and survival of brain cells. Other studies hint that DHA helps brain cells produce energy more efficiently and prevents the formation of cell damage called oxidative stress (which you’ll read more about soon).
Eating seafood regularly will do much more than boost your Brain IQ, of course. After all, studies show that people who eat fish just once a week cut in half the risk of sudden cardiac death, which kills more than 300,000 Americans each year. Eating fish also lowers levels of artery-clogging blood fats called triglycerides and confers a slight drop in blood pressure. Those changes alone could reduce your risk of heart disease and other conditions—including dementia—later in life. As the nutritional benefits of omega-3s have become better known, it’s no wonder that consumption of fish and shellfish has soared 30 percent in the United States over the past generation. However, many people still don’t consume adequate levels of omega-3s. People often ask me if it’s true that fish is “brain food,” like their grandmothers told them. As you can see, the research offers powerful evidence that your grandma was right: eating fish really does seem to be good for the brain. The Brainpower Game Plan gives you plenty of ideas for including this nutritional powerhouse in your weekly meal plan.
Seafood and your mood
Eating fish may be good for your emotional health, too. Several studies have shown that depression rates tend to be low in countries where seafood is a popular menu item. For instance, depression is relatively rare in Iceland, where consumption of seafood is five times higher than in the United States or Canada. Mounting research suggests that fish oil may play a role in combating the blues. For example, University of Pittsburgh researchers showed in a 2007 study that people with the highest blood levels of omega-3 fatty acids were significantly less likely than people with low levels to say they felt mildly or moderately depressed.
Fish benefits for fish haters
Some people who don’t like fish but want to enjoy the brain boost and other health benefits of fish oil turn to other food sources of omega-3 fatty acids, which include flaxseed, walnuts, canola oil, and soybeans. Or they shop for “functional” foods, such as eggs, mayonnaise, breakfast cereal, and others that contain added omega-3 fatty acids. Sounds like a great alternative, but unfortunately, most of those foods do not contain the same omega-3s you get from fish oil, which are known as DHA and EPA. Some of the eggs, mayo, and other food products at your local grocer that are enriched with omega-3s contain a form called alpha-linolenic acid (ALA). That’s the same form found in flaxseed and other non-marine sources.
While nutrition scientists sing the praises of DHA and EPA, far less is known about the health benefits of ALA. Your body does convert ALA to DHA and EPA, but the process is not efficient. Lab studies show that only a small fraction of the ALA you consume ends up as DHA and EPA. (Note to vegetarians: DHA is also found in algae supplements.) Some food products promoted as good sources of omega-3s do contain added DHA and EPA, but usually very little. For instance, according to the Center for Science in the Public Interest (a consumer health watchdog group), a 6-ounce serving of Atlantic salmon has about 100 times more DHA and EPA than a serving of DHA-fortified yogurt or milk. Likewise, one popular brand of yogurt boasts of offering 32 milligrams of DHA per serving. Yet that’s the amount you would get from a small bite of salmon. Including flaxseed, walnuts, canola oil, soybeans, and other sources of ALA in your diet remains a great idea, since they offer other important health benefits. Just keep in mind that eating those foods probably won’t significantly increase your blood levels of DHA and EPA. Eating fish (or taking fish oil supplements) remains the best way to get your dose of omega-3s.
More on Increasing Your Brainpower:
* The Pleasure Principal: Why a Little Indulgence Won’t Hurt Your Health
* Trim Down to Smarten Up
* Best Foods For Focus
* Video: Simple Forgetfulness or Something Serious?
* Purchase the Brainpower Game Plan
Canadian researchers find brain link between anxiety and depression Read more: http://www.montrealgazette.com/health/Canadian+researchers+find+brain+link+between+anxiety+depression/2816873/story.html#ixzz0lAK849Hh
Various prescription medications are pictured in a file photo. By finding a link that can now be isolated and blocked by a small molecular inhibitor developed by Ferguson, doctors may be able to develop more successful medication for depression by treating anxiety.
OTTAWA – Scientists have always known that anxiety and depression were linked. They just couldn't prove it in the brain -- until now.
A discovery about the cellular link between anxiety and depression by Canadian university researchers may provide a better way to treat depression, a condition that affects as much as 20 per cent of this country's population.
"We hadn't known the mechanism by which these two things were physically related," said Stephen Ferguson, a researcher at Robarts Research Institute at the University of Western Ontario.
"Basically, what we're finding is that there's talk between these two receptor systems in the brain, and that if you activate the one receptor system the other becomes sensitized."
The findings, published in a study released Sunday in the journal Nature Neuroscience, also reveal a way to block this link in the brain and potentially reduce anxiety and improve the way depression is treated.
It all has to do with the receptor systems -- made up of proteins on brain cells, which react to neurotransmitters and are the target of depression medication because they are involved in perception and mood -- and the way they activate multiple brain functions.
By finding a link that can now be isolated and blocked by a small molecular inhibitor developed by Ferguson, doctors may be able to develop more successful medication for depression by treating anxiety.
"Most drugs that are used for the treatment of depression block everything the receptor does and what we're doing is blocking one single function, which may allow for the development of drugs with less side effects in the future," said Ferguson.
"If we can block this anxiety-related increase in depression by targeting just one cellular process that these receptors are activating, maybe we can leave other ones intact, reducing the intolerable side effects of these drugs," he said.
The research was conducted on mice and took about five years to complete. It also involved Ferguson's colleagues from the University of Western Ontario, where he teaches pharmacy and physiology, and others, including Carleton University neuroscience professor Hymie Anisman.
Anisman said anxiety is often a precursor to depression, or can make it worse. He said depression medication typically only works for about 60 per cent of patients.
"Now that we know where things are happening in the brain, now we can target these sites to develop treatments to ameliorate anxiety or depression in a way that's better than the ones that currently exist," said Anisman.
The study was funded in part by the Canadian Institutes of Health Research.
"We hadn't known the mechanism by which these two things were physically related," said Stephen Ferguson, a researcher at Robarts Research Institute at the University of Western Ontario.
"Basically, what we're finding is that there's talk between these two receptor systems in the brain, and that if you activate the one receptor system the other becomes sensitized."
The findings, published in a study released Sunday in the journal Nature Neuroscience, also reveal a way to block this link in the brain and potentially reduce anxiety and improve the way depression is treated.
It all has to do with the receptor systems -- made up of proteins on brain cells, which react to neurotransmitters and are the target of depression medication because they are involved in perception and mood -- and the way they activate multiple brain functions.
By finding a link that can now be isolated and blocked by a small molecular inhibitor developed by Ferguson, doctors may be able to develop more successful medication for depression by treating anxiety.
"Most drugs that are used for the treatment of depression block everything the receptor does and what we're doing is blocking one single function, which may allow for the development of drugs with less side effects in the future," said Ferguson.
"If we can block this anxiety-related increase in depression by targeting just one cellular process that these receptors are activating, maybe we can leave other ones intact, reducing the intolerable side effects of these drugs," he said.
The research was conducted on mice and took about five years to complete. It also involved Ferguson's colleagues from the University of Western Ontario, where he teaches pharmacy and physiology, and others, including Carleton University neuroscience professor Hymie Anisman.
Anisman said anxiety is often a precursor to depression, or can make it worse. He said depression medication typically only works for about 60 per cent of patients.
"Now that we know where things are happening in the brain, now we can target these sites to develop treatments to ameliorate anxiety or depression in a way that's better than the ones that currently exist," said Anisman.
The study was funded in part by the Canadian Institutes of Health Research.
A More Accurate Picture Of The Autistic Brain Provided By Dual Approach
A new study, the first of its kind, combines two complementary analytical brain imaging techniques, to provide a more comprehensive and accurate picture of the neuroanatomy of the autistic brain. The study, published in the April issue of neuroimaging journal Human Brain Mapping, was conducted by researchers at The Montreal Neurological Institute and Hospital - The Neuro, McGill University and the Universite de Montreal. The findings provide critical insight into autism and possible markers for the disease for use in early therapy and therapeutic strategies.
Autism is a complex spectrum disorder thought to affect 1 in 166 people. Autistic individuals have difficulties with social interaction, communication and repetitive behaviours, which can lead to isolation and emotional problems. They may also have enhanced abilities particularly in auditory and visual perception.
Although structural brain differences have been reported in autism, the reports are inconsistent. The Neuro research team's objective therefore was to investigate neuroanatomical differences using a dual-analytic approach, combining cortical thickness analysis (CT) and voxel-based morphometry (VBM) together for the first time in the same participants. The team studied a group of young adults with autism of average intelligence and similar language ability relative to closely matched typically developing controls.
"The findings are significant from a functional perspective because the anatomical differences are found in brain regions known to play a functional role in the core features of autism such as social communication and repetitive behaviours, says Dr. Krista Hyde, research fellow with Dr. Alan Evans at The Neuro, and lead investigator in the study. "This is the first step to looking for clues or markers that would help us correlate structural differences with functional and behavioural characteristics."
The advantage in analyzing brain anatomy using CT and VBM is the complementary nature of the two methods, which in combination provide a direct measure of cortical grey matter, regions of the brain that consist primarily of nerve cell bodies. The combined method also provides a measure of subcortical grey matter as well as white matter, regions of the brain composed mainly of nerve cell fibres which have myelin sheaths, the protective covering that insulates and supports nerve cells. "The converging results found from CT and VBM analysis, allows us to make more confident interpretations about the structural brain differences found in autism," adds Dr. Hyde.
Regional differences in grey matter were found in socially-relevant and communication-related brain areas, as well as in areas implicated in repetitive behaviours and those found to play a role in empathic behavior. The study also identifies grey matter increases in autism in the visual cortex and for the first time, in the primary auditory cortex. "We believe that the visual and auditory cortical thickness increases may be related to enhanced visual and auditory perception in autism."
"These new results are extremely important because they offer a more accurate picture of the autistic brain, helping researchers improve early autism treatment strategies," says Dr. Anthony Phillips, Scientific Director of the Canadian Institutes of Health Research (CIHR) Institute of Neurosciences, Mental Health and Addiction. "Autism rates have been rising steadily in Canada, so CIHR is proud to support researchers who devote their time to look into this neurological condition."
The study's findings provide vital insight into autism by identifying structural differences in functionally relevant areas of the brain in a group of individuals with autism using a dual analytic approach for the first time.
The study was funded by The Canadian Institutes of Health Research.
Autism is a complex spectrum disorder thought to affect 1 in 166 people. Autistic individuals have difficulties with social interaction, communication and repetitive behaviours, which can lead to isolation and emotional problems. They may also have enhanced abilities particularly in auditory and visual perception.
Although structural brain differences have been reported in autism, the reports are inconsistent. The Neuro research team's objective therefore was to investigate neuroanatomical differences using a dual-analytic approach, combining cortical thickness analysis (CT) and voxel-based morphometry (VBM) together for the first time in the same participants. The team studied a group of young adults with autism of average intelligence and similar language ability relative to closely matched typically developing controls.
"The findings are significant from a functional perspective because the anatomical differences are found in brain regions known to play a functional role in the core features of autism such as social communication and repetitive behaviours, says Dr. Krista Hyde, research fellow with Dr. Alan Evans at The Neuro, and lead investigator in the study. "This is the first step to looking for clues or markers that would help us correlate structural differences with functional and behavioural characteristics."
The advantage in analyzing brain anatomy using CT and VBM is the complementary nature of the two methods, which in combination provide a direct measure of cortical grey matter, regions of the brain that consist primarily of nerve cell bodies. The combined method also provides a measure of subcortical grey matter as well as white matter, regions of the brain composed mainly of nerve cell fibres which have myelin sheaths, the protective covering that insulates and supports nerve cells. "The converging results found from CT and VBM analysis, allows us to make more confident interpretations about the structural brain differences found in autism," adds Dr. Hyde.
Regional differences in grey matter were found in socially-relevant and communication-related brain areas, as well as in areas implicated in repetitive behaviours and those found to play a role in empathic behavior. The study also identifies grey matter increases in autism in the visual cortex and for the first time, in the primary auditory cortex. "We believe that the visual and auditory cortical thickness increases may be related to enhanced visual and auditory perception in autism."
"These new results are extremely important because they offer a more accurate picture of the autistic brain, helping researchers improve early autism treatment strategies," says Dr. Anthony Phillips, Scientific Director of the Canadian Institutes of Health Research (CIHR) Institute of Neurosciences, Mental Health and Addiction. "Autism rates have been rising steadily in Canada, so CIHR is proud to support researchers who devote their time to look into this neurological condition."
The study's findings provide vital insight into autism by identifying structural differences in functionally relevant areas of the brain in a group of individuals with autism using a dual analytic approach for the first time.
The study was funded by The Canadian Institutes of Health Research.
Brain-Imaging Study Supports the Relevance of a Common Genetic Risk Factor for Alzheimer's Disease in Latinos
Research shows how brain imaging techniques can be used in healthy people to evaluate Alzheimer's disease risk factors
PHOENIX, April 14 /PRNewswire/ -- A brain-imaging study published today in the Archives of Neurology suggests that a major genetic risk factor for Alzheimer's disease in the Anglo population is also a risk factor for the disease in Latinos.While a gene called APOE4 has been firmly established to increase an Anglo person's risk of Alzheimer's disease, its relationship to the disease in different Latino populations has been less clear. In previous studies, researchers from the Banner Alzheimer's Institute and their collaborators in the Arizona Alzheimer's Consortium used a brain-imaging technique called PET to show that cognitively healthy late-middle-aged carriers of the APOE4 gene have lower activity than non-carriers of the gene in brain regions known to be affected by Alzheimer's disease.
In the present study, they extended their findings to 27 Latinos with and without the APOE4 gene, mostly from Arizona's Mexican-American community. As predicted, cognitively healthy Latinos in their 50s and 60s with the APOE4 gene had lower activity than non-carriers of the gene in brain regions known to be affected by Alzheimer's disease.
"This study provides support for the relationship between the APOE4 gene and the risk of Alzheimer's disease in Latinos," said Dr. Jessica Langbaum, staff scientist at the Banner Alzheimer's Institute and the study's lead author. "It also shows how brain imaging techniques can be used in healthy people to evaluate genetic and non-genetic risk factors for this disorder."
Latinos are about 1.5 times more likely than Anglos to develop Alzheimer's disease, according to the Alzheimer's Association. Alzheimer disease is the most common form of dementia. Between the years 2000 and 2050, the number of affected Latinos is projected to increase by 600 percent. Latinos may be at higher risk due to higher amounts of diabetes mellitus, obesity, cardiovascular disease and hypertension, each of which is also a risk factor for Alzheimer's disease.
The researchers have proposed using the same brain imaging techniques in healthy APOE4 carriers to evaluate promising treatments to prevent Alzheimer's disease without having to wait many years to determine whether they go on to develop symptoms. Among other things, the present study supports the inclusion of APOE4 carriers from Latino community in these studies.
About the study
The study was conducted by a team of researchers at Banner Alzheimer's Institute, Translational Genomics Research Institute (TGen), Arizona State University, Mayo Clinic Arizona, University of Arizona, University of California San Diego and the Arizona Alzheimer's Consortium.
The authors include Jessica B.S. Langbaum, PhD; Kewei Chen, PhD; Richard J. Caselli, MD; Wendy Lee, MS; Cole Reschke, BS; Daniel Bandy, MS; Gene E. Alexander, PhD; Christine M. Burns, BA; Alfred W. Kaszniak, PhD; Stephanie A. Reeder, BA; Jason J. Corneveaux, BS; April N. Allen, BS; Jeremy Pruzin, BS, BA; Matthew J. Huentelman, PhD; Adam S. Fleisher, MD; and Eric M. Reiman, MD.
The authors gratefully acknowledge support from National Institute of Mental Health grant R01MH57899 (Dr. Reiman), National Institute on Aging grants R01AG031581 and P30AG19610 (Dr. Reiman), the Evelyn G. McKnight Brain Institute (Dr. Alexander), the state of Arizona (Drs. Reiman, Caselli, Alexander, and Chen), and contributions from the Banner Alzheimer's Foundation and Mayo Clinic Foundation.
About Banner Alzheimer's Institute
Banner Alzheimer's Institute (BAI) is a treatment and research facility dedicated to helping patients with memory and thinking problems. It offers clinical care for patients; provides education, referral and support services for families and caregivers; and conducts leading-edge brain-imaging, clinical trials, brain imaging and genetics studies. The Institute is devoted to finding effective Alzheimer's disease-slowing and prevention treatments in the shortest time possible. BAI is owned and operated by Phoenix-based Banner Health, a nonprofit organization. For more information, visit www.banneralz.org.
About Mayo Clinic
Mayo Clinic is the first and largest integrated, not-for-profit group practice in the world. As a leading academic medical center in the Southwest, Mayo Clinic focuses on providing specialty and surgical care in more than 65 disciplines at its outpatient facility in north Scottsdale and at Mayo Clinic Hospital. The 244-licensed bed hospital is located at 56th Street and Mayo Boulevard (north of Bell Road) in northeast Phoenix, and provides inpatient care to support the medical and surgical specialties of the clinic, which is located at 134th Street and Shea Boulevard in Scottsdale.
About TGen
The Translational Genomics Research Institute (TGen), a nonprofit 501(c)(3) organization, is focused on developing earlier diagnostics and smarter treatments. Translational genomics research is a relatively new field employing innovative advances arising from the Human Genome Project and applying them to the development of diagnostics, prognostics and therapies for cancer, neurological disorders, diabetes and other complex diseases. TGen's research is based on personalized medicine and the institute plans to accomplish its goals through robust and disease-focused research.
About University of Arizona
The University of Arizona is one of the nation's leading public universities, with a long history of academic excellence, research innovation and a student-centered approach. A member of the prestigious Association of American Universities, the UA is ranked 13th among public universities by the National Science Foundation with total research expenditures last year of $530 million. With more than 38,000 students across three campuses representing 50 states and 124 nations, the UA is on the forefront of discoveries – from the depths of space to the medical and genetic mysteries of life, from emerging trends in climate change to the broad complexities of the human condition. For more information, visit www.arizona.edu
About Arizona State University
The Biodesign Institute at Arizona State University integrates diverse fields of science to cure and prevent disease, overcome the limitations of injury, renew the environment and improve national security. By fusing research in biology, engineering, medicine, physics, information technology and cognitive science, the institute accelerates discoveries into uses that can be adopted rapidly by the private sector. For more information, visit http://www.biodesign.asu.edu.
About Arizona Alzheimer's Consortium
The Arizona Alzheimer's Consortium (AAC) capitalizes on the complementary resources of its seven member institutions to promote the scientific understanding and early detection of Alzheimer's disease and find effective disease-stopping and prevention therapies. Established in 1998, the Consortium also seeks to educate Arizona's residents about Alzheimer's disease, research progress in the state and the resources needed to help patients, families, and professionals manage the disease. The AAC is comprised of both the NIA-funded Arizona Disease Core Center (ADCC) and the state-funded Arizona Alzheimer's Research Center (AARC). The AAC's member research institutions include Arizona State University, the Banner Alzheimer's Institute, the Barrow Neurological Institute, Mayo Clinic Arizona, Sun Health Research Institute, the Translational Genomics Research Institute (TGen) and the University of Arizona.
About National Institute on Aging
The NIA leads the federal government effort conducting and supporting research on the biomedical, social and behavioral issues of older people. For more information on aging-related research and the NIA, go to www.nia.nih.gov. The NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer's Disease Education and Referral (ADEAR) Center site at www.nia.nih.gov/Alzheimers.
Contact: | |
Banner Health | |
Brian Browne | |
(brian.browne@bannerhealth.com) | |
623-875-6536 | |
The Lavidge Company | |
Greg Sexton | |
(gsexton@lavidge.com) | |
490-998-2600 | |
Premier urged to release Hunter brain tumour info
The Opposition says the New South Wales Government has an obligation to release the information it has on health concerns in the Upper Hunter Valley.
The ABC's Four Corners program on Monday examined concerns that pollution from mines and power stations is leading to increasing levels of illness in the area. Five residents in a single block in Singleton have been diagnosed with brain tumours.
Premier Kristina Keneally has now promised an investigation into the cancer cases and says she has spoken to health officials.
But the opposition's health spokeswoman, Jillian Skinner, says the Government must tell the public what it knows already.
"I know the Government can report on the incidence of asthma, other chronic illnesses and diseases that cause death - of course they can," she said.
"They've got that information now, its partly reported through the Clinical Excellence Commission. They could publish much more but they've been slow to actually do anything."
NSW Chief Health Officer Kerry Chant says health officials have made contact with the families involved in the reported cluster.
Doctor Chant says while she did not know about the cases before, the department has already started work in the area and an investigation is underway.
"We've been pulling together, undertaking a detailed review of routinely collected data sets to map out the health status of the population in the Hunter-New England region and analyse that by sub-region," she said.
Man beating odds against terminal brain cancer
LOS ANGELES (KABC) -- Glioblastoma is a lethal cancer that starts in the brain and has no cure. Most patients survive about 15 months even with every form of conventional treatment.
But one man says he has been fortunate to find a way to survive and now his goal is to help others do the same. Inside a freezer at UCLA there is a brain tumor sample belonging to 40-year-old Bob Gibbs. Gibbs was diagnosed with glioblastoma in 2004.
Using human tissue, researchers created an experimental vaccine designed to keep Bob's cancer cells from growing back.
"Had I not had the vaccine and went with Standard of Care I don't' believe I would be here today," said Gibbs.
"The way we're approaching it is actually taking the patient's actual tumor tissue and generating the vaccine from that," said UCLA neurosurgeon Dr. Linda Liau.
Dr. Liau says Glioblastoma affects 20,000 Americans every year. It's the same type of cancer that killed Senator Ted Kennedy.
"We can't get to every little tumor cell. That's what makes these tumors difficult to treat and that is why they tend to come back," said Dr. Liau.
Doctors say patients diagnosed with glioblastoma survive about 15 months to two years, and that's with surgery, chemotherapy and radiation. With Dr. Liau's vaccine the survival rate is much longer. Forty-percent of patients survive three years and five percent survive six years.
Bob Gibbs is a seven-year survivor and he's working hard to make sure there are more patients like him. He and his wife started the group Miles for Hope. His sole goal is to raise money for research like Dr. Liau's vaccine and to spread awareness and hope.
"We think we're making a difference by promoting the vaccine, by raising awareness of the vaccine and the disease and by promoting treatments out there," said Gibbs.
A closer look at 1.9 million-year-old brain
It might just be a glimpse of what our ancestors' brains looked like 1.9-million years ago.
The brain, or an impression of it, was spotted in a high-definition scan conducted of the child skull of the newly discovered Australopithecus sediba.
Scientists at the European Synchrotron Radiation Facility in Grenoble, France, believe they have also found, deep in the skull cavity, fossilised insect eggs.
Last week scientists announced to the world a new species called A. sediba, which was found just outside Joburg, in the Cradle of Humankind.
Two individuals were found, a juvenile aged between nine and 13 and a woman, and some palaeoanthropologists believe that the species might be a direct ancestor of man.
"What we have got here is a possible brain impression, and it looks like shrunken brain" said Paul Tafforeau, a palaeoanthropologist at the European Synchrotron Radiation Facility.
What Tafforeau and his team did was conduct a high-quality scan of the juvenile skull, using X-rays generated by a synchrotron. They were able to get an image resolution far greater than more conventional X-ray machines.
The skull was taken to France in February, under tight security.
What caused the brain to shrink, believes Tafforeau, was mummification, which sits comfortably with the hypothesis put forward by Professor Lee Berger of Wits University and his team that the hominids, fell to their deaths down a sinkhole.
"Before fossilisation took place, the brain would have lost most of its water, causing it to shrink to a 20th of its size," explained Tafforeau. "Later, when the cadaver was immersed in water, sediment filled the brain cavity. This created a natural cast of the brain."
Tafforeau is cautious about the discovery and says further research still needs to be done.
If it proves to be the remnant of a brain, this will be the second time that this has been found in the fossil record.
The only other example of a fossilised brain was that of a 300 million-year-old fish.
But because of the shrinkage, Tafforeau believes they won't be able to find out much about the original structure of the brain.
What it would be important for, he explained, was in determining how the hominid was preserved after death.
Also providing clues to those first days after death are three insect eggs found inside the skull. The eggs could belong to a wasp and a fly. Two are open and one closed.
"What we need to establish is, are they fossilised eggs. It could be they are modern. The skull was exposed to the surface... But our preliminary examination suggests that the eggs are dense, which could mean that they are fossilised," Tafforeau said.
But it might take as long as a year for Tafforeau and the team to analyse the data and come to a conclusion.
The scan was also helpful in establishing the age of the juvenile hominid by analysing enamel build-up on the teeth.
"For the first time, what we have got here is the forensic analysis of a death of a hominid 1.9-million years ago," said Tafforeau.
The brain, or an impression of it, was spotted in a high-definition scan conducted of the child skull of the newly discovered Australopithecus sediba.
Scientists at the European Synchrotron Radiation Facility in Grenoble, France, believe they have also found, deep in the skull cavity, fossilised insect eggs.
Last week scientists announced to the world a new species called A. sediba, which was found just outside Joburg, in the Cradle of Humankind.
Two individuals were found, a juvenile aged between nine and 13 and a woman, and some palaeoanthropologists believe that the species might be a direct ancestor of man.
"What we have got here is a possible brain impression, and it looks like shrunken brain" said Paul Tafforeau, a palaeoanthropologist at the European Synchrotron Radiation Facility.
What Tafforeau and his team did was conduct a high-quality scan of the juvenile skull, using X-rays generated by a synchrotron. They were able to get an image resolution far greater than more conventional X-ray machines.
The skull was taken to France in February, under tight security.
What caused the brain to shrink, believes Tafforeau, was mummification, which sits comfortably with the hypothesis put forward by Professor Lee Berger of Wits University and his team that the hominids, fell to their deaths down a sinkhole.
"Before fossilisation took place, the brain would have lost most of its water, causing it to shrink to a 20th of its size," explained Tafforeau. "Later, when the cadaver was immersed in water, sediment filled the brain cavity. This created a natural cast of the brain."
Tafforeau is cautious about the discovery and says further research still needs to be done.
If it proves to be the remnant of a brain, this will be the second time that this has been found in the fossil record.
The only other example of a fossilised brain was that of a 300 million-year-old fish.
But because of the shrinkage, Tafforeau believes they won't be able to find out much about the original structure of the brain.
What it would be important for, he explained, was in determining how the hominid was preserved after death.
Also providing clues to those first days after death are three insect eggs found inside the skull. The eggs could belong to a wasp and a fly. Two are open and one closed.
"What we need to establish is, are they fossilised eggs. It could be they are modern. The skull was exposed to the surface... But our preliminary examination suggests that the eggs are dense, which could mean that they are fossilised," Tafforeau said.
But it might take as long as a year for Tafforeau and the team to analyse the data and come to a conclusion.
The scan was also helpful in establishing the age of the juvenile hominid by analysing enamel build-up on the teeth.
"For the first time, what we have got here is the forensic analysis of a death of a hominid 1.9-million years ago," said Tafforeau.
Brain regions play a fundamental role in empathetic and violent situations
"Just as our species could be considered the most violent, since we are capable of serial killings, genocide and other atrocities, we are also the most empathetic species, which would seem to be the other side of the coin", Luis Moya Albiol, lead author of the study and a researcher at the UV, tells SINC.
This study, published in the most recent issue of the Revista de Neurolog-a, concludes that the prefrontal and temporal cortex, the amygdala and other features of the limbic system (such as insulin and the cingulated cortex) play "a fundamental role in all situations in which empathy appears".
Moya Albiol says these parts of the brain overlap "in a surprising way" with those that regulate aggression and violence. As a result, the scientific team argues that the cerebral circuits - for both empathy and violence - could be "partially similar".
"We all know that encouraging empathy has an inhibiting effect on violence, but this may not only be a social question but also a biological one - stimulation of these neuronal circuits in one direction reduces their activity in the other", the researcher adds.
This means it is difficult for a "more empathetic" brain to behave in a violent way, at least on a regular basis. "Educating people to be empathetic could be an education for peace, bringing about a reduction in conflict and belligerent acts", the researcher concludes.
Techniques for measuring the human brain "in vivo", such as functional magnetic resonance imaging, are making it possible to find out more about the structures of the brain that regulate behaviour and psychological processes such as empathy.
This study, published in the most recent issue of the Revista de Neurolog-a, concludes that the prefrontal and temporal cortex, the amygdala and other features of the limbic system (such as insulin and the cingulated cortex) play "a fundamental role in all situations in which empathy appears".
Moya Albiol says these parts of the brain overlap "in a surprising way" with those that regulate aggression and violence. As a result, the scientific team argues that the cerebral circuits - for both empathy and violence - could be "partially similar".
"We all know that encouraging empathy has an inhibiting effect on violence, but this may not only be a social question but also a biological one - stimulation of these neuronal circuits in one direction reduces their activity in the other", the researcher adds.
This means it is difficult for a "more empathetic" brain to behave in a violent way, at least on a regular basis. "Educating people to be empathetic could be an education for peace, bringing about a reduction in conflict and belligerent acts", the researcher concludes.
Techniques for measuring the human brain "in vivo", such as functional magnetic resonance imaging, are making it possible to find out more about the structures of the brain that regulate behaviour and psychological processes such as empathy.
Here’s how human brain remembers the future
London, Apr 3 (ANI): A group of researchers has discovered that the brain saves energy by forecasting what it is likely to see.
Boffins in the Dept. of Psychology at the Univ. of Glasgow, working in collaboration with the Max-Planck Institute for Brain Research, Frankfurt, Germany, claim that the visual cortex does not simply react to visual stimuli but proactively predicts what it is likely to see in any given context.
And by doing so it uses less energy to process images, but if something unexpected were to appear in that familiar environment, the visual cortex becomes more active in order to process this information, reports New Scientist.
“The brain expects to see things and really just wants to confirm it now and again,” says Lars Muckli at the University of Glasgow, UK.
To reach the conclusion, Muckli and Arjen Alink at the Max Planck Institute for Brain Research asked 12 volunteers to focus on a cross on a screen, above and below which bars flashed on and off to create the illusion of movement.
In order to test a predictable stimulus, a third bar would appear in a position timed to fit in with the illusion of smooth movement. For the unpredictable stimulus it would appear out of sync.
fMRI scans showed that the unpredictable stimulus increased the activity in parts of the brain which deal with the earliest stages of visual processing.
The study has been published in the Journal of Neuroscience
Boffins in the Dept. of Psychology at the Univ. of Glasgow, working in collaboration with the Max-Planck Institute for Brain Research, Frankfurt, Germany, claim that the visual cortex does not simply react to visual stimuli but proactively predicts what it is likely to see in any given context.
And by doing so it uses less energy to process images, but if something unexpected were to appear in that familiar environment, the visual cortex becomes more active in order to process this information, reports New Scientist.
“The brain expects to see things and really just wants to confirm it now and again,” says Lars Muckli at the University of Glasgow, UK.
To reach the conclusion, Muckli and Arjen Alink at the Max Planck Institute for Brain Research asked 12 volunteers to focus on a cross on a screen, above and below which bars flashed on and off to create the illusion of movement.
In order to test a predictable stimulus, a third bar would appear in a position timed to fit in with the illusion of smooth movement. For the unpredictable stimulus it would appear out of sync.
fMRI scans showed that the unpredictable stimulus increased the activity in parts of the brain which deal with the earliest stages of visual processing.
The study has been published in the Journal of Neuroscience
Mimicking the Human Brain
In the human brain, the time-dependent properties of interconnected neurons allow for the processing of information in time and space, due to both memory and computation functions being mixed together. In man-made devices, the physical separation of computing units and memories make it impossible to mimic these complex neural systems.
Researchers have been trying to imitate the integration of neurons and synaptic connections, but as the brain possesses more synapses than neurons, synapse-like devices are necessary to achieve this objective.
In trying to reach this goal, Alibart et al. have fabricated a nanoparticle (NP) organic memory field-effect transistor, which mixes NPs and molecules to implement computation and memory into one device. By changing the size of the NPs and of the transistors, the group managed to tailor the dynamic behavior of the device in the frequency/time domain. Using the charge-storage capability of the NPs and the amplification factor of the organic transistor, it was possible to mimic the short-term plasticity of a biological synapse using a hybrid device.
Nutritional Supplement Magnesium Can Help Boost Brain Functions
A new study suggests that the nutritional supplement magnesium can help boost an individual’s brain power.According to a study published in the journal Neuron, it was found that increasing magnesium in the brain can help enhance learning abilities, working memory and short- and long-term memory in mice. The test subjects also performed higher in a variety of learning tests.
Researchers are excited with this new prospect, noting that it could provide insight to age-related cognitive loss. The scientists noticed a difference in brainpower in both old and young mice, furthering their claim.
"Half the population of the industrialized countries has a magnesium deficit, which increases with aging," said researcher Guosong Liu. "If normal or even higher levels of magnesium can be maintained, we may be able to significantly slow age-related loss of cognitive function and perhaps prevent or treat diseases that affect cognitive function."
The discovery of magnesium’s brain power boost may lead to a market for alternative medications when it comes to memory loss. Liu has done previous research for preventative drugs for Alzheimer’s disease.
Alternative therapies for brain disorders seeing success
Brain Balance Center owners Eric and Tamara Eslich help Ricky Heilbron, 9, who has ADD and Asperger's syndrome, with the monkey bars. Mike Holobeck, a sensory-motor coach at the Golden center, looks on. (RJ Sangosti, The Denver Post)
Basically rewiring brain
"By bombarding his brain for an hour, three times a week, . . . we can basically rewire the brain," said Tamara Eslich, a former chiropractor who, along with her husband, Eric, opened Colorado's first Brain Balance in December. "We are going to find the underlying problem."
Brain Balance now has more than 20 sites across the country.
Another franchise for kids with autism and learning disabilities, LearningRx Brain Training Centers, has 70 sites, including four in Colorado.
Founder Ken Gibson, a former pediatric optometrist, said kids with autism-spectrum disorder often have trouble blending sounds, which makes reading difficult. His therapy focuses on lengthening attention span, short-term memory and speed.
Rapid-fire addition
For a maximum of about $10,000 for a seven-month program, kids at LearningRx sit through demanding sessions doing exercises such as adding numbers in their head as a tutor spouts them in rapid fire.
"It's like a physical workout, but it's mental," Gibson said.
He said the methods of the competition — the right-brain- versus-left-brain therapies at Brain Balance — are based on literature.
"There's not a whole lot of science in that area," Gibson said. "We try to follow a method that is more science-based."
The "brain training" that happens at LearningRx can boost kids' IQs by 15 points and improve reading ability by four years, he said.
With the flood of expensive, alternative therapies — from horseback riding to sensory stimulation — parents of autistic children should use caution before enrolling, said Dr. Robin Gabriels, a psychologist and founder of Children's Hospital's Neuropsychiatric Special Care Program in Aurora.
Choosing the right therapy for an autistic child depends largely on the severity of the child's disorder, Gabriels said.
"There is no one treatment that we can name and say that is the one you need to use," she said.
"When parents come to me and they say, 'Should I try this new expensive diet or this vitamin therapy?' and they really don't have a lot of financial resources, I say, 'Start with what you know works,' " said Gibson, who uses "social stories" accompanied by pictures that teach kids who don't read social cues on how to behave.
Some therapies for sale aren't necessarily based on widely accepted science, Gibson said. For example, she said, autistic children don't necessarily have a right-brain delay.
"We know it's a neurological disorder, but we don't know a specific brain site that has been identified," she said. "That hasn't been done yet.
New Tools to Detect Alzheimer's
Avid, Bayer, General Electric Push Agents to Spot the Disease From Brain Scans
Companies specializing in medical imaging are pushing to develop chemical agents to detect Alzheimer's disease from brain scans, a process that one day may make it possible to predict who will suffer from the progressive ailment before symptoms appear.
![[ALZIMAGE]](http://sg.wsj.net/public/resources/images/MK-BC386A_ALZIM_NS_20100414185104.gif)
Avid Radiopharmaceuticals Inc., a tiny imaging company based in Philadelphia, and multinationals like Bayer AG and General Electric Co., are among those working on imaging compounds to help doctors spot signs of the memory-robbing disease. Such chemical compounds would be a first of their kind and would help their makers tap into the multibillion dollar Alzheimer's diagnostic market.
Currently, Alzheimer's disease can be diagnosed definitively only by taking samples of brain tissue after death and looking for signs of sticky substances called amyloid plaques. An accumulation of such plaque between brain cells is thought to contribute to the disease. However, whether the plaque causes Alzheimer's is much debated.
The imaging compounds under development are molecules with radioactive markers attached, which bind to amyloid plaques. After patients are injected with the compound, regions of the brain take on color under scanning devices, showing where the chemical has adhered and presumably indicating Alzheimer's-related plaque.
The market for diagnosing and treating Alzheimer's is estimated to grow to nearly $10 billion globally in 2014 from $8 billion in 2009, according to BCC Research, a technology market research firm based in Wellesley, Mass. The diagnostics and biomarker segment alone is expected to climb to $2.8 billion in 2014 from $1.1 billion in 2009.
Some 7.7 million Americans older than 65 are expected to have the disease by 2030, up from 5.1 million in 2010 because of the aging population, according to the Alzheimer's Association. Currently available treatments work to treat symptoms, such as memory loss, but don't actually slow the course of the disease. Development of imaging compounds are important for increasing early detection for Alzheimer's patients, although the cost of and access to diagnostic scanning devices are concerns, according to Maria Carrillo, a neuroscientist and spokeswoman for the Alzheimer's Association.
Doctors today must try to diagnose the disease based on their clinical assessment of the patient's memory and cognitive functioning. Some experts estimate that 15% to 20% of people labeled as Alzheimer's patients are misdiagnosed, which can lead to inappropriate treatments.
The hope is that these imaging agents will be "the first time we're able to definitively look inside someone's brain and say, 'Yeah, this is an Alzheimer's patient,' " said Richard Pither, head of research and development for GE's diagnostics division.
These diagnostic tools will be important to developing new treatments as well. Many experimental Alzheimer's treatments appear to work better in patients with less severe forms of the disease but are too weak to have an effect on patients by the time they are diagnosed today.
Closely-held Avid Wednesday presented preliminary data from a late-stage clinical trial showing that the company's compound, called florbetapir, binds to indicators of Alzheimer's in the brain and correctly identified which patients had the disease. These results, presented at the American Academy of Neurology annual conference in Toronto, were the first for this type of experimental compound in a Phase 3 trial, a key step before applying to regulators for approval of a new treatment.
The Avid trial compared the brain scans of six patients with and without memory impairment with findings from their autopsied brains after death. The correlation between the amount of amyloid detected and the brain regions where it was found by brain scans of florbetapir patients was "very strong" compared with the later autopsies, according to neuropathologist Daniel Skovronsky, Avid's chief executive and co-founder. Final results from the study are expected late this year. Because the scans are being compared with usually reliable autopsy findings, meaningful results can be obtained with relatively few subjects.
Bayer is testing florbetaben, a molecule licensed from Avid, and is also in late-stage development. Preliminary data on 150 patients in a Bayer midstage trial, presented Friday, showed that the compound correctly identified those whose doctors had also diagnosed them as having Alzheimer's disease compared with healthy patients. The company began a late-stage clinical trial at the end of 2009 that will compare brain images to autopsies; results are expected near the end of 2011, according to Bayer.
Bayer is also looking to develop molecular imaging targets for cancer, particularly certain solid tumors, as well as other neurodegenerative diseases. For Bayer's health-care division, its diagnostics and imaging unit is one of the four main areas of research and development. The German company expects peak sales of florbetaben could range from €250 million to €500 million, or about $341 million to $683 million a year.
Results from a midstage trial of GE's product, flutemetamol, have also been promising. Brain scans of patients using flutemetamol were found to have more amyloid plaques while healthy participants had virtually none.
Companies specializing in medical imaging are pushing to develop chemical agents to detect Alzheimer's disease from brain scans, a process that one day may make it possible to predict who will suffer from the progressive ailment before symptoms appear.
Currently, Alzheimer's disease can be diagnosed definitively only by taking samples of brain tissue after death and looking for signs of sticky substances called amyloid plaques. An accumulation of such plaque between brain cells is thought to contribute to the disease. However, whether the plaque causes Alzheimer's is much debated.
The imaging compounds under development are molecules with radioactive markers attached, which bind to amyloid plaques. After patients are injected with the compound, regions of the brain take on color under scanning devices, showing where the chemical has adhered and presumably indicating Alzheimer's-related plaque.
The market for diagnosing and treating Alzheimer's is estimated to grow to nearly $10 billion globally in 2014 from $8 billion in 2009, according to BCC Research, a technology market research firm based in Wellesley, Mass. The diagnostics and biomarker segment alone is expected to climb to $2.8 billion in 2014 from $1.1 billion in 2009.
Some 7.7 million Americans older than 65 are expected to have the disease by 2030, up from 5.1 million in 2010 because of the aging population, according to the Alzheimer's Association. Currently available treatments work to treat symptoms, such as memory loss, but don't actually slow the course of the disease. Development of imaging compounds are important for increasing early detection for Alzheimer's patients, although the cost of and access to diagnostic scanning devices are concerns, according to Maria Carrillo, a neuroscientist and spokeswoman for the Alzheimer's Association.
The hope is that these imaging agents will be "the first time we're able to definitively look inside someone's brain and say, 'Yeah, this is an Alzheimer's patient,' " said Richard Pither, head of research and development for GE's diagnostics division.
These diagnostic tools will be important to developing new treatments as well. Many experimental Alzheimer's treatments appear to work better in patients with less severe forms of the disease but are too weak to have an effect on patients by the time they are diagnosed today.
Closely-held Avid Wednesday presented preliminary data from a late-stage clinical trial showing that the company's compound, called florbetapir, binds to indicators of Alzheimer's in the brain and correctly identified which patients had the disease. These results, presented at the American Academy of Neurology annual conference in Toronto, were the first for this type of experimental compound in a Phase 3 trial, a key step before applying to regulators for approval of a new treatment.
The Avid trial compared the brain scans of six patients with and without memory impairment with findings from their autopsied brains after death. The correlation between the amount of amyloid detected and the brain regions where it was found by brain scans of florbetapir patients was "very strong" compared with the later autopsies, according to neuropathologist Daniel Skovronsky, Avid's chief executive and co-founder. Final results from the study are expected late this year. Because the scans are being compared with usually reliable autopsy findings, meaningful results can be obtained with relatively few subjects.
Bayer is testing florbetaben, a molecule licensed from Avid, and is also in late-stage development. Preliminary data on 150 patients in a Bayer midstage trial, presented Friday, showed that the compound correctly identified those whose doctors had also diagnosed them as having Alzheimer's disease compared with healthy patients. The company began a late-stage clinical trial at the end of 2009 that will compare brain images to autopsies; results are expected near the end of 2011, according to Bayer.
Bayer is also looking to develop molecular imaging targets for cancer, particularly certain solid tumors, as well as other neurodegenerative diseases. For Bayer's health-care division, its diagnostics and imaging unit is one of the four main areas of research and development. The German company expects peak sales of florbetaben could range from €250 million to €500 million, or about $341 million to $683 million a year.
Results from a midstage trial of GE's product, flutemetamol, have also been promising. Brain scans of patients using flutemetamol were found to have more amyloid plaques while healthy participants had virtually none.
Anti-Alzheimer’s Brain-Food Diet
Columbia University researchers, led by Yian Gu, have discovered that a diet rich in certain types of fats and proteins can actually help prevent or lessen Alzheimer’s disease in people over 65. The key is to eat Mediterranean: lots of fish, poultry, olive oil, nuts, cruciform vegetables like broccoli, dark leafy greens like spinach, and fruit. These provide essentials like omega-3 and omega-6 fatty acids, vitamin E, vitamin B12, and folate, all of which protect the brain and nervous system. Avoiding saturated fats, like the kind in btter and red meat, are also helpful.
While the change in diet wasn’t a magical preventative, people who did follow the eating pattern were 40% less likely to develop Alzheimer’s disease than their peers. Plus, it sounds delicious, doesn’t it?
Investigational intervention could slow brain shrinkage in Alzheimer's patients
Washington, Apr 14 (ANI): An investigational intervention, which used naturally ocurring antibodies in human blood, has preserved the thinking abilities of a group of mild- to moderate-stage Alzheimer's patients over 18 months and significantly reduced the rate of atrophy (shrinkage) of their brains, says a study.
Researchers at the NewYork-Presbyterian Hospital/Weill Cornell Medical Center, conducted the Phase II clinical trial of GAMMAGARD LIQUID and GAMMAGARD S/D Immune Globulin Intravenous (Human) (IGIV) for Alzheimer's disease (AD).
Dr. Norman Relkin found that patients receiving IGIV once or twice a month for 18 months had significantly lower rates of ventricular enlargement and less whole-brain atrophy than control subjects who initially received placebo.
Relkin's findings were based on two independent analyses of brain-imaging data from 20 patients who underwent serial MRI scans during the Phase II study of IGIV for AD.
"Past AD studies that used MRI measures found no change or an accelerated rate of brain shrinkage after investigational treatments. To the best of my knowledge, this is the first trial in which long-term clinical benefits in Alzheimer's patients were accompanied by objective signs of reduced brain degeneration," said Relkin.
A typical AD patient's brain shrinks three to four times faster than a healthy older adult's as a consequence of accelerated brain cell death.
This shrinkage of brain tissue causes the fluid-filled ventricles at the center of the brain to enlarge at a faster than normal rate.
Changes in the size of the brain and ventricles can be measured accurately by analysing results from two or more MRI scans obtained at an interval of at least several months apart.
The unprecedented reductions in these measures after IGIV reported by the researchers could indicate that IGIV exerts a disease-modifying effect that the current generation of approved AD treatments lack.
Relkin also found that rates of brain shrinkage after IGIV intervention were independent of the subject's age, gender and brain volume at the start of the study but strongly correlated with dose of IGIV and the clinical outcomes after 18 months of intervention.
The team also found that AD patients who responded best to IGIV did not measurably decline over 18 months, and had an average rate of brain shrinkage and average rate of ventricular enlargement comparable to the rate previously reported in normal elderly individuals.
"A dose-related effect of an Alzheimer's intervention on brain ventricular enlargement has never been seen before, and it suggests that IGIV may, indeed, be sparing brain tissue," said Dr. James Brewer, a neurologist and assistant professor of neurology at the University of California at San Diego.
Brewer independently analysed the MRIs from the Phase II IGIV study, and his findings closely matched those obtained by Dr. Dana Moore, a postdoctoral fellow working with Dr. Relkin at Weill Cornell.
"I am particularly looking forward to examining the Phase III data when that study is completed. Since it involves a considerably larger group of patients, it will permit us to obtain more detailed measures of atrophy in the brain regions specifically vulnerable to Alzheimer's disease," said Brewer.
The study has been presented at the American Academy of Neurology (AAN) meeting in Toronto.
Researchers at the NewYork-Presbyterian Hospital/Weill Cornell Medical Center, conducted the Phase II clinical trial of GAMMAGARD LIQUID and GAMMAGARD S/D Immune Globulin Intravenous (Human) (IGIV) for Alzheimer's disease (AD).
Dr. Norman Relkin found that patients receiving IGIV once or twice a month for 18 months had significantly lower rates of ventricular enlargement and less whole-brain atrophy than control subjects who initially received placebo.
Relkin's findings were based on two independent analyses of brain-imaging data from 20 patients who underwent serial MRI scans during the Phase II study of IGIV for AD.
"Past AD studies that used MRI measures found no change or an accelerated rate of brain shrinkage after investigational treatments. To the best of my knowledge, this is the first trial in which long-term clinical benefits in Alzheimer's patients were accompanied by objective signs of reduced brain degeneration," said Relkin.
A typical AD patient's brain shrinks three to four times faster than a healthy older adult's as a consequence of accelerated brain cell death.
This shrinkage of brain tissue causes the fluid-filled ventricles at the center of the brain to enlarge at a faster than normal rate.
Changes in the size of the brain and ventricles can be measured accurately by analysing results from two or more MRI scans obtained at an interval of at least several months apart.
The unprecedented reductions in these measures after IGIV reported by the researchers could indicate that IGIV exerts a disease-modifying effect that the current generation of approved AD treatments lack.
Relkin also found that rates of brain shrinkage after IGIV intervention were independent of the subject's age, gender and brain volume at the start of the study but strongly correlated with dose of IGIV and the clinical outcomes after 18 months of intervention.
The team also found that AD patients who responded best to IGIV did not measurably decline over 18 months, and had an average rate of brain shrinkage and average rate of ventricular enlargement comparable to the rate previously reported in normal elderly individuals.
"A dose-related effect of an Alzheimer's intervention on brain ventricular enlargement has never been seen before, and it suggests that IGIV may, indeed, be sparing brain tissue," said Dr. James Brewer, a neurologist and assistant professor of neurology at the University of California at San Diego.
Brewer independently analysed the MRIs from the Phase II IGIV study, and his findings closely matched those obtained by Dr. Dana Moore, a postdoctoral fellow working with Dr. Relkin at Weill Cornell.
"I am particularly looking forward to examining the Phase III data when that study is completed. Since it involves a considerably larger group of patients, it will permit us to obtain more detailed measures of atrophy in the brain regions specifically vulnerable to Alzheimer's disease," said Brewer.
The study has been presented at the American Academy of Neurology (AAN) meeting in Toronto.
Brain wants us to delay instant gratification, experts claim
Brain secret: It wants us to delay gratification
New research has shown that this circuit underlies a person's ability to resist on the spot reward and delay it for months or even years if it means a better pay-off in the long run.
Lead researcher of the study Dr Jan Peters, from the Department of Systems Neuroscience at the University Medical Center Hamburg-Eppendorf in German, said: 'Humans normally prefer larger over smaller rewards, but this situation can change when the larger rewards are associated with delays.
'Although there is no doubt that humans discount the value of rewards over time, in general, individuals exhibit a particularly significant ability to delay gratification.'
He also said that several ideas have been proposed to explain the reason behind putting value on 'rewards' at different points in time in humans.
But he added: 'Many questions remain unanswered, and the brain regions and mechanisms involved in this process are unclear.'
Dr Peters and co-author Professor Christian B|chel carried out tests where participants had to make a series of choices between smaller immediate and larger delayed rewards while brain activity was measured with brain scans.
The participants were also given 'cues' that referred to future events. And the more cues induced imagery of the event, the more the participants changed their behaviour towards patient, future-minded choices.
Dr Peters added: 'Our results reveal that vividly imagining the future reduced impulsive choice.
'Our data suggests that adjustment of preference functions enable us to make choices that maximize future pay-offs.'
The data is published in the April issue of the journal Neuron
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