Showing posts with label . Neuro science. Show all posts
Showing posts with label . Neuro science. Show all posts
Thursday, June 8, 2017
Saturday, February 25, 2017
Imaging study confirms differences in ADHD brains 02-25
Image credit : Shyam's Imagination Library
The prestigious journal The Lancet has published a large study identifying differences in the brains of people diagnosed with attention-deficit hyperactivity disorder (ADHD).
It found ADHD is associated with the delayed development of five brain regions, and should be considered a brain disorder. This is vindication for people experiencing ADHD whose diagnosis is sometimes called into question as an invented condition used to label normal children who are not meeting unrealistic expectations of “normal” behaviours.
Researchers from 23 centres in nine countries scanned the brains of people of aged four to 63 years, 1,713 with and 1,529 without ADHD. When they analysed all the data they found people with ADHD had slightly smaller brains overall, and in five of the seven specific regions there was a definite but very slight reduction in size.
They found these differences were more marked in children. When they analysed separately those who had and had not been treated with stimulant medication, they found no effect of medication. This suggests the differences are related to ADHD, and not an effect of treatment.
They found these differences were more marked in children. When they analysed separately those who had and had not been treated with stimulant medication, they found no effect of medication. This suggests the differences are related to ADHD, and not an effect of treatment.
Not all cases of ADHD are the same
One important limitation of looking at brain images of people with ADHD relates to the diagnosis of ADHD, which is based on a person meeting a certain set of clinical criteria. Some of these are outcome-based and relate to a person’s ability to carry out tasks. For example, they may avoid tasks that require mental effort or leave tasks incomplete.
The result of this – fewer tasks completed – could have more than one possible cause. The lack of precision in the cause makes it difficult to align the diagnosis exactly with brain images.
Inefficiencies in the “thinking” function of the brain (called “executive functioning deficits”) have been identified in people with ADHD. These inefficiencies would make it harder for people with ADHD to carry out certain tasks, such as tasks that take a long time, are difficult and are not constantly rewarding or reinforcing. Therefore a person with ADHD might find motivation for homework extremely difficult to sustain, but electronic games could hold their attention for a far longer period.
The diagnostic criteria for ADHD ignore the emotional aspect. Using present diagnostic criteria, at least 40% of individuals with ADHD also meet diagnostic criteria for oppositional defiant disorder, a childhood behavioural problem characterised by a negative attitude, disobedience and hostility.
An even larger proportion probably have features of oppositional defiant disorder but do not reach the diagnostic threshold. This very substantial overlap requires explanation. The findings of the Lancet paper may indicate there is an emotional component that is intrinsic to ADHD.
It is possible some people with ADHD do not experience an adequate level of emotional satisfaction or sense of achievement in completing everyday tasks. This deficiency in the emotional reward could be an additional problem for some people with ADHD. These individuals would find tasks not only more difficult but also less satisfying, reducing their motivation to achieve. They might also be more moody and disagreeable.
Individuals with a combination of reduced emotional satisfaction (sometimes termed “reward deficiency”) and executive functioning deficits, would have two different mechanisms that would each serve to reduce their productivity.
Both of these mechanisms would contribute to their symptoms of ADHD, as they would result in fewer tasks completed. So because there is more than one possible underlying mechanism contributing to certain features of ADHD, it could be anticipated that a large cohort of individuals with ADHD would show a mixed picture, with a variety of different brain structures affected.
This would reflect differences in the balance of the deficits contributing to their symptoms. The study results are consistent with this concept – the scans show there is no single brain difference that can categorically diagnose ADHD, but they do involve brain centres related to emotion.
The result of this – fewer tasks completed – could have more than one possible cause. The lack of precision in the cause makes it difficult to align the diagnosis exactly with brain images.
Inefficiencies in the “thinking” function of the brain (called “executive functioning deficits”) have been identified in people with ADHD. These inefficiencies would make it harder for people with ADHD to carry out certain tasks, such as tasks that take a long time, are difficult and are not constantly rewarding or reinforcing. Therefore a person with ADHD might find motivation for homework extremely difficult to sustain, but electronic games could hold their attention for a far longer period.
The diagnostic criteria for ADHD ignore the emotional aspect. Using present diagnostic criteria, at least 40% of individuals with ADHD also meet diagnostic criteria for oppositional defiant disorder, a childhood behavioural problem characterised by a negative attitude, disobedience and hostility.
An even larger proportion probably have features of oppositional defiant disorder but do not reach the diagnostic threshold. This very substantial overlap requires explanation. The findings of the Lancet paper may indicate there is an emotional component that is intrinsic to ADHD.
It is possible some people with ADHD do not experience an adequate level of emotional satisfaction or sense of achievement in completing everyday tasks. This deficiency in the emotional reward could be an additional problem for some people with ADHD. These individuals would find tasks not only more difficult but also less satisfying, reducing their motivation to achieve. They might also be more moody and disagreeable.
Individuals with a combination of reduced emotional satisfaction (sometimes termed “reward deficiency”) and executive functioning deficits, would have two different mechanisms that would each serve to reduce their productivity.
Both of these mechanisms would contribute to their symptoms of ADHD, as they would result in fewer tasks completed. So because there is more than one possible underlying mechanism contributing to certain features of ADHD, it could be anticipated that a large cohort of individuals with ADHD would show a mixed picture, with a variety of different brain structures affected.
This would reflect differences in the balance of the deficits contributing to their symptoms. The study results are consistent with this concept – the scans show there is no single brain difference that can categorically diagnose ADHD, but they do involve brain centres related to emotion.
A valid pathology
The differences in the brains of people with ADHD confirm it is a valid diagnosis and the problems experienced by people with ADHD are genuine.
However, neuroscience has moved ahead of the clinical understanding of ADHD that is based on the definition in the Diagnostic and Statistical Manual of Mental Disorders.
We need more sophisticated but clinically relevant models that recognise ADHD results from a combination of deficits that interact to produce varying symptoms for every person who experiences ADHD.
However, neuroscience has moved ahead of the clinical understanding of ADHD that is based on the definition in the Diagnostic and Statistical Manual of Mental Disorders.
We need more sophisticated but clinically relevant models that recognise ADHD results from a combination of deficits that interact to produce varying symptoms for every person who experiences ADHD.
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Wednesday, January 27, 2016
Breaking the brain’s garbage disposal: Study shows even a small problem causes big effects 01-27
Breaking the brain’s garbage disposal: Study shows even a small problem causes big effects
You wouldn’t think that two Turkish children, some yeast and a bunch of Hungarian fruit flies could teach scientists much.
But in fact, that unlikely combination has just helped an international team make a key discovery about how the brain’s “garbage disposal” process works — and how little needs to go wrong in order for it to break down.
The findings show just how important a cell-cleanup process called autophagy is to our brains. It also demonstrates how even the tiniest genetic change can have profound effects on such an essential function.
The new understanding could lead to better treatments for people whose brain and nerve cells have troubles “taking out the trash.” Some such drugs already exist, but more could follow.
Following a mystery to its end
In a new paper in the online journal eLife, the team describes their painstaking effort to figure out what was wrong in the Turkish siblings, and to understand what it meant. The children have a rare condition called ataxia that makes it harder for them to walk. They also have intellectual disability and developmental delays.
Ataxia is rare–affecting about one in every 20,000 people–and can cause movement problems in people who develop it in adulthood, or a range of symptoms when it arises in children.
Because researchers from the University of Michigan Medical School had published studies about families with multiple cases of ataxia before, Turkish researchers got in touch with them when the children’s parents brought them in for treatment.
That started a long chain of scientific sleuthing that led to today’s publication. First, the U-M team studied samples of the children’s DNA, and used advanced methods to pinpoint the exact genetic mutation that caused their symptoms.
It turned out to be on one of the genes that scientists know play a key role in autophagy, called ATG5. Cells throughout the body trigger their internal garbage crews by turning on this gene and its partners, and using them to make proteins that help clean up the cell.
The junk that these garbage crews clean up includes botched proteins–ones that have been used up or weren’t made right in the first place.
In fact, many forms of ataxia (and lots of other diseases) are caused by genetic problems that result in brain and nerve cells making such damaged, misfolded proteins. The proteins build up inside cells, killing them and causing neurological problems.
So, scientists and drug developers have tried to ramp up autophagy activity. They hope that by cleaning that cellular junk up faster, they can keep it from causing symptoms.
Tiny change – big effects
The children’s ataxia gene problem turned out to be not such a big deal genetically–it was such a slight mutation that it barely changed the way the cells made the protein. But that tiny change was enough to alter the autophagy process, and keep the children’s brain and nerve cells from working properly.
And that’s where the yeast and Hungarian flies come in. Using them, the researchers could see what the children’s problem gene did–and what that meant for the autophagy process. That’s because the autophagy process is so important that organisms ranging from yeast to humans make almost exactly the same ATG5 protein–it’s what scientists call “highly conserved” across species.
What they saw amazed them. The genetic mutation led cells to change just one link in the chain of amino acids that make up the ATG5 protein. The new amino acid even had the same electrical charge as the usual one. But that one changed link happened to be at the exact spot where ATG5 and its partner, called ATG12, connect to one another.
Since the two crucial autophagy partners couldn’t link together as usual, the children’s cells–and the yeast and flies’ cells–couldn’t clean up their cellular trash nearly as well. Autophagy didn’t shut down completely, but less of it happened. And the fruit flies, like the children, had problems walking.
“This is a window into the autophagy system, and the first time where having less autophagy causes ataxia, developmental delays and intellectual disability,” says Margit Burmeister, Ph.D. the U-M neurogeneticist who led the research and is co-senior author on the new paper. “It’s a subtle change, but it shows how important autophagy is in neurological disorders.”
Burmeister and colleagues from the University of Michigan, St. Jude Children’s Research Hospital, Howard Hughes Medical Institute, Istanbul University and Bogazici University in Istanbul and Eötvös Loránd University in Budapest hope the findings lead to autophagy-related treatments.
Meanwhile, they’re still working to understand how the change in ATG12-ATG5 binding actually changes autophagy. They’re looking at cells made with the mutations from other ataxia patients to see if autophagy is also changed.
They’re also looking for more families with ataxias. Each family could hold clues as important as the Turkish children’s mutation did. In fact, Burmeister was in Turkey late in 2015 to work with colleagues to find more potential cases. Small villages with centuries of marriage among people with some relation to one another, and large families, can prove to be important to science.
The acceleration in genetic sequencing and other testing, made possible in the last decade by advances in technology and scientific methods, means they’ll get closer to answers faster. What once took years can now be done in a single year. Having the expertise concentrated at U-M in genetics, autophagy, fruit fly biology, cell biology and more made the work go even faster, says Burmeister. U-M colleagues Daniel Klionsky, Jun Hee Lee and Jun Z. Li were critical to the new research. So were St. Jude colleagues led by Brenda Schulman who made X-ray images of the mutant ATG5 protein, and Zuhal Yapici and Aslihan Tolun, the colleagues in Istanbul and Gabor Juhasz in Budapest.
View at the original source
You wouldn’t think that two Turkish children, some yeast and a bunch of Hungarian fruit flies could teach scientists much.
But in fact, that unlikely combination has just helped an international team make a key discovery about how the brain’s “garbage disposal” process works — and how little needs to go wrong in order for it to break down.
The findings show just how important a cell-cleanup process called autophagy is to our brains. It also demonstrates how even the tiniest genetic change can have profound effects on such an essential function.
The new understanding could lead to better treatments for people whose brain and nerve cells have troubles “taking out the trash.” Some such drugs already exist, but more could follow.
Following a mystery to its end
In a new paper in the online journal eLife, the team describes their painstaking effort to figure out what was wrong in the Turkish siblings, and to understand what it meant. The children have a rare condition called ataxia that makes it harder for them to walk. They also have intellectual disability and developmental delays.
Ataxia is rare–affecting about one in every 20,000 people–and can cause movement problems in people who develop it in adulthood, or a range of symptoms when it arises in children.
Because researchers from the University of Michigan Medical School had published studies about families with multiple cases of ataxia before, Turkish researchers got in touch with them when the children’s parents brought them in for treatment.
That started a long chain of scientific sleuthing that led to today’s publication. First, the U-M team studied samples of the children’s DNA, and used advanced methods to pinpoint the exact genetic mutation that caused their symptoms.
It turned out to be on one of the genes that scientists know play a key role in autophagy, called ATG5. Cells throughout the body trigger their internal garbage crews by turning on this gene and its partners, and using them to make proteins that help clean up the cell.
The junk that these garbage crews clean up includes botched proteins–ones that have been used up or weren’t made right in the first place.
In fact, many forms of ataxia (and lots of other diseases) are caused by genetic problems that result in brain and nerve cells making such damaged, misfolded proteins. The proteins build up inside cells, killing them and causing neurological problems.
So, scientists and drug developers have tried to ramp up autophagy activity. They hope that by cleaning that cellular junk up faster, they can keep it from causing symptoms.
Tiny change – big effects
The children’s ataxia gene problem turned out to be not such a big deal genetically–it was such a slight mutation that it barely changed the way the cells made the protein. But that tiny change was enough to alter the autophagy process, and keep the children’s brain and nerve cells from working properly.
And that’s where the yeast and Hungarian flies come in. Using them, the researchers could see what the children’s problem gene did–and what that meant for the autophagy process. That’s because the autophagy process is so important that organisms ranging from yeast to humans make almost exactly the same ATG5 protein–it’s what scientists call “highly conserved” across species.
What they saw amazed them. The genetic mutation led cells to change just one link in the chain of amino acids that make up the ATG5 protein. The new amino acid even had the same electrical charge as the usual one. But that one changed link happened to be at the exact spot where ATG5 and its partner, called ATG12, connect to one another.
Since the two crucial autophagy partners couldn’t link together as usual, the children’s cells–and the yeast and flies’ cells–couldn’t clean up their cellular trash nearly as well. Autophagy didn’t shut down completely, but less of it happened. And the fruit flies, like the children, had problems walking.
“This is a window into the autophagy system, and the first time where having less autophagy causes ataxia, developmental delays and intellectual disability,” says Margit Burmeister, Ph.D. the U-M neurogeneticist who led the research and is co-senior author on the new paper. “It’s a subtle change, but it shows how important autophagy is in neurological disorders.”
Burmeister and colleagues from the University of Michigan, St. Jude Children’s Research Hospital, Howard Hughes Medical Institute, Istanbul University and Bogazici University in Istanbul and Eötvös Loránd University in Budapest hope the findings lead to autophagy-related treatments.
Meanwhile, they’re still working to understand how the change in ATG12-ATG5 binding actually changes autophagy. They’re looking at cells made with the mutations from other ataxia patients to see if autophagy is also changed.
They’re also looking for more families with ataxias. Each family could hold clues as important as the Turkish children’s mutation did. In fact, Burmeister was in Turkey late in 2015 to work with colleagues to find more potential cases. Small villages with centuries of marriage among people with some relation to one another, and large families, can prove to be important to science.
The acceleration in genetic sequencing and other testing, made possible in the last decade by advances in technology and scientific methods, means they’ll get closer to answers faster. What once took years can now be done in a single year. Having the expertise concentrated at U-M in genetics, autophagy, fruit fly biology, cell biology and more made the work go even faster, says Burmeister. U-M colleagues Daniel Klionsky, Jun Hee Lee and Jun Z. Li were critical to the new research. So were St. Jude colleagues led by Brenda Schulman who made X-ray images of the mutant ATG5 protein, and Zuhal Yapici and Aslihan Tolun, the colleagues in Istanbul and Gabor Juhasz in Budapest.
View at the original source
Wednesday, December 30, 2015
Intelligence ‘networks’ discovered in brain for the first time 12-30
Intelligence ‘networks’ discovered in brain for the first time
Scientists from Imperial College London have identified for the first time two clusters of genes linked to human intelligence.
Called M1 and M3, these so-called gene networks appear to influence cognitive function – which includes memory, attention, processing speed and reasoning.
Crucially, the scientists have discovered that these two networks – which each contain hundreds of genes – are likely to be under the control of master regulator switches. The researchers are now keen to identify these switches and explore whether it might be feasible to manipulate them. The research is at a very early stage, but the scientists would ultimately like to investigate whether it is possible to use this knowledge of gene networks to boost cognitive function.
Dr Michael Johnson, lead author of the study from the Department of Medicine at Imperial College London, said: "We know that genetics plays a major role in intelligence but until now haven’t known which genes are relevant. This research highlights some of genes involved in human intelligence, and how they interact with each other.
What’s exciting about this is that the genes we have found are likely to share a common regulation, which means that potentially we can manipulate a whole set of genes whose activity is linked to human intelligence. Our research suggests that it might be possible to work with these genes to modify intelligence, but that is only a theoretical possibility at the moment – we have just taken a first step along that road."
In the study, published in the journal Nature Neuroscience, the international team of researchers looked at samples of human brain from patients who had undergone neurosurgery for epilepsy. The investigators analysed thousands of genes expressed in the human brain, and then combined these results with genetic information from healthy people who had undergone IQ tests and from people with neurological disorders such as autism spectrum disorder and intellectual disability.
They conducted various computational analyses and comparisons in order to identify the gene networks influencing healthy human cognitive abilities. Remarkably, they found that some of the same genes that influence human intelligence in healthy people were also the same genes that cause impaired cognitive ability and epilepsy when mutated.
Dr Johnson added: "Traits such intelligence are governed by large groups of genes working together – like a football team made up of players in different positions. We used computer analysis to identify the genes in the human brain that work together to influence our cognitive ability to make new memories or sensible decisions when faced with lots of complex information. We found that some of these genes overlap with those that cause severe childhood onset epilepsy or intellectual disability.
"This study shows how we can use large genomic datasets to uncover new pathways for human brain function in both health and disease. Eventually, we hope that this sort of analysis will provide new insights into better treatments for neurodevelopmental diseases such as epilepsy, and ameliorate or treat the cognitive impairments associated with these devastating diseases."
View at the original source
Scientists from Imperial College London have identified for the first time two clusters of genes linked to human intelligence.
Called M1 and M3, these so-called gene networks appear to influence cognitive function – which includes memory, attention, processing speed and reasoning.
Crucially, the scientists have discovered that these two networks – which each contain hundreds of genes – are likely to be under the control of master regulator switches. The researchers are now keen to identify these switches and explore whether it might be feasible to manipulate them. The research is at a very early stage, but the scientists would ultimately like to investigate whether it is possible to use this knowledge of gene networks to boost cognitive function.
Dr Michael Johnson, lead author of the study from the Department of Medicine at Imperial College London, said: "We know that genetics plays a major role in intelligence but until now haven’t known which genes are relevant. This research highlights some of genes involved in human intelligence, and how they interact with each other.
What’s exciting about this is that the genes we have found are likely to share a common regulation, which means that potentially we can manipulate a whole set of genes whose activity is linked to human intelligence. Our research suggests that it might be possible to work with these genes to modify intelligence, but that is only a theoretical possibility at the moment – we have just taken a first step along that road."
In the study, published in the journal Nature Neuroscience, the international team of researchers looked at samples of human brain from patients who had undergone neurosurgery for epilepsy. The investigators analysed thousands of genes expressed in the human brain, and then combined these results with genetic information from healthy people who had undergone IQ tests and from people with neurological disorders such as autism spectrum disorder and intellectual disability.
They conducted various computational analyses and comparisons in order to identify the gene networks influencing healthy human cognitive abilities. Remarkably, they found that some of the same genes that influence human intelligence in healthy people were also the same genes that cause impaired cognitive ability and epilepsy when mutated.
Dr Johnson added: "Traits such intelligence are governed by large groups of genes working together – like a football team made up of players in different positions. We used computer analysis to identify the genes in the human brain that work together to influence our cognitive ability to make new memories or sensible decisions when faced with lots of complex information. We found that some of these genes overlap with those that cause severe childhood onset epilepsy or intellectual disability.
"This study shows how we can use large genomic datasets to uncover new pathways for human brain function in both health and disease. Eventually, we hope that this sort of analysis will provide new insights into better treatments for neurodevelopmental diseases such as epilepsy, and ameliorate or treat the cognitive impairments associated with these devastating diseases."
View at the original source
Monday, March 9, 2015
Neuroimaging study shows how being in love changes the architecture of your brain 03-10
Neuroimaging study shows how being in love changes the architecture of your brain
A research team has used neuroimaging techniques to investigate how being in a romantic relationship produces alterations in the architecture of the brain. They found that being in love is associated with increased connectivity between regions of the brain associated with reward, motivation, emotion regulation, and social cognition.
“This study provides the first empirical evidence of love-related alterations in the underlying functional architecture of the brain,” wrote Hongwen Song and his colleagues, who published their findings February 13 in Frontiers in Neuroscience.
The researchers used resting state functional magnetic resonance imaging (rsfMRI) to examine differences in patterns of brain connectivity in 100 college students.
The students were divided into three groups: the “in-love” group, the “ended-love” group, and the “single” group.
The researchers found increased resting brain activity in the left dorsal anterior cingulate cortex in the in-love group, suggesting this area of the brain is closely related to the state of falling in love.
Brain activity in the bilateral caudate nucleus, on the other hand, was significantly decreased in the ended-love group. This brain structure is associated with detection of reward, expectation, representation of goals, and integration of sensory input.
The researchers also found increased connectivity between the left dorsal anterior cingulate cortex, caudate nucleus, nucleus accumbens, and insula — a brain network associated with reward, motivation, and emotion regulation — among the in-love group.
The increase in connectivity in these brain regions “may be the result of frequent efforts [of in-love participants]to monitor their own emotional state, as well as their lovers’ emotional state, monitoring conflicts while adjusting cognitive strategies in order to resolve conflicts so as to maintain their romantic relationship,” the researchers explained.
In addition, the in-love group showed increased connectivity between the temporoparietal junction, posterior cingulate, medial prefrontal cortex, precuneus, and inferior parietal lobe — a brain network associated with social cognition.
“These results shed light on the underlying neurophysiological mechanisms of romantic love by investigating intrinsic brain activity, and demonstrate the possibility of applying a resting state approach for investigating romantic love,” the researchers concluded.
The Rise and Fall of Cognitive Skills 03-10
The Rise and Fall of Cognitive Skills
Neuroscientists find that different parts of the brain work best at different ages.
Scientists have long known that our ability to think quickly and recall information, also known as fluid intelligence, peaks around age 20 and then begins a slow decline. However, more recent findings, including a new study from neuroscientists at MIT and Massachusetts General Hospital (MGH), suggest that the real picture is much more complex.
The study, which appears in the journal Psychological Science, finds that different components of fluid intelligence peak at different ages, some as late as age 40.
“At any given age, you’re getting better at some things, you’re getting worse at some other things, and you’re at a plateau at some other things. There’s probably not one age at which you’re peak on most things, much less all of them,” says Joshua Hartshorne, a postdoc in MIT’s Department of Brain and Cognitive Sciences and one of the paper’s authors.
“It paints a different picture of the way we change over the lifespan than psychology and neuroscience have traditionally painted,” adds Laura Germine, a postdoc in psychiatric and neurodevelopmental genetics at MGH and the paper’s other author.
Measuring peaks
Until now, it has been difficult to study how cognitive skills change over time because of the challenge of getting large numbers of people older than college students and younger than 65 to come to a psychology laboratory to participate in experiments. Hartshorne and Germine were able to take a broader look at aging and cognition because they have been running large-scale experiments on the Internet, where people of any age can become research subjects.
Their web sites, gameswithwords.org and testmybrain.org, feature cognitive tests designed to be completed in just a few minutes. Through these sites, the researchers have accumulated data from nearly 3 million people in the past several years.
In 2011, Germine published a study showing that the ability to recognize faces improves until the early 30s before gradually starting to decline. This finding did not fit into the theory that fluid intelligence peaks in late adolescence. Around the same time, Hartshorne found that subjects’ performance on a visual short-term memory task also peaked in the early 30s.
Intrigued by these results, the researchers, then graduate students at Harvard University, decided that they needed to explore a different source of data, in case some aspect of collecting data on the Internet was skewing the results. They dug out sets of data, collected decades ago, on adult performance at different ages on the Weschler Adult Intelligence Scale, which is used to measure IQ, and the Weschler Memory Scale. Together, these tests measure about 30 different subsets of intelligence, such as digit memorization, visual search, and assembling puzzles.
Hartshorne and Germine developed a new way to analyze the data that allowed them to compare the age peaks for each task. “We were mapping when these cognitive abilities were peaking, and we saw there was no single peak for all abilities. The peaks were all over the place,” Hartshorne says. “This was the smoking gun.”
However, the dataset was not as large as the researchers would have liked, so they decided to test several of the same cognitive skills with their larger pools of Internet study participants. For the Internet study, the researchers chose four tasks that peaked at different ages, based on the data from the Weschler tests. They also included a test of the ability to perceive others’ emotional state, which is not measured by the Weschler tests.
The researchers gathered data from nearly 50,000 subjects and found a very clear picture showing that each cognitive skill they were testing peaked at a different age. For example, raw speed in processing information appears to peak around age 18 or 19, then immediately starts to decline. Meanwhile, short-term memory continues to improve until around age 25, when it levels off and then begins to drop around age 35.
For the ability to evaluate other people’s emotional states, the peak occurred much later, in the 40s or 50s.
Christopher Chabris, an associate professor of psychology at Union College, said a key feature of the study’s success was the researchers’ ability to gather and analyze so much data, which is unusual in cognitive psychology.
“You need to look at a lot of people to discover these patterns,” says Chabris, who was not part of the research team. “They’re taking the next step and showing a more fine-grained picture of how cognitive abilities differ from one another and the way they change over time.”
More work will be needed to reveal why each of these skills peaks at different times, the researchers say. However, previous studies have hinted that genetic changes or changes in brain structure may play a role.
Researchers have been running large-scale experiments on the Internet, where people of any age can become research subjects. Their websites feature cognitive tests designed to be completed in just a few minutes. Shown here is a “pattern completion test” from their website, testmybrain.org. Image credit: Jose-Luis Olivares/MIT (with image courtesy of the researchers).
“If you go into the data on gene expression or brain structure at different ages, you see these lifespan patterns that we don’t know what to make of. The brain seems to continue to change in dynamic ways through early adulthood and middle age,” Germine says. “The question is: What does it mean? How does it map onto the way you function in the world, or the way you think, or the way you change as you age?”
Accumulated intelligence
The researchers also included a vocabulary test, which serves as a measure of what is known as crystallized intelligence — the accumulation of facts and knowledge. These results confirmed that crystallized intelligence peaks later in life, as previously believed, but the researchers also found something unexpected: While data from the Weschler IQ tests suggested that vocabulary peaks in the late 40s, the new data showed a later peak, in the late 60s or early 70s.
The researchers believe this may be a result of better education, more people having jobs that require a lot of reading, and more opportunities for intellectual stimulation for older people.
Hartshorne and Germine are now gathering more data from their websites and have added new cognitive tasks designed to evaluate social and emotional intelligence, language skills, and executive function. They are also working on making their data public so that other researchers can access it and perform other types of studies and analyses.
“We took the existing theories that were out there and showed that they’re all wrong. The question now is: What is the right one? To get to that answer, we’re going to need to run a lot more studies and collect a lot more data,” Hartshorne says.
Saturday, November 22, 2014
Major brain pathway rediscovered after century-old confusion, controversy 11-22
Major brain pathway rediscovered after century-old confusion, controversy
A couple of years ago a scientist looking at dozens of MRI scans of human brains noticed something
surprising. A large, fiber pathway that seemed to be part of the network of connections that process visual information showed up on the scans, but the researcher couldn’t find it mentioned in any of the modern-day anatomy textbooks he had.
surprising. A large, fiber pathway that seemed to be part of the network of connections that process visual information showed up on the scans, but the researcher couldn’t find it mentioned in any of the modern-day anatomy textbooks he had.
“It was this massive bundle of fibers, visible in every brain I examined,” said Jason Yeatman, a research scientist at the University of Washington’s Institute for Learning & Brain Sciences. “It seemed unlikely that I was the first to have noticed this structure; however, as far as I could tell, it was absent from the literature and from all major neuroanatomy textbooks.”With colleagues at Stanford University, where he was a graduate student at the time, Yeatman started some detective work to figure out the identity of that large, mysterious fiber bundle.
In the paper, to be published Nov. 17 by the Proceedings of the National Academy of Sciences, the team describes the history and controversy of the elusive brain pathway, explains how modern MRI techniques rediscovered it, and gives analytical tools researchers can use to identify the brain structure – now known as the vertical occipital fasciculus.
The “aha moment” in identifying the pathway came while Yeatman and Kevin Weiner, a Stanford postdoctoral researcher, were poring over the yellowed pages of 19th-century brain atlases in the basement of the Stanford Medical Library.
“Kevin found an atlas, written by Carl Wernicke near the turn of the (20th) century, that depicted the vertical occipital fasciculus,” Yeatman said. “The last time that atlas had been checked out was 1912, meaning we were the first to view these images in the last century.”
From there, Yeatman and Weiner, who share lead authorship on the paper, did more library research revealing these possibilities for why the pathway was forgotten:
– A scientific disagreement. In an 1881 neuroanatomy atlas, Wernicke, a well-known anatomist who in 1874 discovered “Wernicke’s area,” which is essential for language, wrote about a fiber pathway in a monkey brain he was examining. He called it “senkrechte Occiptalbündel” (translated as vertical occipital bundle). But its vertical orientation contradicted the belief of one of the most renowned neuroanatomists of the era, Theodor Meynert, who asserted that brain connections could only travel in between the front and the back of the brain, not up and down.
– Haphazard naming methods. The 1880s and 1890s were a fertile time in the neuroanatomy world, but scientists lacked a shared process for naming the brain structures they found. Looking at drawings of the brain from this time period, Yeatman and coauthors saw that the fiber pathway that they were looking for appeared in brain atlases but was called different things, including “Wernicke’s perpendicular fasciculus,” “perpendicular occipital fasciculus of Wernicke,” and “stratum profundum convexitatis.”
“When we started, it was just for our own knowledge and curiosity,” said Weiner, who’s also the director of public information at the Institute for Applied Neuroscience, a nonprofit based in Palo Alto, California.
“But, after a while, we realized that there was an important story to tell that contained a series of missing links that have been buried for so long within this puzzle of historical conversation among many who are considered the founders of the entire neuroscience field.”
The researchers used a type of MRI measure called diffusion-weighted imaging to measure the size of the pathway and see where in the brain it went. Across brain scans taken from 37 subjects, they found that the vertical occipital fasciculus begins in the occipital lobe – the part of the brain’s visual processing system located at the back of the head. From there, the fibers spread out like a sheet, connecting brain regions that are important for seeing objects with other brain regions that coordinate which objects to focus attention upon.
“We believe that signals carried by the VOF play a role in many perceptual processes, from recognizing a friend’s face to rapidly reading a page of text,” said Yeatman, who is now studying brain mechanisms involved in learning to read.
In the paper, the researchers also provide an algorithm that others can use on their own data to find the pathway and measure its properties.
“To support reproducible research, our lab makes a strong effort to share software and data,” said Brian Wandell, senior author of the paper and a psychology professor at Stanford. “We believe this is a powerful way to ensure that our findings can be both checked and used in labs around the world.”
The researchers also hope that the algorithm will enable other researchers to study the pathway, possibly leading to a better understanding of its role in human cognition and in patient populations.
Saturday, April 19, 2014
Turning science on its head 04-19
Turning science on its head
Harvard neuroscientists have made a discovery that turns 160 years of neuroanatomy on its head.
Myelin, the electrical insulating material in the body long known to be essential for the fast transmission of impulses along the axons of nerve cells, is not as ubiquitous as thought, according to new work led by Professor Paola Arlotta of the Harvard Stem Cell Institute (HSCI) and the University’sDepartment of Stem Cell and Regenerative Biology, in collaboration with Professor Jeff Lichtman of Harvard’s Department of Molecular and Cellular Biology.
“Myelin is a relatively recent invention during evolution,” says Arlotta. “It’s thought that myelin allowed the brain to communicate really fast to the far reaches of the body, and that it has endowed the brain with the capacity to compute higher-level functions.”
In fact, loss of myelin is a feature in a number of devastating diseases, includingmultiple sclerosis and schizophrenia.
But the new research shows that despite myelin’s essential roles in the brain, “some of the most evolved, most complex neurons of the nervous system have less myelin than older, more ancestral ones,” said Arlotta, co-director of the HSCI neuroscience program.
What this means, she said, is that the higher one looks in the cerebral cortex — closer to the top of the brain, which is its most evolved part — the less myelin one finds. Not only that, but “neurons in this part of the brain display a brand-new way of positioning myelin along their axons that has not been previously seen. They have ‘intermittent myelin’ with long axon tracts that lack myelin interspersed among myelin-rich segments.”
“Contrary to the common assumptions that neurons use a universal profile of myelin distribution on their axons, the work indicates that different neurons choose to myelinate their axons differently,” Arlotta said. “In classic neurobiology textbooks, myelin is represented on axons as a sequence of myelinated segments separated by very short nodes that lack myelin. This distribution of myelin was tacitly assumed to be always the same, on every neuron, from the beginning to the end of the axon. This new work finds this not to be the case.”
The results of the research by Arlotta and postdoctoral fellow Giulio Srubek Tomassy, the first author on the report, are published in the latest edition of the journal Science.
The paper is accompanied by a “perspective” by R. Douglas Fields of the Eunice Kennedy Shriver National Institute of Child Health and Human Development at the National Institutes of Health, who said that Arlotta and Tomassy’s findings raise important questions about the purpose of myelin, and “are likely to spark new concepts about how information is transmitted and integrated in the brain.”
Arlotta and Tomassy collaborated closely on the new work with postdoctoral fellow Daniel Berger of the Lichtman lab, which generated one of the two massive electron microscopy databases that made the work possible.
“The fact that it is the most evolved neurons, the ones that have expanded dramatically in humans, suggest that what we’re seeing might be the ‘future.’ As neuronal diversity increases and the brain needs to process more and more complex information, neurons change the way they use myelin to achieve more,” said Arlotta.
Tomassy said it is possible that these profiles of myelination “may be giving neurons an opportunity to branch out and ‘talk’ to neighboring neurons.” For example, because axons cannot make synaptic contacts when they are myelinated, one possibility is that these long myelin gaps may be needed to increase neuronal communication and synchronize responses across different neurons. He and Arlotta postulate that the intermittent myelin may be intended to fine-tune the electrical impulses traveling along the axons, in order to allow the emergence of highly complex neuronal behaviors.
Sunday, October 20, 2013
Scientists pinpoint brain’s area for numeral recognition 10-20
Scientists pinpoint brain’s area for numeral recognition
BY BRUCE GOLDMAN
Steve Fisch 
Jennifer Shum and Josef Parvizi led a team that identified a tiny area in the brain that processes numerals.
Scientists at the Stanford University School of Medicine have determined the precise anatomical coordinates of a brain “hot spot,” measuring only about one-fifth of an inch across, that is preferentially activated when people view the ordinary numerals we learn early on in elementary school, like “6” or “38.”
“This is the first-ever study to show the existence of a cluster of nerve cells in the human brain that specializes in processing numerals,” said Josef Parvizi, MD, PhD, associate professor of neurology and neurological sciences and director of Stanford’s Human Intracranial Cognitive Electrophysiology Program . “In this small nerve-cell population, we saw a much bigger response to numerals than to very similar-looking, similar-sounding and similar-meaning symbols.
“It’s a dramatic demonstration of our brain circuitry’s capacity to change in response to education,” he added. “No one is born with the innate ability to recognize numerals.”
The finding pries open the door to further discoveries delineating the flow of math-focused information processing in the brain. It also could have direct clinical ramifications for patients with dyslexia for numbers and with dyscalculia: the inability to process numerical information.
the inferior temporal gyrus, a superficial region of the outer cortex on the brain. The inferior temporal gyrus is already generally known to be involved in the processing of visual information.
The new study, published April 17 in the Journal of Neuroscience, builds on an earlier one in which volunteers had been challenged with math questions. “We had accumulated lots of data from that study about what parts of the brain become active when a person is focusing on arithmetic problems, but we were mostly looking elsewhere and hadn’t paid much attention to this area within the inferior temporal gyrus,” said Parvizi, who is senior author of the study.
Not, that is, until fourth-year medical student Jennifer Shum, who also is doing research in Parvizi’s lab, noticed that, among some subjects in the first study, a spot in the inferior temporal gyrus seemed to be substantially activated by math exercises. Charged with verifying that this observation was consistent from one patient to the next, Shum, the study’s lead author, reported that this was indeed the case. So, Parvizi’s team designed a new study to look into it further.
The new study relied on epileptic volunteers who, as a first step toward possible surgery to relieve unremitting seizures that weren’t responding to therapeutic drugs, had a small section of their skulls removed and electrodes applied directly to the brain’s surface. The procedure, which doesn’t destroy any brain tissue or disrupt the brain’s function, had been undertaken so that the patients could be monitored for several days to help attending neurologists find the exact location of their seizures’ origination points. While these patients are bedridden in the hospital for as much as a week of such monitoring, they are fully conscious, in no pain and, frankly, a bit bored.
Over time, Parvizi identified seven epilepsy patients with electrode coverage in or near the inferior temporal gyrus and got these patients’ consent to undergo about an hour’s worth of tests in which they would be shown images presented for very short intervals on a laptop computer screen, while activity in their brain regions covered by electrodes was recorded. Each electrode picked up activity from an area corresponding to about a half-million nerve cells (a drop in the bucket in comparison to the brain’s roughly 100 billion nerve cells).
To make sure that any numeral-responsive brain areas identified were really responding to numerals — and not just generic lines, angles and curves — these tests were carefully calibrated to distinguish brain responses to visual presentations of the classic numerals taught in Western schools, such as 3 or 50, as opposed to squiggly lines, letters of the alphabet, number-denoting words such as “three” or “fifty,” and symbols that in fact were also numerals but — because they were drawn from the Thai, Tibetan and Devanagari languages — were extremely unlikely to be recognized as such by this particular group of volunteers.
In the first test, subjects were shown series of single numerals and letters — along with false fonts, in which the component parts of numerals or letters had been scrambled but defining curves and angles were retained, and the foreign-number symbols just described. A second test, controlling for meaning and sound, included numerals and their spelled-out versions (for instance, “1” and “one,” or “3” and “three”) and other words with the same sound or a similar one (“won” and “tree,” respectively).
All of our brains are shaped slightly differently. But in almost the identical spot within each study subject’s brain, the investigators observed a significantly larger response to numerals than to similar-shaped stimuli, such as letters or scrambled letters and numerals, or to words that either meant the same as the numerals or sounded like them.
Interestingly, said Parvizi, that numeral-processing nerve-cell cluster is parked within a larger group of neurons that is activated by visual symbols that have lines with angles and curves. “These neuronal populations showed a preference for numerals compared with words that denote or sound like those numerals,” he said. “But in many cases, these sites actually responded strongly to scrambled letters or scrambled numerals. Still, within this larger pool of generic neurons, the ‘visual numeral area’ preferred real numerals to the false fonts and to same-meaning or similar-sounding words.”
It seems, Parvizi said, that “evolution has designed this brain region to detect visual stimuli such as lines intersecting at various angles — the kind of intersections a monkey has to make sense of quickly when swinging from branch to branch in a dense jungle.” The adaptation of one part of this region in service of numeracy is a beautiful intersection of culture and neurobiology, he said.
Having nailed down a specifically numeral-oriented spot in the brain, Parvizi’s lab is looking to use it in tracing the pathways described by the brain’s number-processing circuitry. “Neurons that fire together wire together,” said Shum. “We want to see how this particular area connects with and communicates with other parts of the brain.”
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