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 BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
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 BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
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 BN: Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 1: Cells and Structures: The Anatomy of the Nervous System; Chapter 4: Development of the Brain
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 BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; 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 BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 12: Psychopathology: The Biology 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 BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
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 BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; 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 BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
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 BN: 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: The Biology of Behavioral Disorders; Chapter 4: Development of the Brain
Link ID: 16234 - Posted: 01.10.2012

Heidi Ledford Protective caps known as telomeres that help to preserve the integrity of chromosomes can also predict lifespan in young zebra finches (Taeniopygia guttata), researchers have found. Telomeres are stretches of repetitive DNA sequence that are found at the ends of chromosomes, where they help to maintain cell viability by preventing the fraying of DNA and the fusion of one chromosome to another. The relationship between normal ageing and telomere decline has long been suspected — and even asserted by some companies that measure customers’ telomere length — but the link remains unproven in humans (see 'Spit test offers guide to health'). Most studies of longevity and telomere length have relied on only one or two measurements from an individual during their lifespan. But population ecologist Pat Monaghan of the University of Glasgow, UK, and her colleagues found that measuring telomere length periodically over the course of a zebra finch’s life revealed a tight association between length and lifespan — particularly when those measurements were taken when the birds were only 25 days old. The results are reported online this week in Proceedings of the National Academy of Sciences1. “This study is important,” says María Blasco, a telomere researcher at the Spanish National Cancer Research Centre in Madrid. “It’s the first time that normal differences in telomere length have been shown to be predictive of longevity.” Blasco was not involved in the current study, but serves as chief scientific adviser for Madrid-based company Life Length, which advertises telomere length measurements as a service for determining an individual’s "biological age". © 2012 Nature Publishing Group,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 16233 - Posted: 01.10.2012

By Tina Hesman Saey By kick-starting a gene that is naturally inactivated, chemotherapy drugs could help reverse a genetic brain disorder that is sometimes mistaken for autism or cerebral palsy. The unexpected finding may also spark a new avenue of research on a type of gene regulation known as imprinting. The genetic disorder, Angelman syndrome, occurs in about one in 15,000 live births. It is caused when the copy of a gene called UBE3A inherited from the mother goes missing or is damaged by a mutation. That’s a problem because the copy of the gene inherited from the father is already turned off in brain cells, leaving no way to make UBE3A protein. Genes such as UBE3A that turn off one parent’s copy are called imprinted genes. Until now, researchers knew of no way short of gene therapy to override the imprinting and restore gene activity. Now, researchers from the University of North Carolina at Chapel Hill have discovered that a type of chemotherapy drug called topoisomerase inhibitors can turn on the father’s inactive copy of the gene in brain cells of mice with a version of Angelman syndrome. The team reports the achievement online December 21 in Nature. The prospect that a drug could correct the underlying defect responsible for Angelman syndrome is exciting, says Stormy Chamberlain, a geneticist at the University of Connecticut Health Center in Farmington. “There’s every reason to have hope that it will help our Angelman syndrome kids,” she says. © Society for Science & the Public 2000 - 2011

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 16179 - Posted: 12.23.2011

By NICHOLAS WADE Social behavior among primates — including humans — has a substantial genetic basis, a team of scientists has concluded from a new survey of social structure across the primate family tree. The scientists, at the University of Oxford in England, looked at the evolutionary family tree of 217 primate species whose social organization is known. Their findings, published in the journal Nature, challenge some of the leading theories of social behavior, including: ¶ That social structure is shaped by environment — for instance, a species whose food is widely dispersed may need to live in large groups. ¶ That complex societies evolve step by step from simple ones. ¶ And the so-called social brain hypothesis: that intelligence and brain volume increase with group size because individuals must manage more social relationships. By contrast, the new survey emphasizes the major role of genetics in shaping sociality. Being rooted in genetics, social structure is hard to change, and a species has to operate with whatever social structure it inherits. If social behavior were mostly shaped by ecology, then related species living in different environments should display a variety of social structures. But the Oxford biologists — Susanne Shultz, Christopher Opie and Quentin Atkinson — found the opposite was true: Primate species tended to have the same social structure as their close relatives, regardless of how and where they live. © 2011 The New York Times Company

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress
Link ID: 16172 - Posted: 12.20.2011

By Tina Hesman Saey Nearly everybody knows that Frank Lloyd Wright designed Fallingwater, the house in Pennsylvania that sits above and appears to cascade into a waterfall. I.M. Pei’s glass pyramid at the Louvre in Paris is similarly famous. And Frank Gehry is widely known for the curvi­linear shining steel Walt Disney Concert Hall in Los Angeles. But most people couldn’t name the contractors and subcontractors responsible for translating those great architects’ blueprints into solid structures. Geneticists have the same problem. Details for erecting an organism’s structure are encoded within DNA, written in chemical subunits designated by the letters A, T, C and G. But it has been hard to say exactly who takes those details and oversees the construction of the organism from proteins and other molecular materials. Only now have scientists begun identifying the previously invisible contractors who make sure that materials get where they are supposed to be and in the right order to build a human being or any other creature. Some of these little-known workers belong to a class of molecules called long intergenic noncoding RNAs. Scientists used to think that these “linc­RNAs” were worthless. As their name suggests, these molecules — at least 200 chemical letters long — do not encode information that the body’s manufacturing machinery can use to cobble together proteins. And the lincRNAs originate in what scientists used to view as barren wastelands between protein-coding genes. But new research is showing that these formerly underappreciated workers have important roles in projects both large and microscopic. © Society for Science & the Public 2000 - 2011

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 16107 - Posted: 12.03.2011

By Tina Hesman Saey WASHINGTON — Separation anxiety in some children may be due to extra doses of a particular gene. The gene, GTF2I, is located on human chromosome 7. People missing part of the chromosome that contains GTF2I have a condition called Williams syndrome and are generally extra social. On the other hand, people who have extra copies of that part of chromosome 7 may have social and other types of anxiety: About 26 percent of children with an extra copy the region containing GTF2I have been diagnosed by a doctor as having separation anxiety, human geneticist Lucy Osborne of the University of Toronto said November 15 at a press conference at the Society for Neuroscience’s annual meeting. Osborne and colleagues genetically engineered mice to have a duplicate copy or two of GTF2I, or to be missing one copy of the gene, then tested the effect of the gene dosage on separation anxiety with a squeak test. Week-old baby mice separated from their mothers send out ultrasonic distress calls. “It’s a ‘come get me’ signal,” Osborne said. Baby mice with a normal two copies of GTF2I squeaked an average of 192 times over four minutes when removed briefly from their nests. Mice with three or four copies squeaked nearly twice as much, indicating greater anxiety at being separated from their mothers. Mice missing one copy of the gene were a little bit less vocal. © Society for Science & the Public 2000 - 2011

Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 16051 - Posted: 11.19.2011

By Laura Sanders Human brains all work pretty much the same and use roughly the same genes in the same way to build and maintain the infrastructure that makes people who they are, two new studies show. And by charting the brain’s genetic activity from before birth to old age, the studies reveal that the brain continually remodels itself in predictable ways throughout life. In addition to uncovering details of how the brain grows and ages, the results may help scientists better understand what goes awry in brain disorders such as schizophrenia and autism. “The complexity is mind-numbing,” says neuroscientist Stephen Ginsberg of the Nathan Kline Institute and New York University Langone Medical Center, who wasn’t involved in the studies. “It puts the brain in rarefied air.” In the studies, published in the Oct. 27 Nature, researchers focused not on DNA — virtually every cell’s raw genetic material is identical — but on when, where and for how long each gene is turned on over the course of a person’s life. To do this, the researchers measured levels of mRNA, a molecule whose appearance marks one of the first steps in executing the orders contained in a gene, in postmortem samples of donated brains that ranged in age from weeks after conception to old age. These different patterns of mRNA levels distinguish the brain from a heart, for instance, and a human from a mouse, too, says Nenad Šestan of Yale University School of Medicine and coauthor of one of the studies. “Essentially, we carry the same genes as mice,” he says. “However, in us, these genes are up to something quite different.” © Society for Science & the Public 2000 - 2011

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 15961 - Posted: 10.29.2011

Despite vast differences in the genetic code across individuals and ethnicities, the human brain shows a "consistent molecular architecture," say researchers supported by the National Institutes of Health. The finding is from a pair of studies that have created databases revealing when and where genes turn on and off in multiple brain regions through development. "Our study shows how 650,000 common genetic variations that make each of us a unique person may influence the ebb and flow of 24,000 genes in the most distinctly human part of our brain as we grow and age," explained Joel Kleinman, M.D., Ph.D., of the National Institute of Mental Health (NIMH) Clinical Brain Disorders Branch. Kleinman and NIMH grantee Nenad Sestan, M.D., Ph.D. of Yale University, New Haven, Conn., led the sister studies in the Oct. 27, 2011 issue of the journal Nature. genetic difference vs. transcriptional distance colored by race comparison. Our brains are all made of the same stuff. Despite individual and ethnic genetic diversity, our prefrontal cortex shows a consistent molecular architecture. For example, overall differences in the genetic code (“genetic distance”) between African -Americans (AA) and caucasians (cauc) showed no effect on their overall difference in expressed transcripts (“transcriptional distance”). The vertical span of color-coded areas is about the same, indicating that our brains all share the same tissue at a molecular level, despite distinct DNA differences on the horizontal axis. Each dot represents a comparison between two individuals. The AA::AA comparisons (blue) generally show more genetic diversity than cauc::cauc comparisons (yellow), because caucasians are descended from a relatively small subset of ancestors who migrated from Africa, while African Americans are descended from a more diverse gene pool among the much larger population that remained in Africa. AA::cauc comparisons (green) differed most across their genomes as a whole, but this had no effect on their transcriptomes as a whole. Source: Joel Kleinman, M.D., Ph.D., NIMH Clinical Brain Disorders Branch

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 15960 - Posted: 10.29.2011

By Tina Hesman Saey A genetic variant that makes small tweaks in an important brain protein may cause aging to hit some people’s brains harder than others. Pilots’ performance on a flight simulator test generally declines slightly with age. But a new study shows that pilots with a particular version of a gene called BDNF have a faster drop than others. Researchers also observed a decline in the size of an important learning and memory center in the brains of those with the variant, Ahmad Salehi of the Department of Veterans Affairs Palo Alto Health Care System and Stanford University, and colleagues report online October 25 in Translational Psychiatry. About 38 percent of pilots in the new study carried the variant in either one or both of their copies of the BDNF gene. Over the course of two years the flight simulator scores of all the pilots in the study declined a little with age. But scores of pilots carrying the variant dropped about three times faster than scores of pilots who have the normal version of the gene. The drop in scores was not so dramatic that pilots should be removed from the cockpit, says Salehi. “It certainly did not disable them at all,” he says. But the score drop did reflect a slightly faster decline in factors like reaction time, navigation skills, plane positioning and performance in emergency situations. For some of the pilots, the researchers measured the size of the hippocampus, a structure in the brain that is important for learning and memory. After age 65, men who had the alternate version of the gene also lost more hippocampus volume than men with the normal version of the gene, the researchers found. The size of the hippocampus did not correlate with scores on flight simulator tests, probably because flying a plane requires much more of the brain than just the hippocampus, Salehi says. © Society for Science & the Public 2000 - 2011

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 5: The Sensorimotor System
Link ID: 15953 - Posted: 10.27.2011

Jonathan Weitzman As an identical twin, I have always been fascinated by what determines who we are. Nature's clones are never truly identical, so what explains the differences between my brother and myself? How much of our identity is inherited; how much acquired by interacting with the environment? The field of epigenetics, standing at the interface between our environment and our genes, is beginning to offer answers. Epigenetics explores how genetically identical entities, whether cells or whole organisms, display different characteristics, and how these are inherited. The past century witnessed amazing advances in our understanding of genetics, but secrets remain hidden within the genome. Epigenetics research is now blossoming, offering a potential panacea for these post-genome blues. Two timely books open up this emergent field: Epigenetics by Richard Francis and The Epigenetics Revolution by Nessa Carey offer very different takes. Francis's thoughtful and succinct book focuses on the narrative and the excitement of discovery, rather than on the nitty-gritty details at the molecular level. His personal tour includes anecdotes from his travels around the world and allusions to popular culture. Carey's book is more DNA-centric, focusing on epigenetic mechanisms and the chemistry of chromatin, which defines how DNA is packaged around proteins in the nucleus. Her book combines an easy style with a textbook's thoroughness. © 2011 Nature Publishing Group,

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 15857 - Posted: 09.29.2011

By Lauren Ware In a clear Plexiglas laboratory cage, a mouse sleeps. A thin fiber optic cable projects upward from the top of its head and out through the cage’s lid. The cable lights with a pulse of blue light. The mouse continues to sleep; the light continues to pulse. After a few more pulses, the mouse wakes up. It rubs its face, stretches its legs and runs over to its food cup and begins to eat voraciously, as though it were starving. It keeps eating as the blue light pulses. The optical fiber that carries the blue light goes directly into the mouse’s brain. It targets a specific group of brain cells that have been modified to react to light. The experiment uses a technique called optogenetics, developed seven years ago, which can selectively activate or silence groups of nerve cells, or neurons, in real time. And it allows scientists to interact with the brain and begin to map how it works with a degree of detail that was previously unimaginable. That’s what Scott Sternson has done with the apparently starving mouse at Janelia Farm in Ashburn, Va., an interdisciplinary biomedical research center that is part of the Howard Hughes Medical Institute. In fact, this mouse was well fed and should not have been hungry. Sternson’s research group targeted a type of cell called the agouti-related peptide (AGRP) neuron. AGRP cells live in the hypothalamus and have been linked to feeding behavior in other studies. The scientists used a virus to insert the DNA of a light-sensitive protein from bacteria, channelrhodopsin-2, into the AGRP neurons. Some of the AGRP neurons take up the DNA and begin to produce the protein and send it to the cell membrane. When the blue light is flashed into the mouse’s brain via the optical fiber, the protein causes the neurons to move ions across the cell membrane, effectively stimulating them to fire an electrical signal, the action potential, which neurons use to communicate with each other. Sternson found that the more AGRP neurons are stimulated, the more the mouse eats. And as soon as the light stops, so does the feeding. Miller-McCune © 2011

Related chapters from BN: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 1: Cells and Structures: The Anatomy of the Nervous System
Link ID: 15792 - Posted: 09.13.2011

McMaster University researchers have discovered that a key gene may explain why some people are energetic and others find it hard to get moving. The team was working with mice, some of which had two genes removed. The genes control the AMP-activated protein kinase (or AMPK), an enzyme that is released during exercise. While mice like to run, the mice without the genes were not as active as mice with the genes. "While the normal mice could run for miles, those without the genes in their muscle could only run the same distance as down the hall and back," Gregory Steinberg, associate professor of medicine in the Michael G. DeGroote School of Medicine and Canada Research Chair in Metabolism and Obesity, said in a release Monday. "The mice looked identical to their brothers or sisters, but within seconds we knew which ones had the genes and which one didn't." The researchers found the mice without the AMPK genes had lower levels of mitochondria — sometimes described as cellular power plants — and their muscles were less able to take up glucose while they exercised. By removing the genes, the researchers found that AMPK is the key regulator of the mitochondria, said Steinberg. The research is in the current issue of the Proceedings of the National Academy of Sciences. © CBC 2011

Related chapters from BN: Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 15768 - Posted: 09.06.2011