Chapter 7. Life-Span Development of the Brain and Behavior
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By Greg Miller Nobody knows what causes autism, a condition that varies so widely in severity that some people on the spectrum achieve enviable fame and success while others require lifelong assistance due to severe problems with communication, cognition, and behavior. Scientists have found countless clues, but so far they don’t quite add up. The genetics is complicated. The neuroscience is conflicted. Now, a new study adds an intriguing, unexpected, and sure-to-be controversial finding to the mix: It suggests the brains of children with autism contain small patches where the normally ordered arrangement of neurons in the cerebral cortex is disrupted. “We’ve found locations where there appears to be a failure of normal development,” said Eric Courchesne, a neuroscientist at the University of California, San Diego and an author of the study, which appears today in the New England Journal of Medicine. “It’s been really difficult to identify a lesion or anything in the brain that’s specific and diagnostic of autism,” said Thomas Insel, director of the National Institute of Mental Health, one of several agencies that funded the project. The new study is notable because it applies sophisticated molecular labeling methods to postmortem tissue from people with autism who died as children, which is incredibly hard to come by, Insel says. “If it’s real, if it’s replicated and it’s a consistent finding, it’s more evidence that autism starts prenatally and only manifests itself when kids start to have trouble with language or social behavior around age two or three,” Insel said. “These kinds of changes in cellular architecture would happen during brain development, probably around the first part of the second trimester.” © 2014 Condé Nast
James Hamblin Forty-one million IQ points. That’s what Dr. David Bellinger determined Americans have collectively forfeited as a result of exposure to lead, mercury, and organophosphate pesticides. In a 2012 paper published by the National Institutes of Health, Bellinger, a professor of neurology at Harvard Medical School, compared intelligence quotients among children whose mothers had been exposed to these neurotoxins while pregnant to those who had not. Bellinger calculates a total loss of 16.9 million IQ points due to exposure to organophosphates, the most common pesticides used in agriculture. Last month, more research brought concerns about chemical exposure and brain health to a heightened pitch. Philippe Grandjean, Bellinger’s Harvard colleague, and Philip Landrigan, dean for global health at Mount Sinai School of Medicine in Manhattan, announced to some controversy in the pages of a prestigious medical journal that a “silent pandemic” of toxins has been damaging the brains of unborn children. The experts named 12 chemicals—substances found in both the environment and everyday items like furniture and clothing—that they believed to be causing not just lower IQs but ADHD and autism spectrum disorder. Pesticides were among the toxins they identified. “So you recommend that pregnant women eat organic produce?” I asked Grandjean, a Danish-born researcher who travels around the world studying delayed effects of chemical exposure on children. “That’s what I advise people who ask me, yes. It’s the best way of preventing exposure to pesticides.” Grandjean estimates that there are about 45 organophosphate pesticides on the market, and “most have the potential to damage a developing nervous system.” © 2014 by The Atlantic Monthly Group.
By Jennifer Richler A few days ago, an old friend sent me a panicked email. She had just finished reading Ron Suskind’s beautiful essay in the New York Times Magazine about raising a son with autism: “Reaching My Autistic Son Through Disney.” Suskind describes how, at almost 3 years of age, his son Owen “disappeared.” The child was once “engaged, chatty, full of typical speech,” but then he stopped talking, lost eye contact, even struggled to use a sippy cup. Owen was eventually diagnosed with a regressive form of autism, which Suskind says affects about a third of children with the disorder. “Unlike the kids born with it,” he continues, “this group seems typical until somewhere between 18 and 36 months—then they vanish.” That was the line that alarmed my friend, whose son is nearing his third birthday. “What is this ‘regressive autism?’ ” she asked me, the resident autism expert in her peer group. (I conducted research on autism and regression in autism before becoming a freelance writer.) “I thought we were out of the woods!” I’m sure many parents of young children who read the piece had the same reaction, and it’s completely understandable. It’s also unwarranted. The claim that many kids with autism develop typically for almost three years and then experience a near-complete loss of language, social skills, and motor ability—a claim I’ve read many times before—simply isn’t true. It’s time to set the record straight. © 2014 The Slate Group LLC.
Link ID: 19409 - Posted: 03.26.2014
Claudia Dreifus The biochemist Ricardo E. Dolmetsch has pioneered a major shift in autism research, largely putting aside behavioral questions to focus on cell biology and biochemistry. Dr. Dolmetsch, 45, has done most of his work at Stanford. Since our interviews — a condensed and edited version of which follows — he has taken a leave to join Novartis, where his mission is to organize an international team to develop autism therapies. “Pharmaceutical companies have financial and organizational resources permitting you to do things you might not be able to do as an academic,” he said. “I really want to find a drug.” Q. Did you start out your professional life studying the biochemistry of autism? A. No. In graduate school and as a postdoc, I’d done basic research on the ion channels on the membranes of cells. By my mid-20s, I had my name on some high-profile papers. Then, around 2006, my son who was then 4 was diagnosed with autism. We had suspected it. He didn’t talk much, was hyperactive, very moody. He assembled huge towers based on the color spectrum. He did all sorts of things that were very unusual. Given the signs, why did you wait that long to seek a diagnosis? I’m from Latin America [Cali, Colombia], and my Latin thing was, “This is the way boys are.” But he would just scream for hours and hours, uncontrollable. He didn’t sleep. We didn’t understand it. After a while, his teachers said, “You probably ought to have him seen.” So we went to a psychiatrist and neurologist and ultimately we got differing diagnoses. © 2014 The New York Times Company
Link ID: 19404 - Posted: 03.25.2014
by Barbara J. King Why do little boys tend to behave differently from little girls? Why do boys and girls play differently, for instance, choosing different toys as their favorites? Ask these questions and you invite a firestorm — of more questions. Is the premise behind these queries even accurate? Aren't our sons and daughters really more similar than different, after all? And when behavioral sex differences do occur, aren't parents who inflict sex-stereotypical expectations on their children largely responsible? Seven experts on chimpanzee behavior, led by of Franklin and Marshall College and including the world-famous primatologist , have in Animal Behaviour that speaks, they say, to these issues. Their data on wild chimpanzees from , Tanzania, indicate that human sex differences in childhood are primarily the result of biological, evolutionary mechanisms. The scientists analyzed data on the behavior of 12 male and eight female chimpanzee youngsters, ages 30-36 months. At that age, chimpanzees, who develop quite slowly compared with many other mammals, are still considered infants. As a rule, chimpanzees spend most of their day in close proximity to their mothers clear through their ninth year of life. In the Gombe study, male infants were found to be more gregarious than female chimpanzees; they interacted with significantly more individuals outside the immediate family, including more adult males, than did females. This result held even when the number of the mothers' social partners was controlled. ©2014 NPR
by Simon Makin How much can environmental factors explain the apparent rise in autism spectrum disorders? Roughly 1 per cent of children in the US population are affected by autism spectrum disorder (ASD). Rates in many countries, including the US, have risen sharply in recent years but no one is sure why. It is still not clear whether this is prompted by something in the environment, increased awareness of the condition and changes in diagnoses, or a result of people having children later. The environmental case is hotly debated. There is some evidence that maternal infections during pregnancy can increase the risk. Other studies have pointed to a possible link with antidepressants while others have looked at elevated levels of mercury. But determining prenatal exposure to any substance is difficult because it is hard to know what substances people have been exposed to and when. To get around this, Andrey Rzhetsky and colleagues at the University of Chicago analysed US health insurance claims containing over 100 million patient records – a third of the population – dating from 2003 to 2010. They used rates of genital malformations in newborn boys as a proxy of parents' exposure to environmental risk factors. This is based on research linking a proportion of these malformations to toxins in the environment, including pesticides, lead and medicines. Toxic environment? The team compared the rates of these malformations to rates of ASD county by county. After adjusting for gender, income, ethnicity and socio-economic status, they found that a 1 per cent increase in birth defects – their measure for environmental effects - was associated with an average increase of 283 per cent in cases of ASD. © Copyright Reed Business Information Ltd.
Link ID: 19393 - Posted: 03.21.2014
By Shelly Fan One of the tragedies of aging is the slow but steady decline in memory. Phone numbers slipping your mind? Forgetting crucial items on your grocery list? Opening the door but can’t remember why? Up to 50 percent of adults aged 64 years or older report memory complaints. For many of us, senile moments are the result of normal changes in brain structure and function instead of a sign of dementia, and will inevitably haunt us all. Rather than taking it lying down, scientists are devising interventions to help keep the elderly mind sharp. One popular approach—borrowed from the training of memory experts—is to teach the elderly mnemonics, or little tricks to help encode and recall new information using rhythm, imagery or spatial navigation. By far the most widely used mnemonic device is the method of loci (MoL), a technique devised in ancient Greece. In a 2002 study looking at the neural correlates of superior human memory, nine of 10 memory masters employed the method spontaneously. It involves picturing highly familiar routes through a building (your childhood home) or a town (your way to work). Walk down the route and imagine placing to-be-remembered items at attention-grabbing spots along the way; the more surreal or bizarre you make these images, the better they can help you remember. To recall these stored items, simply retrace your steps. Like fishing lines, the loci are hooked to the memory and help you pull them to the surface. Although generally used to remember objects, numbers or names, the MoL has also been used in people with depression to successfully store bits and pieces of happy autobiographical memories that they can easily retrieve in times of stress. © 2014 Scientific American,
Want to live a long, dementia-free life? Stress your cells out. That’s the conclusion of a new study, which finds that heightened cellular stress causes brain cells to produce a protein that staves off Alzheimer’s disease and other forms of dementia. The work could lead to new ways to diagnose or treat such diseases. “This paper is very impressive,” says neuroscientist Li-Huei Tsai of the Massachusetts Institute of Technology in Cambridge, who was not involved in the new work. “It puts a finger on a particular pathway that can provide some explanation as to why some people are more susceptible to Alzheimer’s.” Alzheimer’s disease, characterized by a progressive loss of memory and cognition, affects an estimated 44.4 million people worldwide, mostly over the age of 65. The illness has been linked to the accumulation of certain proteins in the brain, but what causes symptoms has been unclear. That’s because the brains of some elderly people without dementia have the same clumps of so-called amyloid β and τ proteins typically associated with Alzheimer’s. The new study deals with a protein called repressor element 1-silencing transcription factor (REST), which turns genes and off. Scientists knew that REST played a key role in fetal brain development by controlling the activity of certain genes, but they thought it was absent in adult brains. However, when Bruce Yankner, a neurologist at Harvard Medical School in Boston, looked at all the genes and proteins that change in brains as people age, he found that REST levels begin increasing again when a person hits their 30s. Stumped as to why, he and his colleagues isolated human and mouse brain cells and probed what factors altered REST levels and what consequences those levels had. © 2014 American Association for the Advancement of Science
By Maggie Fox and Erika Edwards Women are carrying the bigger burden of Alzheimer’s disease in the U.S., according to a new report — making up not only most of the cases, but paying more of the cost of caring for the growing population of people with the mind-destroying illness. The new report from the Alzheimer’s Association paints Alzheimer’s as a disease that disproportionately affects women, both as patients and as caregivers. It points out that women in their 60s are about twice as likely to develop Alzheimer’s over the rest of their lives as they are to develop breast cancer. “So women are at the epicenter of Alzheimer's disease today, not only by being most likely to be diagnosed with Alzheimer's, but also by being the caregiver most of the time,” said Maria Carrillo, vice president of the advocacy group. Alzheimer’s affects more than 5 million Americans, a number projected to soar to 13 million over the next 35 years. A study published earlier this year suggested it’s a big killer, taking down more than 500,000 Americans every year. Three out of five of those living with Alzheimer’s are women, the report finds. “The surprising statistic we pulled out of this report actually is that women over 65 have a one in six chance of developing Alzheimer's disease, in comparison to one out of 11 in men,” Carrillo said. And that compares to a one in eight lifetime risk for developing breast cancer.
The cancer gene BRCA1, which keeps tumors in the breast and ovaries at bay by producing proteins that repair damaged DNA, may also regulate brain size. Mice carrying a mutated copy of the gene have 10-fold fewer neurons and other brain abnormalities, a new study suggests. Such dramatic effects on brain size and function are unlikely in human carriers of BRCA1 mutations, the authors of the study note, but they propose the findings could shed light on the gene's role in brain evolution. Scientists have known for a long time that the BRCA1 gene is an important sentinel against DNA damage that can lead to ovarian and breast cancers. More than half of women with a mutated copy of the BRCA1 gene will develop breast cancer, a statistic that has led some who carry the mutation to get preventative mastectomies. But its roles outside the breast and ovaries are less clear, says Inder Verma, a geneticist and molecular biologist at the Salk Institute for Biological Studies in San Diego, California, who headed the new study. Mice bred without BRCA1 die soon after birth, so it’s clear that the gene is necessary to sustain life, but scientists are just starting to unravel its many functions, he says. Several years ago, one of the students in Verma’s lab noticed that BRCA1 is very active in the neuroectoderm, a sliver of embryonic tissue containing neural stem cells that divide and differentiate into the brain’s vast assortment of cell types and structures. Verma and his colleagues wondered why the gene was expressed at such high levels in that region, and what would happen if it were eliminated. They created a strain of mice in which BRCA1 was knocked out only in neural stem cells. As the mice developed, Verma’s team found that the rodents’ brains were only a third of their normal size, with particularly striking reductions in brain areas involved in learning and memory. The grown mice also had a wobbly, drunken gait—a telltale symptom of ataxia, a neurological disorder that affects muscle control and balance, the researchers report online today in the Proceedings of the National Academy of Sciences. © 2014 American Association for the Advancement of Science.
Keyword: Development of the Brain
Link ID: 19378 - Posted: 03.18.2014
by Laura Sanders Candy and sweets make your kid hyper, the common lore goes. But science says that's not true. 1. Sugar makes kids hyper. Lots of parents swear that a single hit of birthday cake holds the power to morph their well-behaved, polite youngster into a sticky hot mess that careens around a room while emitting eardrum-piercing shrieks. Anyone who has had the pleasure to attend a 5-year-old’s birthday party knows that the hypothesis sounds reasonable, except that science has found that it’s not true. Sugar doesn’t change kids’ behavior, a double-blind research study found way back in 1994. A sugary diet didn’t affect behavior or cognitive skills, the researchers report. Sugar does change one important thing, though: parents’ expectations. After hearing that their children had just consumed a big sugar fix, parents were more likely to say their child was hyperactive, even when the big sugar fix was a placebo, another study found. Of course, there are plenty of good reasons not to feed your kids a bunch of sugar, but fear of a little crazed sugar monster isn’t one of them. © Society for Science & the Public 2000 - 2013.
Keyword: Development of the Brain
Link ID: 19376 - Posted: 03.18.2014
by Colin Barras Amyloid plaques, a hallmark of diseases like Alzheimer's, are bad news for humans – but they could have been drivers of the earliest life on Earth. A new study shows that these amyloid clusters can behave as catalysts, backing a theory that they helped trigger the reactions that sustain life, long before modern enzymes appeared. Without enzymes, life's metabolic reactions simply wouldn't occur. But making enzymes from scratch isn't easy. They are normally large, complicated proteins folded into a specific three-dimensional shape. It's difficult to see how these large proteins could have popped out of the primordial soup fully formed. Even if they did, nature faced another problem. There are 20 naturally occurring amino acids, which are the building blocks for all proteins, and each enzyme is made up of a unique sequence of at least 100 amino acids. This means there is a mind-bogglingly vast number – 20100 – of possible enzymes, each with a different amino acid sequence and a slightly different 3D structure. But very few of these 3D structures will work effectively as enzymes because they have to be an exact fit for the substrate they react with – in the same way that a lock can only be opened by one particular key. Even with millions of years to work at the problem, says Ivan Korendovych at Syracuse University in New York, nature would have struggled to build and test all possible enzyme molecules to identify the relatively few that catalyse today's metabolic reactions. © Copyright Reed Business Information Ltd.
Link ID: 19372 - Posted: 03.17.2014
By JAN HOFFMAN COLUMBIA, Mo. – Jilly Dos Santos really did try to get to school on time. She set three successive alarms on her phone. Skipped breakfast. Hastily applied makeup while her fuming father drove. But last year she rarely made it into the frantic scrum at the doors of Rock Bridge High School here by the first bell, at 7:50 a.m. Then she heard that the school board was about to make the day start even earlier, at 7:20 a.m. “I thought, if that happens, I will die,” recalled Jilly, 17. “I will drop out of school!” That was when the sleep-deprived teenager turned into a sleep activist. She was determined to convince the board of a truth she knew in the core of her tired, lanky body: Teenagers are developmentally driven to be late to bed, late to rise. Could the board realign the first bell with that biological reality? The sputtering, nearly 20-year movement to start high schools later has recently gained momentum in communities like this one, as hundreds of schools in dozens of districts across the country have bowed to the accumulating research on the adolescent body clock. In just the last two years, high schools in Long Beach, Calif.; Stillwater, Okla.; Decatur, Ga.;, and Glens Falls, N.Y., have pushed back their first bells, joining early adopters in Connecticut, North Carolina, Kentucky and Minnesota. The Seattle school board will vote this month on whether to pursue the issue. The superintendent of Montgomery County, Md., supports the shift, and the school board for Fairfax County, Va., is working with consultants to develop options for starts after 8 a.m. © 2014 The New York Times Company
By Jessica Wright and SFARI.org It takes more mutations to trigger autism in women than in men, which may explain why men are four times more likely to have the disorder, according to a study published 26 February in the American Journal of Human Genetics. The study found that women with autism or developmental delay tend to have more large disruptions in their genomes than do men with the disorder. Inherited mutations are also more likely to be passed down from unaffected mothers than from fathers. Together, the results suggest that women are resistant to mutations that contribute to autism. “This strongly argues that females are protected from autism and developmental delay and require more mutational load, or more mutational hits that are severe, in order to push them over the threshold,” says lead researcher Evan Eichler, professor of genome sciences at the University of Washington in Seattle. “Males on the other hand are kind of the canary in the mineshaft, so to speak, and they are much less robust.” The findings bolster those from previous studies, but don't explain what confers protection against autism in women. The fact that autism is difficult to diagnose in girls may mean that studies enroll only those girls who are severely affected and who may therefore have the most mutations, researchers note. “The authors are geneticists, and the genetics is terrific,” says David Skuse, professor of behavioral and brain sciences at University College London, who was not involved in the study. “But the questions about ascertainment are not addressed adequately.” © 2014 Scientific American
By RON SUSKIND In our first year in Washington, our son disappeared. Just shy of his 3rd birthday, an engaged, chatty child, full of typical speech — “I love you,” “Where are my Ninja Turtles?” “Let’s get ice cream!” — fell silent. He cried, inconsolably. Didn’t sleep. Wouldn’t make eye contact. His only word was “juice.” I had just started a job as The Wall Street Journal’s national affairs reporter. My wife, Cornelia, a former journalist, was home with him — a new story every day, a new horror. He could barely use a sippy cup, though he’d long ago graduated to a big-boy cup. He wove about like someone walking with his eyes shut. “It doesn’t make sense,” I’d say at night. “You don’t grow backward.” Had he been injured somehow when he was out of our sight, banged his head, swallowed something poisonous? It was like searching for clues to a kidnapping. After visits to several doctors, we first heard the word “autism.” Later, it would be fine-tuned to “regressive autism,” now affecting roughly a third of children with the disorder. Unlike the kids born with it, this group seems typical until somewhere between 18 and 36 months — then they vanish. Some never get their speech back. Families stop watching those early videos, their child waving to the camera. Too painful. That child’s gone. In the year since his diagnosis, Owen’s only activity with his brother, Walt, is something they did before the autism struck: watching Disney movies. “The Little Mermaid,” “Beauty and the Beast,” “Aladdin” — it was a boom time for Disney — and also the old classics: “Dumbo,” “Fantasia,” “Pinocchio,” “Bambi.” They watch on a television bracketed to the wall in a high corner of our smallish bedroom in Georgetown. It is hard to know all the things going through the mind of our 6-year-old, Walt, about how his little brother, now nearly 4, is changing. They pile up pillows on our bed and sit close, Walt often with his arm around Owen’s shoulders, trying to hold him — and the shifting world — in place. © 2014 The New York Times Company
Link ID: 19341 - Posted: 03.10.2014
Alison Abbott A simple blood test has the potential to predict whether a healthy person will develop symptoms of dementia within two or three years. If larger studies uphold the results, the test could fill a major gap in strategies to combat brain degeneration, which is thought to show symptoms only at a stage when it too late to treat effectively. The test was identified in a preliminary study involving 525 people aged over 70. The work identified a set of ten lipid metabolites in blood plasma that distinguished with 90% accuracy between people who would remain cognitively healthy from those who would go on to show signs of cognitive impairment. “These findings are potentially very exciting,” says Simon Lovestone, a neuroscientist at the University of Oxford, UK, and a cordinator of a major European public-private partnership seekimg biomarkers for Alzheimer's. But he points out that only 28 participants developed symptoms similar to those of Alzheimer's disease during the latest work. “So the findings need to be confirmed in independent and larger studies.” There is not yet a good treatment for Alzheimer’s disease, which affects 35 million people worldwide. Several promising therapies have been tested in clinical trials over the last few years, but all have failed. However, those trials involved people who had already developed symptoms. Many neuroscientists fear that any benefits of a treatment would be missed in such a study, because it could be impossible to halt the disease once it has manifested. “We desperately need biomarkers which would allow patients to be identified — and recruited into trials — before their symptoms begin,” says Lovestone. © 2014 Nature Publishing Group,
Link ID: 19340 - Posted: 03.10.2014
By INNA GAISLER-SALOMON WE intuitively understand, and scientific studies confirm, that if a woman experiences stress during her pregnancy, it can affect the health of her baby. But what about stress that a woman experiences before getting pregnant — perhaps long before? It may seem unlikely that the effects of such stress could be directly transmitted to the child. After all, stress experienced before pregnancy is not part of a mother’s DNA, nor does it overlap with the nine months of fetal development. Nonetheless, it is undeniable that stress experienced during a person’s lifetime is often correlated with stress-related problems in that person’s offspring — and even in the offspring’s offspring. Perhaps the best-studied example is that of the children and grandchildren of Holocaust survivors. Research shows that survivors’ children have greater-than-average chances of having stress-related psychiatric illnesses like post-traumatic stress disorder, even without being exposed to higher levels of stress in their own lives. Similar correlations are found in other populations. Studies suggest that genocides in Rwanda, Nigeria, Cambodia, Armenia and the former Yugoslavia have brought about distinct psychopathological symptoms in the offspring of survivors. What explains this pattern? Does trauma lead to suboptimal parenting, which leads to abnormal behavior in children, which later affects their own parenting style? Or can you biologically inherit the effects of your parents’ stress, after all? It may be the latter. In a study that I, together with my colleagues Hiba Zaidan and Micah Leshem, recently published in the journal Biological Psychiatry, we found that a relatively mild form of stress in female rats, before pregnancy, affected their offspring in a way that appeared to be unrelated to parental care. © 2014 The New York Times Company
New findings reveal how a mutation, a change in the genetic code that causes neurodegeneration, alters the shape of DNA, making cells more vulnerable to stress and more likely to die. The particular mutation, in the C9orf72 gene, is the most common cause for amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease), and frontotemporal degeneration (FTD), the second most common type of dementia in people under 65. This research by Jiou Wang, Ph.D., and his colleagues at Johns Hopkins University (JHU) was published in Nature and was partially funded by the National Institutes of Health’s National Institute of Neurological Disorders and Stroke (NINDS). In ALS, the muscle-activating neurons in the spinal cord die, eventually causing paralysis. In FTD neurons in particular brain areas die leading to progressive loss of cognitive abilities. The mutation may also be associated with Alzheimer’s and Huntington’s diseases. DNA contains a person’s genetic code, which is made up of a unique string of bases, chemicals represented by letters. Portions of this code are divided into genes that provide instructions for making molecules (proteins) that control how cells function. The normal C9orf72 gene contains a section of repeating letters; in most people, this sequence is repeated two to 25 times. In contrast, the mutation associated with ALS and FTD can result in up to tens of thousands of repeats of this section.
By Tara Bahrampour, Alzheimer’s disease likely plays a much larger role in the deaths of older Americans than is reported, according to a new study that says the disease may be the third-leading cause of death in the United States. The Centers for Disease Control and Prevention lists Alzheimer’s as the sixth-leading cause of death, far below heart disease and cancer. But the new report, published Wednesday in the medical journal of the American Academy of Neurology, suggests that the current system of relying on death certificates for causes misses the complexity of dying for many older people and underestimates the impact of Alzheimer’s. While the CDC attributed about 84,000 deaths in 2010 to Alzheimer’s, the report estimated that number to be 503,400 among people 75 and older. That puts it in a close third place, behind heart disease and cancer, and well above chronic lung disease, stroke and accidents, which rank third, fourth and fifth. Alzheimer’s is somewhat of a sleeping giant compared with other leading killers that have received more funding over the years. While deaths from these diseases have been going down thanks to better treatment and prevention, the number of people suffering from Alzheimer’s is quickly rising and the disease is always fatal. More than 5 million people in the United States are estimated to have Alzheimer’s. With the aging of the baby-boom generation, this number is expected to nearly triple by 2050 if there are no significant medical breakthroughs, according to the Alzheimer’s Association. © 1996-2014 The Washington Post
Link ID: 19326 - Posted: 03.06.2014
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,