Links for Keyword: Genes & Behavior

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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

By Rachel Ehrenberg That honeybee lazily probing a flower may actually be a stealth explorer, genetically destined to seek adventure from birth. Bees who consistently explore new environments for food have different genetic activity in their brains than their less-adventurous hive mates, scientists report in the March 9 Science. This genetic activity relates to making particular chemical signals, some of which are linked to behaviors such as thrill-seeking in people. “This is an exciting paper that raises a lot of interesting questions,” says neurobiologist Alison Mercer of the University of Otago in New Zealand. To test the notion of whether bees have personality, scientists led by entomologist Gene Robinson of the University of Illinois at Urbana-Champaign focused on scout bees that embark on reconnaissance missions for food. The team, which included bee expert Tom Seeley of Cornell University, placed a hive in an enclosure with a brightly colored feeder full of sugar water and marked the bees that visited. A few days later, the researchers added a new feeder to the enclosure, while keeping the original one full of fresh sugar water. Some of the bees discovered the new feeder and were also marked. Then the researchers removed the new feeder and added a different one in a new place. Again, some of the bees discovered this new feeder. The bees that found the new feeder both times were considered scouts, while the bees that ate only at the same old feeder were considered nonscouts. © Society for Science & the Public 2000 - 2012

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: 16492 - Posted: 03.10.2012

By Tina Hesman Saey Scientists have built a better mouse. But rest easy — these mice don’t require improved traps. The new mice may give scientists an advantage in tracing genetic sources of common diseases and investigating interactions between genes and environmental factors. In a series of 15 papers published in the February issues of Genetics and G3: Genes, Genomes, Genetics, researchers describe the creation of the new-and-improved mice, known as the Collaborative Cross strains, and some of the ways scientists may use the mice in medical studies. Biomedical researchers use inbred strains of mice to mimic human diseases and probe the genetics involved. Every mouse in an inbred strain is a genetic clone. That’s useful because the mice all generally respond in the same way to a drug or to infection with a virus. And altering the function of a single gene and seeing what happens in these mice can help scientists decipher the role of that gene in disease processes. But because all the mice react so uniformly, they don’t reflect the range of responses humans may have. With conventional laboratory mice, it is also difficult to determine how multiple genes interact with each other or how disease-associated genes are influenced by the environment. © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 16401 - Posted: 02.20.2012

For the first time, scientists have tracked the activity, across the lifespan, of an environmentally responsive regulatory mechanism that turns genes on and off in the brain's executive hub. Among key findings of the study by National Institutes of Health scientists: genes implicated in schizophrenia and autism turn out to be members of a select club of genes in which regulatory activity peaks during an environmentally-sensitive critical period in development. The mechanism, called DNA methylation, abruptly switches from off to on within the human brain's prefrontal cortex during this pivotal transition from fetal to postnatal life. As methylation increases, gene expression slows down after birth. Epigenetic mechanisms like methylation leave chemical instructions that tell genes what proteins to make –what kind of tissue to produce or what functions to activate. Although not part of our DNA, these instructions are inherited from our parents. But they are also influenced by environmental factors, allowing for change throughout the lifespan. “Developmental brain disorders may be traceable to altered methylation of genes early in life,” explained Barbara Lipska, Ph.D., a scientist in the NIH’s National Institute of Mental Health (NIMH) and lead author of the study. “For example, genes that code for the enzymes that carry out methylation have been implicated in schizophrenia. In the prenatal brain, these genes help to shape developing circuitry for learning, memory and other executive functions which become disturbed in the disorders. Our study reveals that methylation in a family of these genes changes dramatically during the transition from fetal to postnatal life – and that this process is influenced by methylation itself, as well as genetic variability. Regulation of these genes may be particularly sensitive to environmental influences during this critical early life period.”

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: 16342 - Posted: 02.04.2012

by Virginia Morell As every dog owner knows, teaching Fido to lie down and be calm can be a giant hurdle in obedience class. Now, it turns out that at least among German Shepherds, genetics play a big role in whether your pet earns a gold star. Researchers gave 104 of the dogs the lie-down-and-be-calm test, and three other behavioral exams, all designed to assess the dogs' ability to control their impulses. Later, the scientists compared the canines' DNA, looking specifically at a gene that is connected to the production of dopamine and norepinephrine. These neurotransmitters are involved in our emotional responses and ability to focus, and have been implicated in humans with attention deficit disorder. The 37 German Shepherds with a shortened version of the gene had the most trouble controlling their impulsive behaviors, regardless of their sex, age, or training. But the dogs with long versions of the gene, such as the one in the photo, passed the impulse-tests with the calm of Zen master. The study, reported in the current issue of PLoS ONE, may not only help breeders identify hyperactive dogs, but could prove useful in studies of ADHD in humans. © 2010 American Association for the Advancement of Science.

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: 16269 - Posted: 01.19.2012

by Kai Kupferschmidt Those palm readers predicting your age from your lifeline are making it up. But now scientists say they have found a true lifeline in the cells of Zebra finches. The birds with the longest telomeres—the protective caps at the ends of chromosomes—live the longest, according to a new study. "It is the first time this has been shown for any species," says María Blasco, a telomere researcher at the Spanish National Cancer Research Centre in Madrid, who was not involved in the work. Telomeres are repetitive DNA sequences that, together with some proteins, sit at the ends of chromosomes to keep them from fraying. They have long been known to shorten with age, and when they reach a critical length, cells stop dividing. While abnormally short telomeres have been implicated in some diseases, studies investigating whether longer telomeres lead to a longer life have shown mixed results. Now biologist Pat Monaghan and her colleagues at the University of Glasgow in the United Kingdom have come up with the best evidence yet that telomere length correlates with life span. The scientists measured telomere length in red blood cells of 99 captive zebra finches (Taeniopygia guttata). The birds resemble long-lived animals in that there is little restoration of telomeres in body cells as they age. The first measurement was taken at 25 days; the researchers then followed the birds over their natural life span, ranging from less than a year to nearly 9 years, and measured telomeres again at various time points. They found a highly significant correlation between telomere length at 25 days and life span; birds with longer telomeres lived longer. Length measured at 1 year also predicted life span, but the relationship was weaker, whereas at later time points (after 3, 4, 6, and 7 years) there was no correlation, the team reports online today in the Proceedings of the National Academy of Sciences. © 2010 American Association for the Advancement of Science.

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: 16239 - Posted: 01.10.2012

By Virginia Hughes Among the bloodletting boxes, ether inhalers, kangaroo-tendon sutures and other artifacts stored at the Indiana Medical History Museum in Indianapolis are hundreds of scuffed-up canning jars full of dingy yellow liquid and chunks of human brains. Until the late 1960s the museum was the pathology department of the Central Indiana Hospital for the Insane. The bits of brain in the jars were collected during patient autopsies performed between 1896 and 1938. Most of the jars sat on a shelf until the summer of 2010, when Indiana University School of Medicine pathologist George Sandusky began popping off the lids. Frustrated by a dearth of postmortem brain donations from people with mental illness, Sandusky—who is on the board of directors at the museum—seized the chance to search this neglected collection for genes that contribute to mental disorders. Sandusky is not alone. Several research groups are now seeking ways to mine genetic and other information hidden in old, often forgotten tissue archives—a handful of which can be found in the U.S., along with many more in Europe. Several technical hurdles stand in the way, but if these can be overcome, the archives would offer several advantages. Beyond supplying tissues that can be hard to acquire at a time when autopsies are on the decline, the vintage brains are untainted by modern psychiatric drugs and are often paired with detailed clinical notes that help researchers make more accurate post hoc diagnoses. © 2012 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 16234 - Posted: 01.10.2012