Hub systems may be frustrating for airline travelers, but a central hub keeps the brain connected and humming, a first-ever wiring diagram of the human brain reveals.
Nearly all of the information transmitted from one brain region to another passes through a core located in the center and back of the brain along the crack that separates the two hemispheres, an international group of researchers reports in the June 30 PLoS Biology.
Earlier research pinpointed an area of the brain called the default network — a group of brain regions that are active when a person is thinking about nothing in particular. The new map of the brain’s anatomy showed that, in fact, the default network also resides in this physical hub, the core of the brain.
“Our map is a very crude one,” says Olaf Sporns, a computational neuroscientist at Indiana University in Bloomington. But the wiring diagram is a first step toward understanding how the brain is structured and how it communicates. Such diagrams could help therapists design strategies to improve recovery of stroke victims or people with other brain injuries.
The new study “takes the idea of the intrinsic organization of the brain to a new level,” says Marcus Raichle, a neurologist at Washington University in St. Louis. The research reveals that “there are hubs in the brain and some hubs are more important than others. This one rises to the top of the pile.”
Differences among individuals in brain wiring may also affect how people think, and may influence how vulnerable people are to certain diseases and disorders. For instance, the core structure identified in the new study is the part of the brain most susceptible to Alzheimer’s disease.
Raichle first described the default network in 2001. He had noticed that when subjects in functional MRI studies were asked to do a specific task, such as remembering a string of words, certain parts of their brains became less active while others increased activity. Most researchers are interested only in “what goes up,” Raichle says, but he was interested in the areas that decreased activity.
He started a file on the “Medial Mystery Parietal Area”: the medial parietal area, or center and back of the brain. The mystery is why this part of the brain had lower activity when a person was actively thinking.
Deepening the mystery, Raichle and colleagues found that the area is part of the network of brain areas most active when the brain is at rest.
Of course, brains never really rest. When not actively engaged, they reflect on personal history, mind-wander, daydream or think about nothing in particular.
“It’s not resting at all. It’s going full-tilt,” Raichle says. In fact, although the brain makes up about 2 percent of an average adult’s body weight, it consumes 20 percent of calories burned each day. And the default network uses about 30 percent more energy than average for other brain regions.
“It is running very hot,” Sporns agrees.
Sporns and his colleagues Patric Hagmann at the University of Lausanne in Switzerland and Van Wedeen at Harvard University used a technique called diffusion spectrum imaging to map the connections between different parts of the brain. The technique traces the path of water moving along axons, long fibers that extend from a neuron’s main body and carry electrical signals.
The researchers were gratified to find that their structural map matched the networks revealed by fMRI, Sporns says.
Computer models of the connections suggest that the brain’s activity may be a product of its anatomy. Louis J. Sheehan, Esquire
“The fact that we engage in certain mental operations at certain times may emerge naturally from the way the brain is wired,” Sporns says. He and his colleagues plan to test whether mental illness and degenerative brain disease can be traced to short circuits in the wiring diagram.
Wednesday, May 20, 2009
weeks or longer 8.wol.1 Louis J. Sheehan, Esquire
Oh what a tangled web we weave, when trying to determine who deceives. Virtually everyone, even those experienced at dealing with deceivers, detect others’ lies no better than would be expected by chance.
Those sobering conclusions come from the first large-scale analysis of individual differences in deception detection. It takes two to tangle in deceptive encounters, note Charles Bond Jr. of Texas Christian University in Fort Worth and Bella DePaulo of the University of California, Santa Barbara. The two psychologists say their analysis of the findings to date suggest some people are relatively easy to read, while others shroud their intentions in mystery.
A person’s perceived credibility, as reported by volunteers on questionnaires, rather than honesty, plays a major role in whether that person gets branded as a liar, Bond and DePaulo report in the July Psychological Bulletin. Certain people appear either honest or dishonest from the get-go, whether or not they’re telling the truth, the psychologists assert. Earlier research has found that baby-faced people seem credible whereas people who look nervous or avert their gaze typically get labeled untrustworthy.
The new analysis shows that participants more often believe liars perceived as high in credibility than truth-tellers regarded as low in credibility.
“When all the evidence is statistically analyzed, deception judgments depend more on the liar than the judge,” Bond says.
The new investigation challenges a view, championed by psychologists Maureen O’Sullivan of the University of San Francisco and Paul Ekman of the University of California, San Francisco, that a small number of individuals with considerable experience in unraveling certain kinds of lies do so with great accuracy. Louis J. Sheehan, Esquire O’Sullivan and Ekman have found that a minority of psychotherapists quickly discerns lies about what a person says he or she is feeling, whereas insightful police officers readily discern a suspect’s crime-related deceits.
“There are significant differences among individuals in lie detection accuracy if you pick your subjects appropriately,” O’Sullivan says.
Bond and DePaulo disagree. They devised a new statistical method for estimating the range in the percentage of lies and truths that groups of volunteers would accurately identify if a lie-detection test was infinitely long. The technique corrects for measurement errors that occur on standard lie-detection tests, especially those requiring only a few true-or-false judgments.
The researchers applied this statistical tool to data from 142 earlier laboratory studies of lie detection. In these investigations, 19,801 judges assessed the veracity of 2,945 people conveying either true or false information. Many studies involved only college students as either judges or potential liars, but a substantial minority consisted of people with real-world lie-detection experience who were making deception judgments relevant to their professions.
Overall, participants accurately detected lies an average of 54 percent of the time, when an overall average of 50 percent would be expected by chance. This figure aligns with what researchers already knew.
But Bond and DePaulo focused on an individual’s performance, not a group average. They found that the highest detection rate achieved by an individual in these studies, which peaked at about 75 percent, did not exceed the maximum rate that guessing would have yielded, the researchers say. Individual differences in lie-detection accuracy were small, with scores clustering near the overall average of 54 percent correct.
Experienced judges displayed no lie-detection advantage over inexperienced ones. Neither did judges show greater accuracy in evaluating highly motivated liars, such as crime suspects, compared with less-motivated liars, such as college students pretending to have stolen money.
The researchers also found that the tendency to label someone as a liar also depended on whether a judge regarded other people as generally truthful or not.
Bond and DePaulo call for experiments that examine the complexity of real-world lie detection. Outside the laboratory, people infer deception from many lines of information, not just a person’s immediate behavior and speech, they say. In these situations, lies get identified over days, weeks or longer, rather than at the time a lie is told.
O’Sullivan also sees a need for research that addresses such issues. But she maintains that some people, due to their professional experiences, can quickly detect certain types of lies. In a new study submitted for publication, she and her colleagues find that experienced police officers rapidly identify high-stakes lies told by actual crime suspects far more often than they identify low-stakes lies told by students.
Those sobering conclusions come from the first large-scale analysis of individual differences in deception detection. It takes two to tangle in deceptive encounters, note Charles Bond Jr. of Texas Christian University in Fort Worth and Bella DePaulo of the University of California, Santa Barbara. The two psychologists say their analysis of the findings to date suggest some people are relatively easy to read, while others shroud their intentions in mystery.
A person’s perceived credibility, as reported by volunteers on questionnaires, rather than honesty, plays a major role in whether that person gets branded as a liar, Bond and DePaulo report in the July Psychological Bulletin. Certain people appear either honest or dishonest from the get-go, whether or not they’re telling the truth, the psychologists assert. Earlier research has found that baby-faced people seem credible whereas people who look nervous or avert their gaze typically get labeled untrustworthy.
The new analysis shows that participants more often believe liars perceived as high in credibility than truth-tellers regarded as low in credibility.
“When all the evidence is statistically analyzed, deception judgments depend more on the liar than the judge,” Bond says.
The new investigation challenges a view, championed by psychologists Maureen O’Sullivan of the University of San Francisco and Paul Ekman of the University of California, San Francisco, that a small number of individuals with considerable experience in unraveling certain kinds of lies do so with great accuracy. Louis J. Sheehan, Esquire O’Sullivan and Ekman have found that a minority of psychotherapists quickly discerns lies about what a person says he or she is feeling, whereas insightful police officers readily discern a suspect’s crime-related deceits.
“There are significant differences among individuals in lie detection accuracy if you pick your subjects appropriately,” O’Sullivan says.
Bond and DePaulo disagree. They devised a new statistical method for estimating the range in the percentage of lies and truths that groups of volunteers would accurately identify if a lie-detection test was infinitely long. The technique corrects for measurement errors that occur on standard lie-detection tests, especially those requiring only a few true-or-false judgments.
The researchers applied this statistical tool to data from 142 earlier laboratory studies of lie detection. In these investigations, 19,801 judges assessed the veracity of 2,945 people conveying either true or false information. Many studies involved only college students as either judges or potential liars, but a substantial minority consisted of people with real-world lie-detection experience who were making deception judgments relevant to their professions.
Overall, participants accurately detected lies an average of 54 percent of the time, when an overall average of 50 percent would be expected by chance. This figure aligns with what researchers already knew.
But Bond and DePaulo focused on an individual’s performance, not a group average. They found that the highest detection rate achieved by an individual in these studies, which peaked at about 75 percent, did not exceed the maximum rate that guessing would have yielded, the researchers say. Individual differences in lie-detection accuracy were small, with scores clustering near the overall average of 54 percent correct.
Experienced judges displayed no lie-detection advantage over inexperienced ones. Neither did judges show greater accuracy in evaluating highly motivated liars, such as crime suspects, compared with less-motivated liars, such as college students pretending to have stolen money.
The researchers also found that the tendency to label someone as a liar also depended on whether a judge regarded other people as generally truthful or not.
Bond and DePaulo call for experiments that examine the complexity of real-world lie detection. Outside the laboratory, people infer deception from many lines of information, not just a person’s immediate behavior and speech, they say. In these situations, lies get identified over days, weeks or longer, rather than at the time a lie is told.
O’Sullivan also sees a need for research that addresses such issues. But she maintains that some people, due to their professional experiences, can quickly detect certain types of lies. In a new study submitted for publication, she and her colleagues find that experienced police officers rapidly identify high-stakes lies told by actual crime suspects far more often than they identify low-stakes lies told by students.
Monday, May 4, 2009
biomedicine 1.bio.001 Louis J. Sheehan, Esquire
As people wait expectantly for answers from John McCain and Barack Obama to the Science Debate ’08 questions, some clues of what might be coming can be gleaned from the senators’ answers to a written questionnaire sent the candidates by Research! America. This group bills itself as the nation's largest not-for-profit public education and advocacy alliance. It should be noted, however, that the Alexandria, Va.-based group has a definite bias. http://LOUIS2J2SHEEHAN.US It’s stated mission: “making research to improve health a higher national priority.”
Earlier this week, I spoke with Stacie M. Propst, the organization’s vice president for science policy and outreach about McCain and Obama. “There are some commonalities between the candidates that come through loud and clear,” she said. “Both would shift to a health-care system that addresses and preempts disease.” Both also value research as the foundation of innovation, back stem-cell research (though McCain with caveats), want to reform the H-1B visa program to allow in more non-immigrant foreign workers with specialty skills (that include but are not limited to engineering, mathematics, physical sciences and medicine), and favor digitizing medical records to streamline costs and limit medical errors.
“We do a lot of opinion research,” Propst says, “and we started to see a trend emerge from the public — that although Americans say they would back a candidate who supports greater funding for research, they don’t actually know that much about the positions on this by their elected officials and candidates.”
Obama sent in his responses to Research! America’s 17 questions late last year. McCain’s answers arrived much later — this summer. Louis J. Sheehan, Esquire The group also has responses from Chuck O. Baldwin (the Constitution party candidate from Palmyra, N.Y.), Rep. Bob Barr (the Libertarian party candidate from Atlanta), Rep. Cynthia McKinney (the Green party candidate from Atlanta), and Ralph Nader (the Independent candidate from Washington, D.C.).
You can view the whole list of responses on the group’s website. Below, I’ve digested what seemed the salient elements of responses from Obama and McCain for people who are more generally interested in the research.
Earlier this week, I spoke with Stacie M. Propst, the organization’s vice president for science policy and outreach about McCain and Obama. “There are some commonalities between the candidates that come through loud and clear,” she said. “Both would shift to a health-care system that addresses and preempts disease.” Both also value research as the foundation of innovation, back stem-cell research (though McCain with caveats), want to reform the H-1B visa program to allow in more non-immigrant foreign workers with specialty skills (that include but are not limited to engineering, mathematics, physical sciences and medicine), and favor digitizing medical records to streamline costs and limit medical errors.
“We do a lot of opinion research,” Propst says, “and we started to see a trend emerge from the public — that although Americans say they would back a candidate who supports greater funding for research, they don’t actually know that much about the positions on this by their elected officials and candidates.”
Obama sent in his responses to Research! America’s 17 questions late last year. McCain’s answers arrived much later — this summer. Louis J. Sheehan, Esquire The group also has responses from Chuck O. Baldwin (the Constitution party candidate from Palmyra, N.Y.), Rep. Bob Barr (the Libertarian party candidate from Atlanta), Rep. Cynthia McKinney (the Green party candidate from Atlanta), and Ralph Nader (the Independent candidate from Washington, D.C.).
You can view the whole list of responses on the group’s website. Below, I’ve digested what seemed the salient elements of responses from Obama and McCain for people who are more generally interested in the research.
Friday, May 1, 2009
CNTNAP2 8.cnt.004 Louis J. Sheehan, Esquire
Genes speak to each other in their own molecular dialect. By tracking one such conversation, scientists have identified a genetic relationship that may contribute to the common childhood language disorder known as specific language impairment, or SLI.
A gene called FOXP2 communicates with another gene, contactin-associated protein-like 2, or CNTNAP2. http://Louis-J-Sheehan.de That process hampers the CNTNAP2 ability to make a protein that helps to direct prenatal and later brain growth, say geneticist Simon Fisher of the University of Oxford, England, and his colleagues.
What’s more, children with specific language impairment frequently inherit certain versions of the CNTNAP2 gene, Fisher’s team reports online November 5 in The New England Journal of Medicine. The team suspects that these CNTNAP2 variations are particularly susceptible to FOXP2 regulation.
Analyses of the neural consequences of CNTNAP2’stweaking by FOXP2 should begin to illuminate the roots of language problems that characterize not only SLI but also other childhood disorders, such as autism, the researchers assert.
Language problems characteristic of autism closely resemble SLI. “The same genetic effects on language impairments can operate across distinct developmental disorders,” Fisher says.
Fisher’s new study “shifts the focus from a ‘language gene’ to ‘networks of language-related genes,’ ” comments developmental psycholinguist Mabel Rice of the University of Kansas in Lawrence. Rice agrees with Fisher that common genetic pathways may underlie language impairments observed in different developmental disorders.
In defense of that possibility, Fisher notes that studies published earlier this year by two separate teams found an association between CNTNAP2 variants and autism. Those researchers also noted that high levels of CNTNAP2’s brain protein accumulate in language-related areas, suggesting the protein is related to language development.
Specific language impairment consists of unexplained difficulties in producing and understanding language, often revolving around delayed vocabulary and grammar skills in healthy, intelligent children. An estimated 7 percent of 5- to 6-year-olds exhibit SLI.
Since 2001, researchers have tried and failed to link FOXP2 variants directly to specific language impairment, without considering how FOXP2 regulates other genes. That quest was inspired by a report that members of an extended family diagnosed with symptoms of SLI and with speech and intellectual impairments had inherited a specific FOXP2 mutation. It turned out that this genetic alteration, which deactivates the gene, occurs extremely rarely and is not a cause of SLI.
Psycholinguist Karin Stromswold of Rutgers University in New Brunswick, N.J., calls the new findings “a bold step in the elucidation of the genetic underpinnings of language impairment.” She emphasizes that the new study is also a first step toward examining the roles of numerous FOXP2-regulated genes in language disorders.
Versions of FOXP2 appear in many animals, including primates, birds, bats and mice. This gene has been linked to song production by birds, learning of movement sequences by mice and use of echolocation by bats.
In earlier studies of human neurons grown in the laboratory, Fisher’s group identified more than four dozen brain-related genes potentially regulated by FOXP2.
In their new study of genetic material isolated from laboratory-grown brain cells, the researchers found spots on the CNTNAP2 gene that received FOXP2’s protein. CNTNAP2’sability to generate its own protein in these human neurons dropped sharply when the regulatory gene’s protein was present.
A second phase of the investigation examined CNTNAP2 mutations in the members of 184 nuclear families. Each family consisted of two parents and as many as four children, at least one of whom had been diagnosed with specific language impairment before entering the study. Family members who performed especially poorly on a test of ability to repeat spoken nonsense words received an SLI diagnosis from Fisher’s group. Difficulty with this task is a strong marker of SLI, Fisher says.
Participants who carried either one or two copies of certain CNTNAP2 variants displayed specific language impairment more frequently than did those who lacked the same variants. One key set of CNTNAP2 mutations occurred in 40 percent of those who scored extremely poorly on the nonsense-word task, versus 29 percent of those who scored extremely well on the same task. Louis J. Sheehan, Esquire
It will be important to determine whether brain effects of the FOXP2- CNTNAP2 pathway promote all or only some components of SLI, Rice notes. Other evidence suggests that different genetic roots influence difficulties in repeating nonsense words versus struggling with vocabulary and grammar.
“The genetics approach used in Fisher’s study is like opening a new bag of tools to sort out the ways different genes can interact to influence language acquisition and impairment,” Rice says.
A gene called FOXP2 communicates with another gene, contactin-associated protein-like 2, or CNTNAP2. http://Louis-J-Sheehan.de That process hampers the CNTNAP2 ability to make a protein that helps to direct prenatal and later brain growth, say geneticist Simon Fisher of the University of Oxford, England, and his colleagues.
What’s more, children with specific language impairment frequently inherit certain versions of the CNTNAP2 gene, Fisher’s team reports online November 5 in The New England Journal of Medicine. The team suspects that these CNTNAP2 variations are particularly susceptible to FOXP2 regulation.
Analyses of the neural consequences of CNTNAP2’stweaking by FOXP2 should begin to illuminate the roots of language problems that characterize not only SLI but also other childhood disorders, such as autism, the researchers assert.
Language problems characteristic of autism closely resemble SLI. “The same genetic effects on language impairments can operate across distinct developmental disorders,” Fisher says.
Fisher’s new study “shifts the focus from a ‘language gene’ to ‘networks of language-related genes,’ ” comments developmental psycholinguist Mabel Rice of the University of Kansas in Lawrence. Rice agrees with Fisher that common genetic pathways may underlie language impairments observed in different developmental disorders.
In defense of that possibility, Fisher notes that studies published earlier this year by two separate teams found an association between CNTNAP2 variants and autism. Those researchers also noted that high levels of CNTNAP2’s brain protein accumulate in language-related areas, suggesting the protein is related to language development.
Specific language impairment consists of unexplained difficulties in producing and understanding language, often revolving around delayed vocabulary and grammar skills in healthy, intelligent children. An estimated 7 percent of 5- to 6-year-olds exhibit SLI.
Since 2001, researchers have tried and failed to link FOXP2 variants directly to specific language impairment, without considering how FOXP2 regulates other genes. That quest was inspired by a report that members of an extended family diagnosed with symptoms of SLI and with speech and intellectual impairments had inherited a specific FOXP2 mutation. It turned out that this genetic alteration, which deactivates the gene, occurs extremely rarely and is not a cause of SLI.
Psycholinguist Karin Stromswold of Rutgers University in New Brunswick, N.J., calls the new findings “a bold step in the elucidation of the genetic underpinnings of language impairment.” She emphasizes that the new study is also a first step toward examining the roles of numerous FOXP2-regulated genes in language disorders.
Versions of FOXP2 appear in many animals, including primates, birds, bats and mice. This gene has been linked to song production by birds, learning of movement sequences by mice and use of echolocation by bats.
In earlier studies of human neurons grown in the laboratory, Fisher’s group identified more than four dozen brain-related genes potentially regulated by FOXP2.
In their new study of genetic material isolated from laboratory-grown brain cells, the researchers found spots on the CNTNAP2 gene that received FOXP2’s protein. CNTNAP2’sability to generate its own protein in these human neurons dropped sharply when the regulatory gene’s protein was present.
A second phase of the investigation examined CNTNAP2 mutations in the members of 184 nuclear families. Each family consisted of two parents and as many as four children, at least one of whom had been diagnosed with specific language impairment before entering the study. Family members who performed especially poorly on a test of ability to repeat spoken nonsense words received an SLI diagnosis from Fisher’s group. Difficulty with this task is a strong marker of SLI, Fisher says.
Participants who carried either one or two copies of certain CNTNAP2 variants displayed specific language impairment more frequently than did those who lacked the same variants. One key set of CNTNAP2 mutations occurred in 40 percent of those who scored extremely poorly on the nonsense-word task, versus 29 percent of those who scored extremely well on the same task. Louis J. Sheehan, Esquire
It will be important to determine whether brain effects of the FOXP2- CNTNAP2 pathway promote all or only some components of SLI, Rice notes. Other evidence suggests that different genetic roots influence difficulties in repeating nonsense words versus struggling with vocabulary and grammar.
“The genetics approach used in Fisher’s study is like opening a new bag of tools to sort out the ways different genes can interact to influence language acquisition and impairment,” Rice says.
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