Links for Keyword: Genes & Behavior

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By Tina Hesman Saey COLD SPRING HARBOR, N.Y. – Taming foxes changes not only the animals’ behavior but also their brain chemistry, a new study shows. The finding could shed light on how the foxes’ genetic cousins, wolves, morphed into man’s best friend. Lenore Pipes of Cornell University presented the results May 10 at the Biology of Genomes conference. The foxes she worked with come from a long line started in 1959 when a Russian scientist named Dmitry Belyaev attempted to recreate dog domestication, but using foxes instead of wolves. He bred silver foxes (Vulpes vulpes), which are actually a type of red fox with white-tipped black fur. Belyaev and his colleagues selected the least aggressive animals they could find at local fox farms and bred them. Each generation, the scientists picked the tamest animals to mate, creating ever friendlier foxes. Now, more than 50 years later, the foxes act like dogs, wagging their tails, jumping with excitement and leaping into the arms of caregivers for caresses. At the same time, the scientists also bred the most aggressive foxes on the farms. The descendents of those foxes crouch, flatten their ears, growl, bare their teeth and lunge at people who approach their cages. The foxes’ tame and aggressive behaviors are rooted in genetics, but scientists have not found DNA changes that account for the differences. Rather than search for changes in genes themselves, Pipes and her colleagues took an indirect approach, looking for differences in the activity of genes in the foxes’ brains. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18164 - Posted: 05.16.2013

Ed Yong The US adolescents who signed up for the Study of Mathematically Precocious Youth (SMPY) in the 1970s were the smartest of the smart, with mathematical and verbal-reasoning skills within the top 1% of the population. Now, researchers at BGI (formerly the Beijing Genomics Institute) in Shenzhen, China, the largest gene-sequencing facility in the world, are searching for the quirks of DNA that may contribute to such gifts. Plunging into an area that is littered with failures and riven with controversy, the researchers are scouring the genomes of 1,600 of these high-fliers in an ambitious project to find the first common genetic variants associated with human intelligence. The project, which was launched in August 2012 and is slated to begin data analysis in the next few months, has spawned wild accusations of eugenics plots, as well as more measured objections by social scientists who view such research as a distraction from pressing societal issues. Some geneticists, however, take issue with the study for a different reason. They say that it is highly unlikely to find anything of interest — because the sample size is too small and intelligence is too complex. Earlier large studies with the same goal have failed. But scientists from BGI’s Cognitive Genomics group hope that their super-smart sample will give them an edge, because it should be enriched with bits of DNA that confer effects on intelligence. “An exceptional person gets you an order of magnitude more statistical power than if you took random people from the population — I’d say we have a fighting chance,” says Stephen Hsu, a theoretical physicist from Michigan State University in East Lansing, who acts as a scientific adviser to BGI and is one of the project’s leaders. © 2013 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 1: An Introduction to Brain and Behavior
Link ID: 18159 - Posted: 05.15.2013

Stephen S. Hall Male sexual dysfunction is never pretty, even in nematodes. In normal roundworm courtship, a slender male will sidle up to a plump hermaphrodite, make contact, and then initiate a set of steps leading up to insemination: a sinuous backwards motion as he searches for the sexual cleft, a pause to probe, and finally the transfer of sperm. The whole business is usually over in a couple of minutes. “It's very slithery, and affectionate,” says Cornelia Bargmann, who has been observing the behaviour of this particular worm, Caenorhabditis elegans, for 25 years. Last October, scientists in Bargmann's laboratory at the Rockefeller University, New York, reported the discovery of a gene that seems to be crucial to successful mating. Disrupting the action of this gene causes male sexual confusion of almost epic pathos: nematodes with certain mutations poke tentatively at an inert hermaphrodite, making confused, fruitless curlicues around the potential mate. Occasionally the mutant male succeeds, but often he literally falls off the job and begins the search anew for a mate. Jennifer Garrison, a postdoc of Bargmann's who tracked the behaviour of these males, just shakes her head as she replays the scene on her computer screen. “Really sad,” she says. There are two punchlines to this story of thwarted invertebrate mating. One is the charming squeamishness with which Bargmann describes it, hesitating at words such as “vulva” and “spicule” and other anatomical gewgaws of roundworm reproduction. “As a well-brought-up Southern girl,” she says with a laugh, “it's still difficult to talk about this!” © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17828 - Posted: 02.20.2013

IF TWO animals have identical brain cells, how different can they really be? Extremely. Two worm species have exactly the same set of neurons, but extensive rewiring allows them to lead completely different lives. Ralf Sommer of the Max Planck Institute for Developmental Biology in Tübingen, Germany, and colleagues compared Caenorhabditis elegans, which eats bacteria, with Pristionchus pacificus, which hunts other worms. Both have a cluster of 20 neurons to control their foregut. Sommer found that the clusters were identical. "These species are separated by 200 to 300 million years, but have the same cells," he says. P. pacificus, however, has denser connections than C. elegans, with neural signals passing through many more cells before reaching the muscles (Cell, doi.org/kbh). This suggests that P. pacificus is performing more complex motor functions, says Detlev Arendt of the European Molecular Biology Laboratory in Heidelberg, Germany. Arendt thinks predators were the first animals to evolve complex brains, to find and catch moving prey. He suggests their brains had flexible wiring, enabling them to swap from plant-eating to hunting. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17749 - Posted: 02.04.2013

by Michael Balter CAMBRIDGE, UNITED KINGDOM—Siberia may not be everyone's idea of a tourist destination, but it has been home to humans for tens of thousands of years. Now a new study of indigenous Siberian peoples presented here earlier this month at a meeting on human evolution reveals how natural selection helped people adapt to the frigid north. The findings also show that different living populations adapted in somewhat different ways. Siberia occupies nearly 10% of Earth's land mass, but today it's home to only about 0.5% of the world's population. This is perhaps not surprising, since January temperatures average as low as -25°C. Geneticists have sampled only a few of the region's nearly one dozen indigenous groups; some, such as the 2000-member Teleuts, descendants of a once powerful group of horse and cattle breeders also known for their skill in making leather goods, are in danger of disappearing. Previous research on cold adaptation included two Siberian populations and implicated a couple of related genes. For example, genes called UCP1 and UCP3 tend to be found in more active forms in populations that live in colder climes, according to work published in 2010 by University of Chicago geneticist Anna Di Rienzo and her colleagues. These genes help the body's fat stores directly produce heat rather than producing chemical energy for muscle movements or brain functions, a process called "nonshivering thermogenesis." The new study sampled Siberians much more intensely, including 10 groups that represent nearly all of the region's native populations. © 2010 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 17730 - Posted: 01.29.2013

Ewen Callaway Even as home experiments go, Hopi Hoekstra’s one was peculiar: she built a giant plywood box in her garage in San Diego, California, filled it with more than a tonne of soil and then let a pet mouse dig away. “This thing was bursting at its seams and held together with duct tape,” says the evolutionary biologist, now at Harvard University in Cambridge, Massachusetts. “But it worked.” It allowed her to study the genetics of burrowing behaviour in a controlled setting. Armed with plastic casts of the burrows and state-of-the-art sequencing, Hoekstra’s team discovered clusters of genes that partly explain why the oldfield mouse (Peromyscus polionotus) builds elaborate two-tunnel burrows, whereas its close relative, the deer mouse (Peromyscus maniculatus), goes for a simple hole in the ground1. The findings highlight an underappreciated benefit of a genomics revolution that is moving at breakneck speed. Thanks to cheap and quick DNA sequencing, scientists interested in the genetics of behaviour need not limit themselves to a handful of favourite lab organisms. Instead, they can probe the genetic underpinnings of behaviours observed in the wild, and glean insights into how they evolved. “In my mind, the link between genes and behaviour in natural populations and organisms is the next great frontier in biology,” says Hoekstra. Oldfield mice are native to the southeastern United States, where they burrow in soils ranging from sandy beaches to silt-rich clays. Wherever they dig, their holes look much the same, with a long entrance tunnel and a second tunnel that stops short of the surface and allows them to escape predators. Such invariability hints that the trait is encoded in DNA, says Hoekstra. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17693 - Posted: 01.17.2013

by Elizabeth Norton To humans, all fire ants may look alike. But the tiny, red, stinging bugs known as Solenopsis invicta have two types of social organization, and these factions are as recognizable to the ants as rival football teams are to us. Researchers once thought that the groups' distinct physiological and behavioral profiles stemmed from a variant in a single gene. Now, a new study provides the first evidence that the gene in question is bound up in a bundle of some 600 other genes, versions of which are all inherited together. This "supergene" takes up a large chunk of what may be the first known social chromosome, analogous to the chromosomes that determine sex in humans. The differences between the two types of fire ants start with the winged queens, according to evolutionary geneticist Laurent Keller of the University of Lausanne in Switzerland. A so-called monogyne queen is large, fat, and fertile. Once she's mated, she can fly long distances to start her colony, nourishing her eggs from her fat stores, and then wait until her larvae grow up into workers. A monogyne colony will accept only the original queen and kill any other that shows up; these ants are very aggressive in general. By contrast, a polygyne queen is smaller and needs mature workers to help set up a colony. Thus polygyne communities will accept multiple queens from nearby nests—unless, that is, one happens to be a monogyne, in which case, they kill her. In 1998, working with entomologist and geneticist Kenneth Ross of the University of Georgia in Athens, Keller showed that the two groups of fire ants had distinct versions of a gene known as Gp-9. All of the monogynes had two copies of one form; among the polygynes, many had one normal and one mutated copy of the gene. At first glance, the finding made sense. © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 17691 - Posted: 01.17.2013

By Razib Khan In Slate there is an important piece up, The Early Education Racket, which attempts to reassure upper middle striving types that it isn’t the end of the world if their children don’t get into the right preschool. It is important because there are many people out there with lots of money (or perhaps more accurately, just enough money) and no common sense. Though the author, Melinda Wenner Moyer, offers that she’s not “making a Bell Curve argument here,” the general thesis that there are diminishing returns to inputs on childhood environment is well known to anyone with a familiarity with behavior genetics. Here’s a piece in Psychology Today from 1993, So Long, Superparents: If you are doubtful of this, I recommend you read The Nurture Assumption. This book was published in 1999, and Steve Pinker reported on the results in The Blank Slate a few years later, where I first encountered the thesis. The basic insight, that parental home environment seems to have minimal predictive power in explaining variation in outcomes, is still not very well known. The two primary issues to keep in mind are: 1) A substantial proportion of the variation in I.Q. and personality is heritable in a genetic sense. Many observations of parent-child similarities presumed that they were due to learning and emulation, but statistical analysis suggests this is not the case. Today, with genomic understanding of sibling relatedness (recall that though siblings should be related 0.50, there is some variation about this value) this seems more true than ever; much of the difference between siblings seems to be due to the variation of their genetic make up.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17688 - Posted: 01.17.2013

By Gary Stix The Atlantic featured a captivating fantasy in its November issue about a scenario to assassinate the U.S. president in 2016 by using a bioweapon specifically tailored to his genetic makeup—a virus that targeted the commander in chief and no one else. A great plot for a Hollywood thriller. But will we really see four years from now an engineered pathogen that could home in on just one person’s DNA, a lethal microbe that could be transmitted from person to person by a sneeze? The authors, including “genomic futurist” Andrew Hessel and cybercrime expert Marc Goodman, both faculty at Ray Kurzweil’s Singularity University, acknowledge that the plausibility of a hit on the president by the time of the next election might be reaching a bit. A personal gene bomb monogrammed for Barack Obama is still beyond the technical acumen of the best genetic engineers. But there is one good use beyond the cloaks and daggers to which the president’s genes might eventually be put. As Obama begins his second term next week, he has begun to contemplate his historical legacy. For his third act—that is, once he leaves office—he might consider extending that legacy further by undertaking a whole genome scan. Obama’s genome, as much as that of anyone alive, might help a bit in the long-running search for genes associated with emotional and psychological resilience. Anyone who runs for president and gets the nomination has to display a measure of mental toughness, and so might carry a set of such genes. Romney was a toughie too—recall the first debate—but he was also to the manner born, doing what was expected for someone of his breeding. © 2013 Scientific American

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 11: Emotions, Aggression, and Stress
Link ID: 17684 - Posted: 01.15.2013

By Susan Lunn, CBC News It's the time of year when people take stock of the past 12 months, and make resolutions for the New Year. That's kind of what Svante Paabo is doing — but the Swedish archeological geneticist is looking over a time span of 30,000 years. He's almost finished mapping the DNA of neanderthal man, a distant cousin of modern humans. Paabo has found that many people today carry within their DNA about 3 to 5 per cent in common with neanderthals. Paabo says it's important to learn more about our caveman cousins' DNA to reveal the differences between us and them, differences that have seen modern humans surive and thrive over the millennia, while neanderthals have become extinct. "I really hope that over the next 10 years we will understand much more of those things that set us apart. Which changes in our genome made human culture and technology possible? And allowed us to expand and become 7, 8, 9 billion people and spread all over the world?," he asked at a recent genetic conference in Ottawa. The room was packed with people from across North America who wanted to hear Paabo speak. He's recognized as the inspiration for Michael Crichton's Jurassic Park. © CBC 2012

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17642 - Posted: 12.29.2012

  By Jason G. Goldman In 1976, psychologists John and Sandra Condry of Cornell University had 204 human adults view videotaped footage of an infant boy named David and infant girl named Dana, and asked them to describe the infants’ facial expressions and dispositions. They described their findings in an article in the journal Child Development. In the video, infants were shown responding to various stimuli, which were not visible to the viewer. For example, they’d be shown a teddy bear, so that their reaction could be recorded. They were also videotaped responding to a loud buzzer and to a jack-in-the-box. Participants described David’s response to the jack-in-the-box, for example, as “anger,” while they described Dana’s response to the same toy as “fear.” Participants rated David’s emotional responses to all three stimuli as more “intense” than Dana’s. Here’s the catch: David and Dana were the same infant. Each of the experiment participants were shown the same video of the same infant. Half of them were told the infant was a nine-month-old boy named David, and half were told the infant was a nine-month-old girl named Dana. That they described the “two” infants in such different ways was evidence that the participants’ perceptions were at least based in part upon pre-existing biases and preconceptions about the different ways in which boys and girls experience the world. Now, a group of researchers from Tokyo and Berlin have published a new finding about the relationship between personality and genetics in captive elephants. They collected genetic information from the blood, feces, tissues, cheek swabs, or hair of 196 Asian (Elephas maximus) and African elephants (Loxodonta africana) in Japanese, American, and Canadian zoos, and sanctuaries in Thailand. Personality information was collected for a seventy-five of those elephants by distributing to questionnaires to their keepers. Each elephant was assessed by more than one keeper. An improved understanding of elephant personality would be not only extremely interesting from a basic science perspective, but also extremely useful for more effectively maintaining captive elephant populations in zoos and sanctuaries. The better that zookeepers and curators understand the psychology of the animals in their collections, the better the quality of care can be, which directly impacts animal welfare. © 2012 Scientific American  

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17313 - Posted: 09.29.2012

Nicky Guttridge Subtle differences in the DNA of honeybees are reflected in the bees' roles within the hive. These DNA modifications are normally fixed, but research published today in Nature Neuroscience1 reveals the first example of reversible changes to DNA associated with behaviour. All honeybees (Apis mellifera) are born equal, but this situation doesn’t last long. Although genetically identical, the bees soon take on the specific roles of queen or worker. These roles are defined not just by behavioural differences, but by physical ones. Underlying them are minor modifications to their DNA: ‘epigenetic’ changes that leave the DNA sequence intact, but that add chemical tags in the form of methyl (CH3) molecules to sections of the DNA. This in turn alters the way a gene is expressed2. Once a bee is a queen or worker, they fulfil that role for life — the change is irreversible. But that is not the case for the subdivisions among the workers. The workers start out as nurses, which look after and feed the queen and larvae, and most then go on to become foragers, which travel out from the hive in search of pollen. Again the two types have very different methylation patterns in their DNA. This time, however, as the latest results show, the DNA modifications are reversible: if a forager reverts to being a nurse, its methylation pattern reverts too. © 2012 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17265 - Posted: 09.17.2012

By Tina Hesman Saey The human genetic instruction book just got more readable. Nearly a decade after the Human Genome Project assembled the genome’s 3 billion chemical units, an international consortium has revealed how the components fit together into sentences and chapters. Already, the genome’s tales are revealing how genetic variants contribute to disease, giving researchers insights into human evolution and even changing how scientists define a gene. “The questions we can now ask are more sophisticated and will yield better answers than the ones we were asking nine years ago,” says Eric Green, director of the National Human Genome Research Institute, which coordinated and funded the mammoth Encyclopedia of DNA Elements, or ENCODE, project. Results from ENCODE, which involves more than 400 researchers around the globe, appear in the Sept. 6 Nature, with more than 30 companion papers published in Science, Genome Research, Genome Biology, Cell and BMC Genetics. When scientists announced the completion of the Human Genome Project in 2003, researchers could pick out genes that carry instructions for building proteins. But that information comprises less than 2 percent of the genome. Some people passed the rest of the genome off as “junk DNA.” © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17230 - Posted: 09.07.2012

By Tina Hesman Saey If variety lends life flavor, then humans are kicking things up to a previously unrecognized notch on the spice-o-meter. New efforts to decipher the genetic blueprints of thousands of people have turned up more than half a million tweaks in human DNA, many more than scientists expected. Most of these tweaks are new to science, and a majority fall into a class called “rare variants,” found in 0.5 percent of the population or less. Some of the variety recently uncovered is so uncommon that it shows up in people living in a single geographic region, or even in only one person. Despite their limited spread, the newly discovered rare variants could profoundly affect susceptibility to disease or how well drugs work. They may also help researchers reconstruct recent human migrations around the world. For years, scientists have been examining the chemical units of DNA called nucleotides that act as letters in the human genetic instruction book. So researchers thought they had a good handle on how often to expect single-letter changes in the A’s, G’s, T’s and C’s in that book. Such changes stem from errors in copying and are spotted via comparison with some majority-rule blueprint. They can go by terms like “single nucleotide polymorphisms” or “mutations” depending on where and when they show up. When looking at 202 genes predicted to be important in diseases from 14,002 people, John Novembre of the University of California, Los Angeles and colleagues unearthed five times as many rare genetic variants as expected. © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 17149 - Posted: 08.11.2012

By Dan Hurley, New studies are raising the hope of finding a pill to improve the intellectual abilities of people with Down syndrome. One study, published online by the journal Translational Psychiatry, is the first ever to show that a drug might improve the verbal memory of people with the disorder. Although the benefits appeared modest and the study was small, Down syndrome experts meeting last week in Washington called it a major development after more than a decade of research in mice and test tubes. “A lot of us are well aware of progress we’ve seen . . . in the past five to 10 years,” said Jamie Edgin, a developmental psychologist at the University of Arizona in Tucson. Among those advances, she said, are tests designed to measure the cognitive abilities of people with Down syndrome. The development of mice with the genetic equivalent of Down syndrome, essential for studies of possible drug treatments, has been another milestone. “There’s a lot of excitement,” Edgin said. The drug used in the recent study, Namenda, is approved for treating Alzheimer’s disease. Although it has shown only a slim and temporary benefit for that condition, a 2007 study of mice with the genetic equivalent of Down syndrome showed that it almost entirely normalized their ability to learn and remember. The effects in humans appeared far less striking. Alberto Costa, a physician and neuroscientist at the University of Colorado in Denver, ran a test involving 42 young adults with Down syndrome, half of whom received a placebo. After 16 weeks, most of the people who received Namenda performed better on tests of memory than they had at the beginning of the study. But the effect was statistically significant on only one of the 14 tests, which some researchers at last week’s meeting said they considered disappointing. © 1996-2012 The Washington Post

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 13: Memory, Learning, and Development
Link ID: 17107 - Posted: 07.31.2012

Daniel H. Geschwind & Genevieve Konopka The decoding of the human and chimpanzee genomes was heralded as an opportunity to truly understand how changes in DNA resulted in the evolution of our cognitive features. However, more than a decade and much detective work later, the functional consequences of such changes have proved elusive, with a few exceptions1, 2. Now, writing in Cell, Dennis et al.3 and Charrier et al.4 describe the evolutionary history and function of the human gene SRGAP2 and provide evidence for molecular and cellular mechanisms that may link the gene's evolution with that of our brain. It was already known that SRGAP2 is involved in brain development5 and that humans have at least three similar copies of the gene, whereas non-human primates carry only one6. However, the study of duplicated, or very similar, segments of DNA is hampered by the fact that most human cells carry two sets of chromosomes (one inherited from each parent), which makes it difficult to distinguish duplicated copies from the different parental forms of the gene. To circumvent this problem, Dennis et al.3 searched for copies of SRGAP2 in the genome of a hydatidiform mole — an abnormal, non-viable human embryo that results from the fusion of a sperm with an egg that has lost its genetic material; it therefore has chromosomes derived from a single parent. The authors showed that humans carry four non-identical copies (named A–D) of SRGAP2 at different locations on chromosome 1. By comparing the genes' sequences with that of the SRGAP2 gene from the orang-utan and chimpanzee, the authors estimated that SRGAP2 was duplicated in the human lineage about 3.4 million years ago, resulting in SRGAP2A (the ancestral version that we share with other primates) and SRGAP2B. Further duplications of SRGAP2B gave rise to SRGAP2C about 2.4 million years ago and to SRGAP2D about 1 million years ago (Fig. 1a). © 2012 Nature Publishing Group

Related chapters from BP7e: Chapter 6: Evolution of the Brain and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 0: ; Chapter 13: Memory, Learning, and Development
Link ID: 16945 - Posted: 06.21.2012

by Moheb Costandi Researchers have yet to understand how genes influence intelligence, but a new study takes a step in that direction. An international team of scientists has identified a network of genes that may boost performance on IQ tests by building and insulating connections in the brain. Intelligence runs in families, but although scientists have identified about 20 genetic variants associated with intelligence, each accounts for just 1% of the variation in IQ scores. Because the effects of these genes on the brain are so subtle, neurologist Paul Thompson of the University of California, Los Angeles, devised a new large-scale strategy for tackling the problem. In 2009, he co-founded the ENIGMA Network, an international consortium of researchers who combine brain scanning and genetic data to study brain structure and function. Earlier this year, Thompson and his colleagues reported that they had identified genetic variants associated with head size and the volume of the hippocampus, a brain structure that is crucial for learning and memory. One of these variants was also weakly associated with intelligence. Those carrying it scored on average 1.29 points better on IQ tests than others, making it one of the strongest candidate intelligence genes so far. The researchers have now used the same strategy to identify more genetic variants associated with brain structure and IQ. In the new study, they analyzed brain images and whole-genome data from 472 Australians, including 85 pairs of identical twins, 100 pairs of nonidentical twins, and their nontwin siblings. They identified 24 genetic variations within six different genes, all of which were linked to differences in the structural integrity of major brain pathways. © 2010 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 1: An Introduction to Brain and Behavior
Link ID: 16942 - Posted: 06.20.2012

by Linda Geddes They might share the same DNA and cramped living space, but as these images reveal, life is anything but identical for unborn twins. This unprecedented glimpse into their inner world is afforded through a recently developed form of magnetic resonance imaging (MRI), which is being turned on twins for the first time. Whereas conventional MRI takes snapshots of thin slices of the body as it penetrates through it, so-called cinematic-MRI takes repeated images of the same slice, then stitches them together to create a videoMovie Camera. This means that a moving structure such as a fetus – or several fetuses – can be visualised in unprecedented detail. "A lot of the so-called videos in the womb are very processed, so they do a lot of reconstructing and computer work afterwards. These are the raw images that are acquired immediately," says Marisa Taylor-Clarke of the Robert Steiner MR Unit at Imperial College London, who recorded the images. She has been using the technique to study twin-to-twin transfusion syndrome, a relatively common complication in which the blood supplies of twins sharing the same placenta become connected. As the twin receiving its sibling's blood grows larger, the growth of the donor twin becomes stunted. In the worst cases it can prove fatal to both twins. Fortunately, an operation that involves blocking the shared blood vessels usually saves them, but its impact on brain development is relatively unknown. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16892 - Posted: 06.09.2012

Ewen Callaway Medical geneticists are giving genome sequencing its first big test in the clinic by applying it to some of their most baffling cases. By the end of this year, hundreds of children with unexplained forms of intellectual disability and developmental delay will have had their genomes decoded as part of the first large-scale, national clinical sequencing projects. These programmes, which were discussed last month at a rare-diseases conference hosted by the Wellcome Trust Sanger Institute near Cambridge, UK, aim to provide a genetic diagnosis that could end years of uncertainty about a child’s disability. In the longer term, they could provide crucial data that will underpin efforts to develop therapies. The projects are also highlighting the logistical and ethical challenges of bringing genome sequencing to the consulting room. “The overarching theme is that genome-based diagnosis is now hitting mainstream medicine,” says Han Brunner, a medical geneticist at the Radboud University Nijmegen Medical Centre in the Netherlands, who leads one of the projects. About 2% of children experience some form of intellectual disability. Many have disorders such as Down’s syndrome and fragile X syndrome, which are linked to known genetic abnormalities and so are easily diagnosed. Others have experienced environmental risk factors, such as fetal alcohol exposure, that rule out a simple genetic explanation. However, a large proportion of intellectual disability cases are thought to be the work of single, as-yet-unidentified mutations. © 2012 Nature Publishing Group

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 16679 - Posted: 04.19.2012

By Eryn Brown, Los Angeles Times Scientists have published a new map of gene variations that influence the risk for various brain diseases and conditions, including Alzheimer’s. More than 200 researchers involved in Project ENIGMA (for Enhancing Neuro Imaging Genetics through Meta-Analysis) pored over thousands of MRI images and DNA screens from 21,151 healthy people. They looked for specific, heritable gene variations that appeared to cause disease. They sought out gene variants associated with reduced brain size, which is a marker for Alzheimer’s disease and dementia, as well as mental health disorders such as schizophrenia and bipolar disorder. They also discovered gene variants associated with larger brain size and increased intelligence. The collaboration was led by the Laboratory of Neuro Imaging at UCLA and researchers in Australia and in the Netherlands, who recruited scientists at more than 100 institutions to pool brain scans and genetic information. “By sharing our data with Project ENIGMA, we created a sample large enough to reveal clear patterns in genetic variation and show how these changes physically alter the brain,” Paul Thompson, a professor of neurology and psychiatry at UCLA who helped lead the effort, said in a statement. The research was published online Sunday by the journal Nature Genetics. Copyright © 2012, Los Angeles Times

Related chapters from BP7e: Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 2: Cells and Structures: The Anatomy of the Nervous System; Chapter 13: Memory, Learning, and Development
Link ID: 16652 - Posted: 04.16.2012