Links for Keyword: Epigenetics

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By Marissa Fessenden, A new technique classifies neurons by surveying chemical tags that turn genes on or off on the neurons’ DNA1. The approach represents a new way to chart the brain’s cellular diversity. It could reveal how patterns of chemical tags known as methyl groups are altered in autism. Methyl groups bind to the DNA base cytosine. Patterns of methylation can be inherited, but they can also change in response to environmental factors, such as exposure in the womb to stress hormones or to the mother’s diet. Studies have reported altered methylation patterns in postmortem brains of people with autism. Methylation patterns also vary by cell type. In a new study, published 11 August in Science, researchers classified neurons from mouse and human brain tissue by their methylation patterns. The researchers looked at cells from specific layers of the brain’s outer shell, the cerebral cortex. They used a chemical cocktail to isolate the cells’ nuclei, and placed a single nucleus in each well of a 384-well plate. They then treated the nuclei with a chemical that converts cytosines without methyl groups to the RNA base uracil. They sequenced the DNA to pinpoint the remaining cytosines, yielding a map of every methyl group. © 2017 Scientific American,

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 24073 - Posted: 09.19.2017

By Becca Cudmore A mother rat’s care for her pup reaches all the way into her offspring’s DNA. A young rat that gets licked and groomed a lot early on in life exhibits diminished responses to stress thanks to epigenetic changes in the hippocampus, a brain region that helps transform emotional information into memory. Specifically, maternal solicitude reduces DNA methylation and changes the structure of DNA-packaging proteins, triggering an uptick in the recycling of the neurotransmitter serotonin and the upregulation of the glucocorticoid receptor. These changes make the nurtured rat’s brain quicker to sense and tamp down the production of stress hormones in response to jarring experiences such as unexpected sound and light. That pup will likely grow into a calm adult, and two studies have shown that female rats who exhibit a dampened stress response are more likely to generously lick, groom, and nurse their own young. Caring for pups is one example of what casual observers of behavior might call an animal’s instinct—generally considered to be an innate, genetically encoded phenomenon. But could such epigenetic changes, when encoded as ancestral learning, also be at the root of maternal care and other seemingly instinctual behaviors we see across the animal kingdom? “We don’t have a general theory for the mechanics of instinct as we do for learning, and this is something that has troubled me for a very long time,” says University of Illinois entomologist Gene Robinson. He studies social evolution in the Western honey bee and recently coauthored a perspective piece in Science together with neurobiologist Andrew Barron of Macquarie University in Sydney, Australia, suggesting methylation as a possible mechanism for the transgenerational transmission of instinctual behavior, rather than those behaviors being hardwired in the genome (356:26-27, 2017). Robinson and Barron suggest that instinctual traits, such as honey bees’ well-known waggle dance or a bird’s in-born ability to sing its species’ songs, are the result of traits first learned by their ancestors and inherited across generations by the process of methylation. This differs from classical thoughts on animal learning, which say that if a behavior is learned, it is not innate, and will not be inherited. © 1986-2017 The Scientist

Related chapters from BN8e: 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: 23861 - Posted: 07.22.2017

Ian Sample Science editor Older men tend to have “geekier” sons who are more aloof, have higher IQs and a more intense focus on their interests than those born to younger fathers, researchers claim. The finding, which emerged from a study of nearly 8,000 British twins, suggests that having an older father may benefit children and boost their performance in technical subjects at secondary school. Researchers in the UK and the US analysed questionnaires from 7,781 British twins and scored them according to their non-verbal IQ at 12 years old, as well as parental reports on how focused and socially aloof they were. The scientists then combined these scores into an overall “geek index”. Magdalena Janecka at King’s College London said the project came about after she and her colleagues had brainstormed what traits and skills helped people to succeed in the modern age. “If you look at who does well in life right now, it’s geeks,” she said. Drawing on the twins’ records, the scientists found that children born to older fathers tended to score slightly higher on the geek index. For a father aged 25 or younger, the average score of the children was 39.6. That figure rose to 41 in children with fathers aged 35 to 44, and to 47 for those with fathers aged over 50. The effect was strongest in boys, where the geek index rose by about 1.5 points for every extra five years of paternal age. The age of the children’s mothers seemed to have almost no effect on the geek index. © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 23757 - Posted: 06.21.2017

By Andy Coghlan The switching-off of genes in the human brain has been watched live for the first time. By comparing this activity in different people’s brains, researchers are now on the hunt for abnormalities underlying disorders such as Alzheimer’s disease and schizophrenia. To see where genes are most and least active in the brain, Jacob Hooker at Harvard Medical School and his team developed a radioactive tracer chemical that binds to a type of enzyme called an HDAC. This enzyme deactivates genes inside our cells, stopping them from making the proteins they code for. When injected into people, brain scans can detect where this tracer has bound to an enzyme, and thus where the enzyme is switching off genes. Live epigenetics The switching-off of genes by HDACs is a form of epigenetics – physical changes to the structure of DNA that modify how active genes are without altering their code. Until now, the only way to examine such activity in the brain has been by looking at post-mortem brain tissue. In the image above from the study, genes are least active in the red regions, such as the bulb-shaped cerebellum area towards the bottom right. The black and blue areas show the highest levels of gene activity – where barely any HDACs are present – and the yellow and green areas fall in between. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 22544 - Posted: 08.11.2016

Carl Zimmer Our genes are not just naked stretches of DNA. They’re coiled into intricate three-dimensional tangles, their lengths decorated with tiny molecular “caps.” These so-called epigenetic marks are crucial to the workings of the genome: They can silence some genes and activate others. Epigenetic marks are crucial for our development. Among other functions, they direct a single egg to produce the many cell types, including blood and brain cells, in our bodies. But some high-profile studies have recently suggested something more: that the environment can change your epigenetic marks later in life, and that those changes can have long-lasting effects on health. In May, Duke University researchers claimed that epigenetics could explain why people who grow up poor are at greater risk of depression as adults. Even more provocative studies suggest that when epigenetic marks change, people can pass them to their children, reprogramming their genes. But criticism of these studies has been growing. Some researchers argue that the experiments have been weakly designed: Very often, they say, it’s impossible for scientists to confirm that epigenetics is responsible for the effects they see. Three prominent researchers recently outlined their skepticism in detail in the journal PLoS Genetics. The field, they say, needs an overhaul. “We need to get drunk, go home, have a bit of a cry, and then do something about it tomorrow,” said John M. Greally, one of the authors and an epigenetics expert at the Albert Einstein College of Medicine in New York. © 2016 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 22391 - Posted: 07.02.2016

Chris Woolston A story about epigenetics in the 2 May issue of The New Yorker has been sharply criticized for inaccurately describing how genes are regulated. The article by Siddhartha Mukherjee — a physician, cancer researcher and award-winning author at Columbia University in New York — examines how environmental factors can change the activity of genes without altering the DNA sequence. Jerry Coyne, an evolutionary ecologist at the University of Chicago in Illinois, posted two widely discussed blog posts calling the piece “superficial and misleading”, largely because it ignored key aspects of gene regulation. Other researchers quoted in the blog posts called the piece “horribly damaging” and “a truly painful read”. Mukherjee responded by publishing a point-by-point rebuttal online. Speaking to Nature, he says he now realizes that he erred by omitting key areas of the science, but that he didn’t mean to mislead. “I sincerely thought that I had done it justice,” he says. Mukherjee’s article, ‘Same But Different’, takes a personal view of epigenetics — a term whose definition is highly contentious in the field. The story features his mother and aunt, identical twins who have distinct personalities. Mukherjee, who won a Pulitzer Prize in 2011 for his best-selling book The Emperor of All Maladies: A Biography of Cancer (Scribner, 2010), writes that identical twins differ because: “Chance events — injuries, infections, infatuations; the haunting trill of that particular nocturne — impinge on one twin and not on the other. Genes are turned on and off in response to these events, as epigenetic marks are gradually layered above genes, etching the genome with its own scars, calluses, and freckles.” The article is drawn from a book by Mukherjee that is due out later this month, called The Gene: An Intimate History (Scribner, 2016). © 2016 Nature Publishing Group

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22197 - Posted: 05.10.2016

By Aleszu Bajak In its May 2 issue, The New Yorker magazine published a report titled “Same But Different,” with the subhead: “How epigenetics can blur the line between nature and nurture.” The piece was written by Siddhartha Mukherjee, a physician and author of the Pulitzer prize-winning book “The Emperor of all Maladies: A Biography of Cancer.” In his New Yorker story, Mukherjee, with deft language and colorful anecdotes, examines a topic that is very much du jour in science writing: Epigenetics. Google defines epigenetics as “the study of changes in organisms caused by modification of gene expression, rather than alteration of the genetic code itself.” Merriam Webster’s definition is similar — but not exactly the same: “The study of heritable changes in gene function that do not involve changes in DNA sequence.” The slight variation in definition is telling in itself — and it’s really that “heritable” part that has sparked intense interest not just among scientists, but in the popular mind. Steven Henikoff, a molecular biologist at the Fred Hutchinson Cancer Research Center in Seattle, called Siddhartha Mukherjee’s lyrical take on epigenetics “baloney.” It’s the idea that external factors like diet, or stress or even lifestyle choices can impact not just your own genes, but the genetic information you pass down to all of your descendants. Spend your life smoking cigarettes and eating fatty foods, the thinking goes, and you’ll not just make yourself sick, you’ll predispose your offspring — and their offspring, and their offspring — to associated diseases as well. It’s heady stuff, but much of it remains speculative and poorly supported, which is where Mukherjee may have run into trouble. The publication of his story — an excerpt from his forthcoming book “The Gene: An Intimate History” — was met with swift criticism from biologists working in epigenetics and the broader field of gene regulation. They argue that Mukherjee played fast and loose with his description of epigenetic processes and misled readers by casting aside decades of research into how genes are regulated during development. Copyright 2016 Undark

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 22194 - Posted: 05.09.2016

By Elizabeth Pennisi Whether foraging for food, caring for young, or defending the nest, the worker castes of carpenter ants toil selflessly for their queen and colony. Now, biologists have figured out how to make some of those worker ants labor even harder, or change their very jobs in ant society, all by making small chemical modifications to their DNA. The finding calls attention to a new source of behavioral flexibility, and drives home the idea that so-called epigenetic modifications can connect genes to the environment, linking nature to nurture. The work is “a pioneering study establishing a causal link between epigenetics and complex social behavior,” says Ehab Abouheif, an evolutionary developmental biologist at McGill University, Montreal, in Canada. “These mechanisms may extend far beyond ants to other organisms with social behavior.” Insect biologists have long debated whether the division of labor in these sophisticated species with castes is driven by colony needs or is innate. Evidence in honey bees had pointed toward a genetic difference between queens and workers. In the past several years, however, work in both honey bees and ants had indicated that epigenetic modifications—changes to DNA other than to its sequence of bases (or DNA “letters”)—influence caste choices, indicating environmental factors can be pivotal. But subsequent research about one type of change, methylation, led to contradictory conclusions. © 2016 American Association for the Advancement of Science.

Related chapters from BN8e: 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: The Biology of Behavioral Disorders
Link ID: 21744 - Posted: 01.02.2016

By Mitch Leslie Male mice bequeath an unexpected legacy to their progeny. Two studies published online this week in Science reveal that sperm from the rodents carry pieces of RNAs that alter the metabolism of their offspring. The RNAs spotlighted by the studies normally help synthesize proteins, so the findings point to an unconventional form of inheritance. The results are “exciting and surprising, but not impossible,” says geneticist Joseph Nadeau of the Pacific Northwest Diabetes Research Institute in Seattle, Washington. “Impossible” is exactly how biologists once described so-called epigenetic inheritance, in which something other than a DNA sequence passes a trait between generations. In recent years, however, researchers have found many examples. A male mouse’s diet and stress level, for instance, can tweak offspring metabolism. Researchers are still trying to determine how offspring inherit a father’s metabolic attributes and physiological condition. Some evidence implicates chemical modification of DNA. Other work by neuroscientist Tracy Bale of the University of Pennsylvania Perelman School of Medicine in Philadelphia and colleagues has found that mammalian sperm pack gene-regulating molecules called microRNAs. The new work highlights a different class of RNAs, transfer RNAs (tRNAs). In one study, genomicist Oliver Rando of the University of Massachusetts Medical School in Worcester and colleagues delved into a case of epigenetic inheritance in which the progeny of mice fed a low-protein diet show elevated activity of genes involved in cholesterol and lipid metabolism. When Rando’s group analyzed sperm from the protein-deprived males, they uncovered an increased abundance of fragments from several kinds of tRNAs. The researchers concluded the sperm acquired most of these fragments while passing through the epididymis, a duct from the testicle where the cells mature. © 2016 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 21741 - Posted: 01.02.2016

Carl Zimmer In 2013, an obese man went to Hvidovre Hospital in Denmark to have his stomach stapled. All in all, it was ordinary bariatric surgery — with one big exception. A week before the operation, the man provided a sperm sample to Danish scientists. A week after the procedure, he did so again. A year later, he donated a third sample. Scientists were investigating a tantalizing but controversial hypothesis: that a man’s experiences can alter his sperm, and that those changes in turn may alter his children. That idea runs counter to standard thinking about heredity: that parents pass down only genes to their children. People inherit genes that predispose them to obesity, or stress, or cancer — or they don’t. Whether one’s parents actually were obese or constantly anxious doesn’t rewrite those genes. Yet a number of animal experiments in recent years have challenged conventional thinking on heredity, suggesting that something more is at work. In 2010, for example, Dr. Romain Barres of the University of Copenhagen and his colleagues fed male rats a high-fat diet and then mated them with females. Compared with male rats fed a regular diet, those on the high-fat diet fathered offspring that tended to gain more weight, develop more fat and have more trouble regulating insulin levels. Eating high-fat food is just one of several experiences a father can have that can change his offspring. Stress is another. Male rats exposed to stressful experiences — like smelling the odor of a fox — will father pups that have a dampened response to stress. © 2015 The New York Times Company

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 21676 - Posted: 12.05.2015

Helen Thomson Genetic changes stemming from the trauma suffered by Holocaust survivors are capable of being passed on to their children, the clearest sign yet that one person’s life experience can affect subsequent generations. The conclusion from a research team at New York’s Mount Sinai hospital led by Rachel Yehuda stems from the genetic study of 32 Jewish men and women who had either been interned in a Nazi concentration camp, witnessed or experienced torture or who had had to hide during the second world war. They also analysed the genes of their children, who are known to have increased likelihood of stress disorders, and compared the results with Jewish families who were living outside of Europe during the war. “The gene changes in the children could only be attributed to Holocaust exposure in the parents,” said Yehuda. Her team’s work is the clearest example in humans of the transmission of trauma to a child via what is called “epigenetic inheritance” - the idea that environmental influences such as smoking, diet and stress can affect the genes of your children and possibly even grandchildren. The idea is controversial, as scientific convention states that genes contained in DNA are the only way to transmit biological information between generations. However, our genes are modified by the environment all the time, through chemical tags that attach themselves to our DNA, switching genes on and off. Recent studies suggest that some of these tags might somehow be passed through generations, meaning our environment could have and impact on our children’s health. © 2015 Guardian News and Media Limited

Related chapters from BN8e: 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: 21325 - Posted: 08.22.2015

by Helen Thomson For the first time, scientists have discovered a mechanism in humans that could explain how your lifestyle choices may impact your children and grandchildren's genes. Mounting evidence suggests that environmental factors such as smoking, diet and stress, can leave their mark on the genes of your children and grandchildren. For example, girls born to Dutch women who were pregnant during a long famine at the end of the second world war had twice the usual risk of developing schizophrenia. Likewise, male mice that experience early life stress give rise to two generations of offspring that have increased depression and anxiety, despite being raised in a caring environment. This has puzzled many geneticists, as genetic information contained in sperm and eggs is not supposed to be affected by the environment, a principle called the August Weismann barrier. But we also know the activity of our own genes can be changed by our environment, through epigenetic mechanisms . These normally work by turning a gene on or off by adding or subtracting a methyl group to or from its DNA. These methyl groups can inactivate genes by making their DNA curl up, so that enzymes can no longer access the gene and read its instructions. Such epigenetic mechanisms are high on the list of suspects when it comes to explaining how environmental factors that affect parents can later influence their children, such as in the Dutch second world war study, but just how these epigenetic changes might be passed on to future generations is a mystery. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: 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: The Biology of Behavioral Disorders
Link ID: 21022 - Posted: 06.06.2015

Catherine Brahic THE nature versus nurture debate is getting a facelift this week, with the publication of a genetic map that promises to tell us which bits of us are set in stone by our DNA, and which bits we can affect by how we live our lives. The new "epigenomic" map doesn't just look at genes, but also the instructions that govern them. Compiled by a consortium of biologists and computer scientists, this information will allow doctors to pinpoint precisely which cells in the body are responsible for various diseases. It might also reveal how to adjust your lifestyle to counter a genetic predisposition to a particular disease. "The epigenome is the additional information our cells have on top of genetic information," says lead researcher Manolis Kellis of the Massachusetts Institute of Technology. It is made of chemical tags that are attached to DNA and its packaging. These tags act like genetic controllers, influencing whether a gene is switched on or off, and play an instrumental role in shaping our bodies and disease. Researchers are still figuring out exactly how and when epigenetic tags are added to our DNA, but the process appears to depend on environmental cues. We inherit some tags from our parents, but what a mother eats during pregnancy, for instance, might also change her baby's epigenome. Others tags relate to the environment we are exposed to as children and adults. "The epigenome sits in a very special place between nature and nurture," says Kellis. Each cell type in our body has a different epigenome – in fact, the DNA tags are the reason why our cells come in such different shapes and sizes despite having exactly the same DNA. So for its map, the Roadmap Epigenomics Consortium collected thousands of cells from different adult and embryonic tissues, and meticulously analysed all the tags. © Copyright Reed Business Information Ltd.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 20591 - Posted: 02.18.2015

By Helen Briggs BBC News A mother's diet around the time of conception can permanently influence her baby's DNA, research suggests. Animal experiments show diet in pregnancy can switch genes on or off, but this is the first human evidence. The research followed women in rural Gambia, where seasonal climate leads to big differences in diet between rainy and dry periods. It emphasises the need for a well-balanced diet before conception and in pregnancy, says a UK/US team. Scientists followed 84 pregnant women who conceived at the peak of the rainy season, and about the same number who conceived at the peak of the dry season. Nutrient levels were measured in blood samples taken from the women; while the DNA of their babies was analysed two to eight months after birth. Lead scientist Dr Branwen Hennig, from the London School of Hygiene & Tropical Medicine, said it was the first demonstration in humans that a mother's nutrition at the time of conception can change how her child's genes will be interpreted for life. She told BBC News: "Our results have shown that maternal nutrition pre-conception and in early pregnancy is important and may have implications for health outcomes of the next generation. "Women should have a well-balanced food diet prior to conception and during pregnancy." BBC © 2014

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 8: Hormones and Sex
Link ID: 19556 - Posted: 04.30.2014

Virginia Hughes When Brian Dias became a father last October, he was, like any new parent, mindful of the enormous responsibility that lay before him. From that moment on, every choice he made could affect his newborn son's physical and psychological development. But, unlike most new parents, Dias was also aware of the influence of his past experiences — not to mention those of his parents, his grandparents and beyond. Where one's ancestors lived, or how much they valued education, can clearly have effects that pass down through the generations. But what about the legacy of their health: whether they smoked, endured famine or fought in a war? As a postdoc in Kerry Ressler's laboratory at Emory University in Atlanta, Georgia, Dias had spent much of the two years before his son's birth studying these kinds of questions in mice. Specifically, he looked at how fear associated with a particular smell affects the animals and leaves an imprint on the brains of their descendants. Dias had been exposing male mice to acetophenone — a chemical with a sweet, almond-like smell — and then giving them a mild foot shock. After being exposed to this treatment five times a day for three days, the mice became reliably fearful, freezing in the presence of acetophenone even when they received no shock. Ten days later, Dias allowed the mice to mate with unexposed females. When their young grew up, many of the animals were more sensitive to acetophenone than to other odours, and more likely to be startled by an unexpected noise during exposure to the smell. Their offspring — the 'grandchildren' of the mice trained to fear the smell — were also jumpier in the presence of acetophenone. What's more, all three generations had larger-than-normal 'M71 glomeruli', structures where acetophenone-sensitive neurons in the nose connect with neurons in the olfactory bulb. In the January issue of Nature Neuroscience1, Dias and Ressler suggested that this hereditary transmission of environmental information was the result of epigenetics — chemical changes to the genome that affect how DNA is packaged and expressed without altering its sequence. © 2014 Nature Publishing Group,

Related chapters from BN8e: 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: 19325 - Posted: 03.05.2014

Stephen S. Hall Hochelaga was the original Iroquoian name for the village that ultimately became Montreal, but it is also the name of a rough-hewn French–Canadian neighbourhood located east of — and a world away from — the cosmopolitan city centre. The district's tidy two- and three-storey brick duplexes, adorned with Montreal's characteristic wrought-iron staircases, predominantly house families that have, because of poverty and lack of education, never quite attained thriving middle-class status. During the 1980s, public-school officials identified Hochelaga and many other impoverished neighbourhoods in the eastern part of Montreal as places where kindergarten children disproportionately displayed severe behavioural problems, such as physical aggression. The school system asked a young University of Montreal psychologist named Richard Tremblay for help. “Their parents didn't have a high-school diploma, and many of the mothers had their first child before the age of 20,” Tremblay says of the families he began to study, as he walks along Rue Ontario in Hochelaga on a sunny afternoon in September. Those were the women, he adds, “most at risk of having children who have problems”. Over the past three decades, Hochelaga and similar neighbourhoods have served as living laboratories in the study of the roots of aggression. Since 1984, Tremblay and his collaborators have followed more than 1,000 children from 53 schools in the city from childhood into adulthood. And in 1985, he initiated a ground-breaking experiment in which some families of at-risk children were given support and counselling to help curb bad behaviour. His research overturned ideas about when aggressive behaviour first emerges, and showed that early intervention can deflect children away from adult criminality. © 2013 Nature Publishing Group

Related chapters from BN8e: Chapter 15: Emotions, Aggression, and Stress; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 13: Memory, Learning, and Development
Link ID: 19082 - Posted: 12.31.2013

by Bethany Brookshire “You are what you eat.” We’ve all heard that one. What we eat can affect our growth, life span and whether we develop disease. These days, we know that we also are what our mother eats. Or rather, what our mothers ate while we were in the womb. But are we also what our father eats? A new study shows that in mice, a dietary deficiency in dad can be a big downer for baby. The dietary staple in the study was folic acid, or folate. Folate is one of the B vitamins and is found in dark leafy greens (eat your kale!) and has even been added to some foods like cereals. It is particularly essential to get in the diet because we cannot synthesize it on our own. And it plays roles in DNA repair and DNA synthesis, as well as methylation of DNA. It’s particularly important during development. Without adequate folate, developing fetuses are prone to neural tube disorders, such as spina bifida. Some of the neural tube disorders caused by folate deficiency could result from breaks in the DNA itself. But folic acid is also important in the epigenome. Epigenetics is a mechanism that allows cells to change how genes are used without changing the genes themselves. Instead of altering the DNA itself, epigenetic alterations put chemical “marks” or “notes” —methyl or acetyl groups — on the DNA and the proteins associated with it. The marks can either make a gene more accessible (acetylation) or less accessible (methylation), making it more or less likely to be made into a protein. This means that each cell type can have a different epigenome, allowing a neuron to function differently than a muscle cell, even though they contain the same DNA. Folate affects DNA synthesis, but it can also affect DNA methylation. In fact, DNA methylation requires the presence of folate. So low folate could affect whether genes are turned off or on and by how much. In a developing fetus, that could contribute to developmental problems. © Society for Science & the Public 2000 - 2013.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19035 - Posted: 12.14.2013

By Dan Hurley Darwin and Freud walk into a bar. Two alcoholic mice — a mother and her son — sit on two bar stools, lapping gin from two thimbles. The mother mouse looks up and says, “Hey, geniuses, tell me how my son got into this sorry state.” “Bad inheritance,” says Darwin. “Bad mothering,” says Freud. For over a hundred years, those two views — nature or nurture, biology or psychology — offered opposing explanations for how behaviors develop and persist, not only within a single individual but across generations. And then, in 1992, two young scientists following in Freud’s and Darwin’s footsteps actually did walk into a bar. And by the time they walked out, a few beers later, they had begun to forge a revolutionary new synthesis of how life experiences could directly affect your genes — and not only your own life experiences, but those of your mother’s, grandmother’s and beyond. The bar was in Madrid, where the Cajal Institute, Spain’s oldest academic center for the study of neurobiology, was holding an international meeting. Moshe Szyf, a molecular biologist and geneticist at McGill University in Montreal, had never studied psychology or neurology, but he had been talked into attending by a colleague who thought his work might have some application. Likewise, Michael Meaney, a McGill neurobiologist, had been talked into attending by the same colleague, who thought Meaney’s research into animal models of maternal neglect might benefit from Szyf’s perspective.

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 19017 - Posted: 12.11.2013

Ewen Callaway Certain fears can be inherited through the generations, a provocative study of mice reports1. The authors suggest that a similar phenomenon could influence anxiety and addiction in humans. But some researchers are sceptical of the findings because a biological mechanism that explains the phenomenon has not been identified. According to convention, the genetic sequences contained in DNA are the only way to transmit biological information across generations. Random DNA mutations, when beneficial, enable organisms to adapt to changing conditions, but this process typically occurs slowly over many generations. Yet some studies have hinted that environmental factors can influence biology more rapidly through 'epigenetic' modifications, which alter the expression of genes, but not their actual nucleotide sequence. For instance, children who were conceived during a harsh wartime famine in the Netherlands in the 1940s are at increased risk of diabetes, heart disease and other conditions — possibly because of epigenetic alterations to genes involved in these diseases2. Yet although epigenetic modifications are known to be important for processes such as development and the inactivation of one copy of the X-chromsome in females, their role in the inheritance of behaviour is still controversial. Kerry Ressler, a neurobiologist and psychiatrist at Emory University in Atlanta, Georgia, and a co-author of the latest study, became interested in epigenetic inheritance after working with poor people living in inner cities, where cycles of drug addiction, neuropsychiatric illness and other problems often seem to recur in parents and their children. “There are a lot of anecdotes to suggest that there’s intergenerational transfer of risk, and that it’s hard to break that cycle,” he says. © 2013 Nature Publishing Group

Related chapters from BN8e: 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: 18990 - Posted: 12.02.2013

By Puneet Kollipara Identical twin mice sharing the same mazelike environment develop distinct personalities based on how much they explore their surroundings, researchers report in the May 10 Science. After death, those differences were reflected in the animals’ brains. The study “highlights something for which we had some intuition before, but actually quantifies it,” says Fred Gage, a neuroscientist at the Salk Institute for Biological Studies in La Jolla, Calif. Some character and biological differences between identical twins may originate as early as pregnancy. But twins become more and more different as life goes on, even when they grow up together. Scientists have recognized that having distinct experiences within the same environment might boost such personality differences, but that’s difficult to test in humans. Studying it in animals has multiple benefits. “You can keep the genes constant and also keep the environment constant,” says Gerd Kempermann of the Center for Regenerative Therapies Dresden in Germany. “It’s much more controlled than in a human situation.” Researchers led by Kempermann put 40 genetically identical female mice in an elaborate cage and observed their behavior. The cage had multiple levels linked together by tubes and contained toys and other features that the animals could explore. The researchers equipped each mouse with a microchip that tracked its location, using the animals’ movements as a measure of exploratory behavior. Initially, the mice differed only slightly in their tendency to roam. As they grew older, all tended to explore more often, but the differences among the mice grew more pronounced. © Society for Science & the Public 2000 - 2013

Related chapters from BN8e: Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 13: Memory, Learning, and Development
Link ID: 18145 - Posted: 05.11.2013